Effect of left atrial to left femoral artery bypass and renin-angiotensin system blockade on renal blood flow and function during and after thoracic aortic occlusion

Temporary thoracic aortic occlusion can result in renal insufficiency with or without adjuncts to avoid distal hypoperfusion. In a canine model of thoracic aortic occlusion, left atrial to left femoral bypass was compared with blockade of the renin-angiotensin system. Renin-angiotensin system blockade with the converting enzyme inhibitor, MK422, resulted in restoration of baseline renal blood flow and glomerular filtration 30 minutes after cross-clamp release. Left atrial to left femoral bypass resulted in significant reduction in both renal blood flow and glomerular filtration 30 minutes after cross-clamp release. Stimulation of the renin-angiotensin system plays a significant role in the altered renal hemodynamics and glomerular filtration rates after thoracic aortic occlusion.     

Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome

We studied the effect of thoracic aortic occlusion and cerebrospinal fluid (CSF) drainage on regional spinal cord blood flow and its correlation with neurologic outcome. Using isotope-tagged microspheres, we determined blood flow to the gray and white matter of five regions of the spinal cord in dogs: group I (control), group II (cross-clamp only), group III (cross-clamp plus CSF drainage). At 60 minutes after thoracic aortic occlusion in group II, median gray matter blood flow (GMBF) in the lower thoracic and lumbar cord decreased from 23.1 and 27.0 ml/100 gm/min at baseline to 4.0 and 2.5 ml/100 gm/min, respectively. The addition of CSF drainage improved GMBF during aortic cross-clamping in the lower thoracic and lumbar cord to 11.3 (p less than 0.05) and 15.1 ml/100 gm/min (p less than 0.03), respectively. After removal of the aortic cross-clamp, median blood flow more than tripled from baseline blood flow in group II, whereas CSF drainage prevented significant reperfusion hyperemia. Both low GMBF during cross-clamping and reperfusion hyperemia were associated with a worse neurologic outcome. In group II, no dog was neurologically normal, and more than 60% of the dogs had spastic paraplegia. In contrast, almost 60% of dogs in group III were normal, and none had spastic paraplegia (p less than 0.001). We conclude that CSF drainage in dogs during thoracic aortic occlusion maintained spinal cord perfusion above critical levels, diminished reperfusion hyperemia, and improved neurologic outcome.     

Effects of aortic occlusion on regional spinal cord blood flow and somatosensory evoked potentials in sheep

Somatosensory evoked potentials (SEPs) were recorded continuously during aortic occlusion in sheep, with simultaneous measurement of spinal cord blood flow (SCBF) by radiolabeled microspheres. Aortic occlusion was associated with disappearance of the SEPs in seven of nine sheep in 7.8 +/- 4.1 (SD) minutes. SCBF at the time of initial cross clamping and 30 minutes after the onset of ischemia revealed a severe reduction in white and gray matter flow in the thoracolumbar cord. Release of the aortic clamp was associated with reactive hyperemia in these ischemic regions. In two animals, the SEP persisted during aortic cross clamping. The total SCBF in the thoracic and lumbar regions of these two animals exceeded 20 ml/100 g/min after 30 minutes of ischemia and was significantly greater than the flow recorded in sheep whose evoked response disappeared. The relation between spinal cord ischemia and evoked potential alterations is discussed in detail.     

The effect of hyperemia on spinal cord function after temporary thoracic aortic occlusion

Nineteen mongrel dogs had 30 minutes of thoracic aortic occlusion to determine the effects that blockade of the renin-angiotensin system may have on preserving spinal cord blood flow and function during a period of temporary spinal cord ischemia. Cross-clamping of the thoracic aorta causes renal ischemia and activates the renin-angiotensin system with resulting increased production of angiotensin II. Angiotensin II is a potent peripheral constrictor and elevated levels may constrict collateral spinal cord circulation. At the time of aortic cross-clamping, 10 dogs received 100 mg/kg of MK422 (intravenous enalapril maleate), a converting enzyme inhibitor, and nine animals served as controls. The blockade of the renin-angiotensin system had no preserving effects on spinal cord flow as measured by microspheres and on spinal cord function as graded with the Tarlov scale. However, the paraplegic animals all had significantly increased lower thoracic and lumbar spinal cord flows 30 minutes after clamp release when compared with those animals that remained neurologically intact. In conclusion, marked hyperemia occurring after a period of hypoperfusion may lead to spinal cord edema and compartment syndrome with resulting paraplegia.     

The effect of mannitol and dopamine on the renal response to thoracic aortic cross-clamping

Postoperative renal failure and insufficiency are important complications of operations that require thoracic aortic cross-clamping. Successful application of pharmacologic methods to protect renal function would be clinically useful. The ability of mannitol and dopamine to prevent renal dysfunction in a canine model of thoracic aortic cross-clamping was studied. Twenty animals were divided into four equal groups, and all underwent thoracic aortic cross-clamping for 60 minutes. An intra-aortic infusion of saline (control), mannitol, dopamine, or mannitol plus dopamine was started before, and continued during, the period of aortic occlusion. Glomerular filtration rate was significantly depressed 60 minutes after clamp release, and although there was some recovery in treated animals 150 minutes after clamp release, it remained significantly decreased (52% to 73% of baseline values, p less than 0.01). Renal blood flow was significantly reduced 60 minutes after clamp release, and there was no recovery in any group at 150 minutes (38% to 56% of baseline values, p less than 0.01). No significant differences in osmolar clearance or fractional excretion of sodium were evident between groups. These data reveal that the profound reductions in glomerular filtration and renal blood flow induced by thoracic aortic cross-clamping were not attenuated by mannitol or dopamine and suggest that efforts to protect renal function should be directed toward improving renal blood flow in the post-clamp period.     

A sheep model for thoracic aortic surgery in the presence of systemic coagulopathy.

Surgical repair of aneurysms, traumatic injuries, or congenital anomalies of the thoracic aorta are associated with high morbidity and mortality mainly as a result of excessive and uncontrollable hemorrhage from diffuse coagulopathy. We developed a model in sheep that simulates this coagulopathic state for experimentation with thoracic aorta surgery. This experimental animal model involves administering a 600-mg aspirin suppository once a day for the 2 days preceding surgery and a final dose on-call to surgery. Prior to cross-clamping the aorta, an intravenous (i.v.) bolus of heparin (400 IU/kg) was administered. Thirty minutes later, the i.v. heparin bolus was repeated. Pre- and intraoperative activated clotting time was 101 +/- 10 s and >1500 s (p < .0001); prothrombin time, 21 +/- 1 s and >100 s (p < .0001); and activated partial thromboplastin time, 20 +/- 1 s and >50 s (p < .0001), respectively. We utilized a partial cross-clamp-and-sew technique to anastomose a woven, gelatin-impregnated, 16-mm tube graft end-to-side to the descending thoracic aorta. Mean total blood loss was 1367 +/- 282 mL, which included mean blood loss from time of release of aortic cross-clamp to close (422 +/- 135 mL) and mean total blood output from chest tube drain (945 +/- 203 mL). The mean time to achieve hemostasis at suture lines after aortic cross-clamp release was 15.5 +/- 6.6 min. In conclusion, a sheep model with induced coagulation defects was successfully developed and reproducible for experimentation involving thoracic aortic surgery.     

Should initial clamping for abdominal aortic aneurysm repair be proximal or distal to minimise embolisation?

OBJECTIVES: to determine whether clamping proximally or distally on the infrarenal aorta during abdominal aortic aneurysm (AAA) repair increases the overall embolic potential. MATERIALS AND METHODS: a sheath was placed in the mid-infrarenal aorta of 16 dogs. In eight animals a cross-clamp was placed at the aortic trifurcation, and in another eight animals it was placed in the immediate subrenal position. Under fluoroscopy blood flow within the infrarenal aorta was evaluated by contrast and particle injections. Grey-scale analysis was used to calculate contrast density. Particle distribution was followed fluoroscopically and confirmed pathologically. RESULTS: fifty-seven+/-24% of injected contrast remained within the aorta with distal clamping while 97+/-7% did so with proximal clamping (p<0.01). With distal aortic clamping 6.2+/-1. 3 out of 10 injected particles remained within the aorta after 15 seconds and only 0.8+/-0.8 remained after 5 min. With proximal aortic clamping, all 10 of the particles remained within the aortic lumen for the full 5 minutes (p<0.001). CONCLUSIONS: initial distal clamping minimises distal embolisation, but may result in renal and/or visceral embolisation. Initial proximal clamping prevents proximal embolisation and does not promote distal embolisation. We recommend initial proximal clamping in aortic aneurysm surgery to minimise the overall risk of embolisation.     

Stapled aortic anastomoses: a minimally invasive, feasible alternative to videoscopic aortic suturing?

Widespread applications of totally laparoscopic aortic reconstructions have been limited by the long cross-clamp time required to suture the aortic anastomosis despite improvement in instrumentation. The authors' hypothesis was that a "one-step anastomosis concept" using an intraluminal stapler would allow shorter cross-clamp time but similar patency and imperviousness as videoscopic suturing techniques. An intraluminal stapler (Endopath-ILS, Ethicon) with a modified anvil was used to perform videoscopic-assisted thoracic aorta-to-iliac artery bypass with a 21 mm by 8 mm polytetrafluoroethylene (PTFE) graft in 22 sheep through a minimally invasive approach using a 5 cm thoracotomy. The graft-to-iliac artery anastomoses were hand sutured through a flank incision. Twelve sheep were used to establish the technique and 10 subsequent animals constituted the study group. Aortic cross-clamp time, imperviousness, and need for additional sutures were recorded and compared to previously reported data using videoscopic suturing in pigs. Patency was assessed by comparing lower limb arterial pressures. Macroscopic and microscopic examinations of the anastomoses were performed at different time-points within the first 3 months. Videoscopic-assisted stapled anastomoses were also performed on atherosclerotic aortas of 3 human cadavers. Stapled anastomoses between the thoracic aorta and PTFE graft were completed in 8 of 10 animals. Two animals were euthanized after stapler failure and anastomotic bleeding. Sutures to strengthen the anastomosis had to be used in 4 cases. Mean aortic cross-clamp time in 8 successful cases was 4.3 +/-2.9 minutes (range 2-11 minutes) and was significantly shorter than clamp time of videoscopic suturing technique (48.7 +/-9.4 minutes, p < 0.0001). Imperviousness was good or excellent in 4 animals and fair in 4 animals. All anastomoses were patent at the end of the procedure. Examination of the anastomosis of the 2 failed interventions showed medial aortic tear surrounding the anastomosis in 1 case and misfired staples in the other. No graft occlusion was noted during follow-up ranging from 0 to 12 weeks. At the time of harvest, no bleeding was noted after epinephrine and volume infusion to increase mean arterial pressure to 200 mm Hg for 15 minutes. Macroscopic examination of the anastomoses revealed adequate healing with circumferential stapling of the prosthesis to the aortic wall and no stenosis or thrombus except in 1 false aneurysm (1/7, 14%). Surface electron microscopy showed cells coverage of the anastomosis surface. When applied on human cadaver thoracic and abdominal aorta with atherosclerotic changes, clamping times of less than 5 minutes were achieved. However, imperviousness tested with saline was poor. An automatic stapling device allows performance of a graft-to-aorta anastomosis through a minimally invasive approach with shorter clamping time than a videoscopic suturing technique. However, the current technique of aortic stapling is unreliable and further improvements are needed.     

Improvement in thoracic aortic pressure after proximal aortic cross-clamping by balloon occlusion of the distal aorta

Spinal cord hypoperfusion injury is a devastating complication of cross-clamping the proximal thoracic aorta. The collateral circulation around the cross-clamp is generally poorly developed, and the run-off is immense, resulting in extremely low thoracic aortic and spinal cord perfusion pressures. The authors postulated that balloon occlusion of the abdominal aorta might confine this reduced collateral flow around the cross-clamp to the thoracic aorta. In 8 of 16 dogs subjected to aortic cross-clamping of the aorta just beyond the arch vessels, the abdominal aorta was also occluded by a balloon. Thoracic aortic pressure and spinal cord perfusion pressure were significantly higher in the animals with aortic balloon occlusion than in those without balloon occlusion (77 +/- 8 mm Hg versus 26 +/- 1 mm Hg, p less than 0.01, and 67 +/- 8 mm Hg versus 18 +/- 2 mm Hg, p less than 0.01, at 10 minutes after cross-clamping). Abdominal aortic balloon occlusion increases thoracic aortic pressure after the aorta is cross-clamped proximally. Further studies are necessary in primates to assess the effect of this procedure in spinal cord perfusion and the rate of paraplegia.     

The effects of fenoldopam on renal function in patients undergoing elective aortic surgery

BACKGROUND AND OBJECTIVE: Postoperative renal impairment is a recognized complication of infrarenal aortic cross-clamping. Our hypothesis was that the renal vasodilating and natriuretic effects of fenoldopam mesylate, a selective dopamine (DA1) agonist, would preserve renal function in patients undergoing elective infrarenal aortic cross-clamping. METHODS: A prospective, randomized, double blind controlled clinical trial was performed. Twenty-eight ASA II-III patients undergoing elective aortic surgery requiring infrarenal aortic cross-clamping were studied. According to random allocation, patients received either fenoldopam (0.1 microg kg(-1) min(-1)) or placebo intravenously prior to surgical skin incision until release of the aortic clamp. Plasma creatinine, creatinine clearance, urinary output, fractional excretion of sodium, and free water clearance were measured: (a) prior to admission to hospital; (b) during the period from insertion of the urinary catheter until application of the aortic cross-clamp; (c) during the period of aortic cross-clamping; (d) 0-4 h, and (e) 4-8 h after release of the clamp and on days 1, 2, 3, and 5 postoperatively. RESULTS: Fenoldopam (0.1 microg kg(-1)min(-1)) administration was not associated with haemodynamic instability. On application of the aortic cross-clamp creatinine clearance decreased significantly in the placebo (83 +/- 20 to 42 +/- 29 mL min(-1) (mean +/- SD)) (P < 0.01) but not in the fenoldopam group, and this decrease persisted for at least 8 h after release of the cross-clamp (83 +/- 20 to 54 +/- 33 mL min(-1) (mean +/- SD)) (P < 0.05). Plasma creatinine concentration increased significantly from baseline on the first postoperative day in the placebo group (87 +/- 12 to 103 +/- 28 micromolL(-1) (mean +/- SD)) (P < 0.01) but not in the fenoldopam group. CONCLUSIONS: These findings are consistent with the hypothesis that fenoldopam possesses a renoprotective effect during and after infrarenal aortic cross-clamping.     

Hemodynamic Benefit of Positive End-expiratory Pressure during Acute Descending Aortic Occlusion

Background: Acute aortic occlusion in vascular surgery patients abruptly increases arterial resistance and blood pressure, which, in turn, makes subsequent volume expansion during cross-clamp application difficult. The use of vasodilatory drugs or volatile anesthetic agents to attenuate this response may have persistent detrimental effects after clamp removal. Another potential therapy that produces rapid effects on myocardial loading conditions is positive end-expiratory pressure (PEEP). In a porcine model of acute aortic clamping, the hemodynamic consequences of 15 cm H2O PEEP with and without plasma volume expansion were studied.

Methods: Forty anesthetized pigs underwent 30-min occlusion of the abdominal aorta 1 cm above the origin of the celiac artery. Animals were randomly divided into four treatment groups (n = 10 each) to receive 15 cm H2O PEEP or zero end-expiratory pressure (ZEEP) with or without plasma volume expansion using 6% hetastarch (10 ml/kg) during cross-clamp application. Mean aortic pressure was measured with a transducer-tipped catheter placed in the ascending aorta; stroke volume was calculated using thermodilution cardiac output. End-expiratory pressure was discontinued upon aortic declamping, and animals were studied over the ensuing 30-min period.

Results: Aortic occlusion doubled systemic vascular resistance in all groups. Mean aortic blood pressure increased significantly in both ZEEP groups at 1 and 5 min but not in animals treated with 15 cm H2O PEEP. The application of PEEP with aortic cross-clamping reduced cardiac output and stroke volume by nearly 50%. Cardiac output and stroke volume increased after volume expansion regardless of end-expiratory pressure. After aortic declamping, aortic blood pressure decreased in all groups but was significantly greater in the PEEP + volume group than in either ZEEP group. Similarly, 5 min after declamping, stroke volume was greatest in the PEEP + volume animals.     

Hemodynamic benefit of positive end-expiratory pressure during acute descending aortic occlusion

BACKGROUND: Acute aortic occlusion in vascular surgery patients abruptly increases arterial resistance and blood pressure, which, in turn, makes subsequent volume expansion during cross-clamp application difficult. The use of vasodilatory drugs or volatile anesthetic agents to attenuate this response may have persistent detrimental effects after clamp removal. Another potential therapy that produces rapid effects on myocardial loading conditions is positive end-expiratory pressure (PEEP). In a porcine model of acute aortic clamping, the hemodynamic consequences of 15 cm H(2)O PEEP with and without plasma volume expansion were studied.(2) METHODS: Forty anesthetized pigs underwent 30-min occlusion of the abdominal aorta 1 cm above the origin of the celiac artery. Animals were randomly divided into four treatment groups (n = 10 each) to receive 15 cm H(2)O PEEP or zero end-expiratory pressure (ZEEP) with or without plasma volume expansion using 6% hetastarch (10 ml/kg) during cross-clamp application. Mean aortic pressure was measured with a transducer-tipped catheter placed in the ascending aorta; stroke volume was calculated using thermodilution cardiac output. End-expiratory pressure was discontinued upon aortic declamping, and animals were studied over the ensuing 30-min period. RESULTS: Aortic occlusion doubled systemic vascular resistance in all groups. Mean aortic blood pressure increased significantly in both ZEEP groups at 1 and 5 min but not in animals treated with 15 cm H(2)O PEEP. The application of PEEP with aortic cross-clamping reduced cardiac output and stroke volume by nearly 50%. Cardiac output and stroke volume increased after volume expansion regardless of end-expiratory pressure. After aortic declamping, aortic blood pressure decreased in all groups but was significantly greater in the PEEP + volume group than in either ZEEP group. Similarly, 5 min after declamping, stroke volume was greatest in the PEEP + volume animals. CONCLUSIONS: Fifteen cm H(2)O PEEP reduces the hypertensive response to acute aortic occlusion and allows concomitant volume expansion. Consequently, stroke volume and blood pressure are better maintained after clamp removal in PEEP + volume animals. The use of PEEP during acute aortic occlusion in patients may allow rapid control of loading conditions to attenuate systemic hypertension while permitting simultaneous volume expansion.     

Studies of myocardial protection in the immature heart. V. Safety of prolonged aortic clamping with hypocalcemic glutamate/aspartate blood cardioplegia

This study tests the hypothesis that multidose, hypocalcemic aspartate/glutamate-enriched blood cardioplegia provides safe and effective protection during prolonged aortic clamping of immature hearts. Of 17 puppies (6 to 8 weeks of age, 3 to 5 kg) placed on vented cardiopulmonary bypass, five were subjected to 60 minutes of 37 degrees C global ischemia without cardioplegic protection and seven underwent 120 minutes of aortic clamping with 4 degrees C multidose aspartate/glutamate-enriched blood cardioplegia ([Ca++] = 0.2 mmol/L), preceded and followed by 37 degrees C blood cardioplegic induction and reperfusion. Five puppies underwent blood cardioplegic perfusion for 10 minutes without intervening ischemia to assess the effect of the cardioplegic solution and the delivery techniques. Left ventricular performance was assessed 30 minutes after bypass was discontinued (Starling function curves). Hearts were studied for high-energy phosphates and tissue amino acids. One hour of normothermic ischemia resulted in profound functional depression, with peak stroke work index only 43% of control (0.7 +/- 0.1 versus 1.7 +/- 0.2 gm x m/kg, p less than 0.05). There was 70% depletion of adenosine triphosphate (7.6 +/- 1 versus control 20.3 +/- 1 mumol/gm dry weight, p less than 0.05) and 75% glutamate loss (6.6 +/- 1 versus control 26.4 +/- 3 mumol/gm, p less than 0.05). In contrast, after 2 hours of aortic clamping with multidose blood cardioplegia preceded and followed by 37 degrees C blood cardioplegia, there was complete recovery of left ventricular function (peak stroke work index 1.6 +/- 0.2 gm x m/kg) and maintenance of adenosine triphosphates, glutamate, and aspartate levels at or above control levels adenosine triphosphate 18 +/- 2 mumol/gm, aspartate 21 +/- 1 versus control 2 mumol/gm, and glutamate 25.4 +/- 2 mumol/gm). Puppy hearts receiving blood cardioplegic perfusion without ischemia had complete recovery of control stroke work index. We conclude that methods of myocardial protection used in adults, with amino acid-enriched, reduced-calcium blood cardioplegia, can be applied safely to the neonatal heart and allow for complete functional and metabolic recovery after prolonged aortic clamping.     

Influence of the descending thoracic aortic cross clamping on bispectral index value and plasma propofol concentration in humans

BACKGROUND: In this study, the authors investigated changes in Bispectral Index (BIS) values and plasma propofol concentrations (Cp) after aortic cross clamping in the descending thoracic aortic aneurysm repair surgery during propofol anesthesia. METHODS: Prospectively, in 10 patients undergoing thoracic aortic surgery during total intravenous anesthesia with propofol, BIS values were recorded during cross clamping of the descending thoracic aorta. In this study, the rate of propofol infusion was controlled to keep the BIS value between 30 and 60 throughout surgery. Simultaneously, Cp values in the blood samples taken from the right radial artery (area proximal to cross clamping) and the left femoral artery (area distal to cross clamping) were measured. RESULTS: Approximately 15 min after initiating aortic cross clamping, BIS values in all cases started to decrease abruptly. Cp values of samples taken from the radial artery after cross clamping of the aorta were significantly (P < 0.05) increased compared with pre-cross clamp values (1.8 +/- 0.4 microg/ml), and the mean Cp after aortic cross clamping varied between 3.0 and 5.3 microg/ml. In addition, there were significant differences in the Cp values between radial arterial and femoral arterial blood samples throughout aortic cross clamping. Cp values in samples from the radial artery were approximately two to seven times higher than those from the femoral artery. CONCLUSIONS: This study showed that Cp values increased and BIS values decreased rapidly after aortic cross clamping in thoracic aortic aneurysm repair surgery during propofol anesthesia. These findings suggested that all anesthesiologists should control the infusion rate carefully, taking the abrupt changes in its pharmacokinetics into consideration, especially during cross clamping of the descending thoracic aorta.     

Influence of the Descending Thoracic Aortic Cross Clamping on Bispectral Index Value and Plasma Propofol Concentration in Humans

Background: In this study, the authors investigated changes in Bispectral Index (BIS) values and plasma propofol concentrations (Cp) after aortic cross clamping in the descending thoracic aortic aneurysm repair surgery during propofol anesthesia.

Methods: Prospectively, in 10 patients undergoing thoracic aortic surgery during total intravenous anesthesia with propofol, BIS values were recorded during cross clamping of the descending thoracic aorta. In this study, the rate of propofol infusion was controlled to keep the BIS value between 30 and 60 throughout surgery. Simultaneously, Cp values in the blood samples taken from the right radial artery (area proximal to cross clamping) and the left femoral artery (area distal to cross clamping) were measured.

Results: Approximately 15 min after initiating aortic cross clamping, BIS values in all cases started to decrease abruptly. Cp values of samples taken from the radial artery after cross clamping of the aorta were significantly (P < 0.05) increased compared with pre-cross clamp values (1.8 +/- 0.4 [mu]g/ml), and the mean Cp after aortic cross clamping varied between 3.0 and 5.3 [mu]g/ml. In addition, there were significant differences in the Cp values between radial arterial and femoral arterial blood samples throughout aortic cross clamping. Cp values in samples from the radial artery were approximately two to seven times higher than those from the femoral artery.     

Halothane and Xanthine Oxidase Increase Hepatocellular Enzyme Release and Circulating Lactate after Ischemia-Reperfusion in Rabbits

Background: Multiple-organ injury often occurs after aortic occlusion-reperfusion. Oxidants derived from xanthine oxidase have been implicated as a source of injury after aortic occlusion-reperfusion. Halogenated anesthetics modify oxidant-mediated injury. The current study determined if halothane modifies hepatocellular enzyme release (e.g., alanine aminotransferase) and circulating lactate after aortic occlusion-reperfusion.

Methods: Rabbits were randomly assigned to one of four groups that underwent 40 min of thoracic aortic occlusion and 2 h of reperfusion: Two groups were given either halothane or fentanyl plus droperidol anesthesia and two groups were given either anesthetic and sodium tungstate (xanthine oxidase inactivator). Each of the four groups was then matched with a similarly treated group that did not undergo aortic occlusion.

Results: Halothane anesthesia was associated with significantly (P < 0.05) increased release of alanine aminotransferase (34 +/- 9 U/l at baseline and 539 +/- 370 U/l at 120 min of reperfusion; mean +/- SD) and increased plasma lactate concentrations (2.8 +/- 2.0 mM at baseline and 12.1 +/- 9.7 mM at 120 min of reperfusion) after aortic occlusion-reperfusion compared with fentanyl plus droperidol anesthesia (alanine aminotransferase, 33 +/- 12 U/l and 148 +/- 109 U/l; lactate, 3.4 +/- 2.0 mM and 3.8 +/- 1.2 mM at baseline and 120 min of reperfusion, respectively). Inactivation of xanthine oxidase significantly decreased the release of hepatocellular enzymes (P < 0.05) and decreased circulating lactate in animals anesthetized with halothane after aortic occlusion-reperfusion.     

The effect of the pneumatic antishock garment (PASG) on hemodynamics, hemorrhage, and survival in penetrating thoracic aortic injury

To determine if the increased blood pressure associated with application of a pneumatic antishock garment (PASG) affects outcome in thoracic hemorrhage, we assessed hemodynamics, blood loss, and survival in three groups of eight anaesthetized piglets with a 2.5-mm laceration of the descending thoracic aorta. Baseline measurements were made before aortic hemorrhage. During one hour of aortic hemorrhage or until death of the animal, the PASG was not inflated in Group I while the PASG in the other two groups was inflated to maintain carotid artery pressure at 15 torr below baseline (Group II) and at baseline (Group III), respectively. Survival was 100% in Group I, 50% in Group II, and 0% in Group III. Hemorrhage at 22.5 +/- 4.0 mL/min stopped after 18-24 minutes in Group I; the survivors in Group II bled at a rate of 32.5 +/- 3.0 mL/min compared with 43.6 +/- 4.0 mL/min over 26-35 minutes in the Group II nonsurvivors. Group III pigs bled at 107.5 +/- 8.0 mL/min over the 10-18 minutes of survival. The intended blood pressure could not be maintained beyond 30 minutes. Bleeding stopped in Group I when the blood pressure fell to 58.2 +/- 4.5 torr from a baseline of 119.0 +/- 10.0 torr. The blood pressure fell to 48.0 +/- 5.0 torr in the four Group-II survivors. After a transient maintenance of baseline blood pressure in Group III, a precipitous drop in blood pressure with death in 10-18 minutes occurred in all these animals. In this porcine model of thoracic aortic injury, PASG inflation increases hemorrhage and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right and left ventricular performance during and after abdominal aortic aneurysm repair.

To evaluate the effect of aortic occlusion and limb reperfusion on global and regional function of the right and left ventricle during infrarenal abdominal aortic aneurysm repair, 23 patients underwent five intraoperative first-pass radionuclide angiocardiograms: 1) before the skin incision, 2) at aortic cross-clamp, 3) 20 minutes after aortic occlusion, 4) at unclamping, and 5) after skin closure. A subset of twelve patients had simultaneous transesophageal echocardiography to evaluate left ventricular wall stress. Parameters measured included the electrocardiogram (ECG), heart rate, blood pressure, pulmonary artery pressure, the cardiac output, the left and right ventricular ejection fractions, left ventricular volumes, and left ventricular wall stress. Significant changes (p less than 0.01) were observed at aortic clamping in the left ventricular ejection fraction (from 0.56 to 0.48), end-diastolic volume (from 171 to 225 ml), end-systolic volume (from 85 to 127 ml), mean blood pressure (from 82 to 91 mmHg), and meridional end-systolic wall stress (from 53 to 67 10(3) dyne/cm2). Once the clamp was removed, significant variations were seen in the left ventricular ejection fraction (from 0.51 to 0.58), end-diastolic volume (from 205 to 187 ml), end-systolic volume (from 105 to 94 ml), mean blood pressure (from 84 to 69 mmHg), and meridional end-systolic wall stress (from 67 to 46 10(3) dyne/cm2). No differences were observed between the two aortic occlusion studies, and the baseline level of function was recovered in all parameters during the last study. These data quantify the changes in heart function that occur during abdominal aortic aneurysm operation and demonstrate that the majority of the adaptations that occurred were due to a variation in afterload.     

RETRACTED ARTICLE: Hemodynamics, intra-mucosal pH and regulators of circulation during perioperative epidural analgesia

PURPOSE: To evaluate the effects of perioperative epidural analgesia on hemodynamics, splanchnic perfusion and regulators of circulation. METHODS: Twenty patients undergoing aortic surgery were randomised into two groups: epidural analgesia group (EAG): epidural analgesia with bupivacaine (15 ml, 0.125%) was started before surgery. Eight and 16 hr postoperatively 10 ml bupivacaine 0.125% and 1 mg morphine were given. Control group (COG): patients received no epidural catheter. Monitoring included pulmonary artery catheter and gastric tonometer. Norepinephrine, epinephrine, renin, ADH, ANP and endothelin were measured: before epidural analgesia (T0), before aortic clamping (T1), 20 min after aortic clamping (T2), after declamping the first leg (T3), at end of surgery (T4), one hour (T5) and 24 hr postoperatively (T6). RESULTS: At T5 mean arterial blood pressure decreased in EAG compared with baseline (86 +/- 16 to 75 +/- 8 mmHg) and compared with COG (75 +/- 8 vs 84 +/- 11 mmHg). At T2 pulmonary capillary wedge pressure and cardiac index increased and at T6 decreased in both groups. Systemic vascular resistance decreased at T I and at T3-T5 in EAG compared with COG and at T1 and T3-T6 to baseline (1472 +/- 448 to 1027 +/- 184 dyn x sec x cm(-5) x m(-2)). In EAG and in COG, pHi decreased compared with baseline but without group differences. In both groups, epinephrine, norepinephrine, renin, and ADH levels increased from baseline. Endothelin and ANP levels showed no changes. CONCLUSIONS: Perioperatively administrated epidural bupivacaine has no beneficially effects on hemodynamics, pHi or release of regulators of circulation.     

Intrathecal perfusion of an oxygenated perfluorocarbon prevents paraplegia after aortic occlusion.

A canine model was used to evaluate the effects of continuous intrathecal perfusion of an oxygenated perfluorocarbon emulsion on systemic and cerebral hemodynamics and neurologic outcome after 70 minutes of normothermic aortic occlusion. Twelve mongrel dogs were instrumented to monitor proximal and distal arterial blood pressure, cerebrospinal fluid pressure, spinal cord perfusion pressure, and somatosensory evoked potentials. The intrathecal perfusion apparatus consisted of two perfusing catheters, placed in the intrathecal space through a laminectomy, and a draining catheter percutaneously inserted in the cisterna cerebellomedullaris. The aorta was cross-clamped just distal to the left subclavian artery for 70 minutes. Animals were randomized into two groups: group 1 (n = 6) animals were treated with intrathecal perfusion of saline solution, whereas group 2 (n = 6) animals received oxygenated Fluosol-DA 20%. Data were acquired at baseline, during the cross-clamp period, and after reperfusion. Normothermic Fluosol or saline solution was infused at a rate of 15 mL/min beginning 15 minutes before cross-clamping and continued throughout the ischemic interval. There was no difference in proximal arterial blood pressure (97.2 versus 95.4 mm Hg; p > 0.05) or distal arterial blood pressure (14.6 versus 15.0; p > 0.05) between the two groups throughout the cross-clamp interval. Cerebrospinal fluid pressure rose significantly in both groups with the onset of intrathecal perfusion of either saline solution or Fluosol (7 +/- 1 versus 24 +/- 5 and 8 +/- 1 versus 40 +/- 4 mm Hg, respectively; p < 0.05). The rise in cerebrospinal fluid pressure was sustained throughout the perfusion interval in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)