Azygos venous blood flow in portal hypertension

Azygos venous blood flow estimated by the continuous thermodilution method was measured in 48 patients with portal hypertension. In patients with cirrhosis, azygos venous blood flow was 326 +/- 139ml/min (mean SD) and was significantly higher than in patients without portal hypertension (163 +/- 61ml/min). In patients with idiopathic portal hypertension and extrahepatic portal obstruction, azygos venous blood flow was 411 +/- 227ml/min and 328 +/- 85ml/min respectively. Azygos venous blood flow was significantly correlated with the hepatic venous pressure gradient but neither with cardiac output nor with size of esophageal varices. In eleven cirrhotic patients, azygos venous blood flow and other hemodynamic parameters were measured before and after the nonshunting operation of esophageal transection, splenectomy and esophagogastric devascularization. Azygos venous blood flow and hepatic venous pressure gradient were significantly reduced after operation. On the other hand, cardiac output did not change significantly after surgical procedure. Relatively high postoperative azygos venous blood flow indicates its important role in the postoperative collateral circulation.     

Central and Splanchnic Haemodynamics in the Dog During Controlled Hypotension with Sodium Nitroprusside

The effects of controlled hypotension induced by sodium nitroprusside (SNP) on central and splanchnic haemodynamics were studied in ten artificially ventilated dogs under neurolept anaesthesia. SNP was given intravenously as a continuous infusion in order to maintain a mean arterial blood pressure (MABP) of about 50 mmHg. Observations were made before (control) and at 20 and 60 min after the start of the SNP infusion. The mean SNP dosage was 13.7 micrograms X kg-1 X min-1. Systemic vascular resistance (SVR) decreased by 47%. After 20 min there was a 17% decrease in cardiac output, while the hepatic arterial blood flow was diminished by 39%, and portal venous blood flow by 16%. Cardiac output and portal venous blood flow tended to return towards control values at 60 min, while the hepatic arterial blood flow remained depressed. The total oxygen uptake was unaltered after 20 min, but slightly decreased after 60 min. There were no changes in hepatic or preportal tissue oxygen consumption, nor in hepatic lactate uptake. It is concluded that SNP-induced hypotension was achieved primarily by a profound reduction of SVR, and initially also by a slight decrease in cardiac output. Although splanchnic and hepatic blood flows decreased, there were no signs of hypoxia in the preportal tissues or in the liver.     

Arterialization of the portal blood with a new model of flow diversion: an experimental study

Arterialization of the portal blood with double shunts, cavo-mesenteric venous and femoro-femoral arterio-venous, was attempted in dogs. The experimental model was studied in three groups. Group-I was concerned with the condition immediately after establishment of the model. Group-II-A was referred to the study on the established model with hepatic artery ligation for seven days. Group-II-B was evaluated under hepatic artery ligation and absent participation in arterialization and shunts. The ratio of portal venous flow (PVF) to cardiac output (CO) in group-I revealed significant increase from 23 +/- 6% to 56 +/- 9% (p less than 0.01). Portal venous PO2 (PVO2) also increased from 48 +/- 7 mmHg to 65 +/- 9 mmHg (p less than 0.01). Portal venous pressure, however, remained below 200 mmH2O. Persistent increase of CO (150% of the control) and PVF/CO were seen in observation of group-II-A. Histopathological appearance of the liver was normal in group-II-A. Group-II-B revealed a high mortality rate (8/9) with necrosis of the liver by seventh postoperative day. The experimental model provides the useful flow diversion with arterialized blood to the portal flow. The arterialization of the portal flow may play an important role in the recovery of the ischemic liver cell in the preservation of the liver graft and in hepatic regeneration after extended resection.     

Hemodynamic Patterns in Human Hepatic Cirrhosis: A Prospective Randomized Study of the Hemodynamic Sequelae of Distal Splenorenal (Warren) and Mesocaval Shunts

Increasingly successful operative management of gastroesophageal variceal hemorrhage has been achieved by newer techniques of portal venous reconstruction. Although it is postulated that the clinical success may be due to more selectivity in portal venous shunting, direct determination of the effect of portasystemic shunt on portal vein blood flow has not been possible. Direct determinations of portal vein blood flow were performed preoperative on unanesthetized, hemodynamically stable cirrhotic patients by observation of radiopaque water-insoluble droplets. Patients were then randomized into elective distal splenorenal (Warren) or mesocaval shunt and determinations were performed postoperatively under similar conditions when clinically possible. Although portal vein blood flow was not significantly different before (929 +/- 147 ml/min) or after 899 +/- 271 ml/min) distal splenorenal shunt, there was a large change in portal vein blood flow after mesocaval shunt, decreasing from 772 +/- 177 ml/min (hepatopetal) to -1021 +/- 310 ml/min (hepatofugal) p < 0.01). After either procedure total hepatic blood flow (as determined by cardiac green clearance) was not significantly changed, nor was renal blood flow; however, cardiac output was significantly increased after mesocaval shunt. Thus the theoretical hemodynamic goals of the selective distal splenorenal shunt, i.e., preservation of the hepatopetal flow within the portal vein, is achieved as determined in the early postoperative period. The correlation between these changes and the eventual clinical outcome remains to be determined.     

Cardiovascular function during induced hypotension by fenoldopam or sodium nitroprusside in anesthetized dogs.

Fenoldopam, a selective dopamine1 receptor agonist, has been recommended for induced hypotension because it effectively lowers arterial blood pressure and improves renal perfusion. We examined cardiovascular functions during hypotension induced by fenoldopam or sodium nitroprusside. In eight halothane-anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers for the assessment of LV contractility using the analysis of the pressure-diameter relationship. Blood flow distribution was measured by radioactive microspheres. Doses of fenoldopam and nitroprusside were titrated to reduce mean arterial blood pressure to 60 mm Hg. After 40 min of hypotension, fenoldopam and nitroprusside caused similar increases in heart rate (17% +/- 4% vs 19% +/- 10%, respectively) and decreases in systemic vascular resistance (-24% +/- 5% vs -27% +/- 4%). Hypotension induced by fenoldopam was associated with higher LV end-diastolic pressure (4.4 +/- 0.6 vs 2.5 +/- 1.1 mm Hg) and end-systolic meridional wall stress (33.0 +/- 4.3 vs 17.8 +/- 2.1 g/cm2) when compared with nitroprusside. There were no significant changes in cardiac output and cardiac contractility as expressed by the slope (Ees) of the LV end-systolic pressure-diameter relationship, velocity of shortening of the diameter, and percentage of wall thickening of the LV. In contrast to nitroprusside, which decreased renal blood flow from 197 +/- 19 to 163 +/- 15 mL/min, renal blood flow increased during fenoldopam-induced hypotension from 187 +/- 20 to 239 +/- 18 mL/min. The increase in renal perfusion was similar in upper, middle, and lower regions of the kidney; however, it was more in the medulla compared with the cortex (37% +/- 17% vs 25% +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential effects on portal and effective hepatic blood flow. A comparison between transjugular intrahepatic portasystemic shunt and small-diameter H-graft portacaval shunt.

OBJECTIVE: This study was undertaken to determine the effects of transjugular intrahepatic portasystemic shunt (TIPS) and small-diameter prosthetic H-graft portacaval shunt (HGPCS) on portal and effective hepatic blood flow. SUMMARY BACKGROUND DATA: Mortality after TIPS is higher than after HGPCS for bleeding varices. This higher mortality is because of hepatic failure, possibly a result of excessive diminution of hepatic blood flow. METHODS: Forty patients randomized prospectively to undergo TIPS or HGPCS had effective hepatic blood flow determined 1 day preshunt and 5 days postshunt using low-dose galactose clearance. Portal blood flow was determined using color-flow Doppler ultrasound. RESULTS: Treatment groups were similar in age, gender, and Child's class. Each procedure significantly reduced portal pressures and portasystemic pressure gradients. Portal flow after TIPS increased (21 mL/second +/- 11.9 to 31 mL/second +/- 16.9, p < 0.05), whereas it remained unchanged after HGPCS (26 mL/second +/- 27.7 to 14 mL/second +/- 41.1, p = n.s.). Effective hepatic blood flow was diminished significantly after TIPS (1684 mL/minute +/- 2161 to 676 mL/minute +/- 451, p < 0.05) and was unaffected by HGPCS (1901 mL/ minute +/- 1818 to 1662 mL/minute +/- 1035, p = n.s.). CONCLUSIONS: Both TIPS and HGPCS achieved significant reductions in portal vein pressure gradients. Portal flow increased after TIPS, although most portal flow was diverted through the shunt. Effective hepatic flow is reduced significantly after TIPS but well preserved after HGPCS. Hepatic decompensation and mortality after TIPS may be because, at least in part, of reductions in nutrient hepatic flow.     

Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.

To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.     

Effect of low-dose vasopressin infusion on vital organ blood flow in the conscious normal and septic sheep

The effect of low-dose vasopressin (AVP) on vital regional circulations may be clinically relevant but has not been fully described. We sought to determine the effect of low-dose AVP on systemic haemodynamics, coronary, mesenteric and renal circulations in the conscious normal and septic mammal. We studied seven Merino sheep using a prospective randomized cross-over double-blind placebo-controlled animal design. We inserted flow probes around aorta, coronary, mesenteric and renal arteries and, three weeks later, we infused low-dose AVP (0.02 IU/min) or placebo in the normal and septic state induced by intravenous E. coli. In normal sheep, AVP (0.02 IU/min) induced a 17% decrease in mesenteric blood flow (393.0+/-134.9 vs 472.1+/-163.8 ml/min, P<0.05) and a 14% decrease in mesenteric conductance (P<0.05). In septic sheep, AVP decreased heart rate and cardiac output by 28% and 22%, respectively (P<0.05). It also decreased mesenteric blood flow and mesenteric conductance by 23% (flow: 468.5+/-159.7 vs 611.3+/-136.3 ml/min, P<0.05; conductance: 6.3+/-2.7 vs 8.2+/-2.7 ml/min/mmHg; P<0.05). Renal blood flow was unchanged but urine output and creatinine clearance increased (P<0.05). We conclude that low-dose AVP infusion has similar effects in the normal and septic mammalian circulation: bradycardia, decreased cardiac output, decreased mesenteric blood flow and conductance and increased urine output and creatinine clearance. This information is important to clinicians considering its administration in humans.     

A pilot study on early versus delayed hypertonic saline dextran resuscitation in a porcine model of near-lethal liver injury: early hemodynamic response and short-term survival

BACKGROUND: We studied the effects of early versus delayed fluid resuscitation on hemodynamic response and short-term survival in a porcine model of severe hepatic injury associated with hemorrhagic shock. MATERIALS AND METHODS: Eighteen anesthetized swine were randomized after standardized liver injury into two groups: early resuscitation (ER, n = 9) and delayed resuscitation (DR, n = 9). The ER and DR groups were resuscitated with hypertonic saline dextran (HSD) 20 min and 40 min after the injury, respectively. Mean arterial pressure (MAP), cardiac output (CO), and arterial blood gases were measured in addition to vascular blood flow rates in the aorta, hepatic artery and portal vein. The duration of follow-up was 100 min. RESULTS: MAP decreased from 112 +/- 4 to 23 +/- 2 mmHg (P < 0.05) during 20 min after the injury. Bolus infusion of HSD significantly elevated MAP, CO, and flow rates in the aorta, portal vein and common hepatic artery in both groups. Portal vein flow remained relatively high during the shock. Intra-abdominal bleeding (ER, 701 +/- 42 mL; DR 757 +/- 78 mL) and the mortality rate (ER 44%; DR 33%) did not differ between the groups 100 min after injury (P > 0.05). Aortic flow, portal vein flow, common hepatic artery flow, MAP, CO, PaO(2), PaCO(2), base deficit, pH, hemoglobin measurements, and the volume of blood shed into the intraperitoneal cavity did not affect survival in the Cox regression analysis. CONCLUSIONS: Early versus delayed fluid infusion with HSD resulted in a comparable hemodynamic response and survival 100 min after injury. No rebleeding was observed.     

Effects of enflurane and isoflurane on hepatic and renal circulations in chronically instrumented dogs

Seven dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic, portal, and renal blood flows. Each animal was studied on two separate occasions, awake and during 1.2, 1.4, 1.75, and 2.0 MAC isoflurane and enflurane. Both anesthetics induced tachycardia; to a greater degree than isoflurane, enflurane lowered mean aortic blood pressure in a dose-dependent manner (-37, -45, -48, and -62% vs. -19, -25, -41, and -44%, respectively) and cardiac output (-20, -26, -41, and -48% vs. -3, -5, -11, and -15%, respectively). With isoflurane, cardiac output decreased only at 1.75 and 2.0 MAC, and portal blood flow did not change significantly, whereas hepatic arterial blood flow increased at 1.75 and 2 MAC (by 28 and 33%, respectively). With enflurane, no significant changes were recorded in hepatic arterial blood flow, whereas portal blood flow decreased in a dose-dependent manner. Except at 2 MAC, hepatic circulation did not differ between anesthetics. Likewise, neither anesthetic significantly changed renal blood flow, except for enflurane at 2.0 MAC, which was associated with a 35% reduction. Both anesthetics led to similar systemic, hepatic, and renal vasodilations. Our data suggest that high concentrations of enflurane are associated with decreases in portal, total hepatic, and renal blood flows, most likely as a result of an anesthetic-induced cardiac depression.     

Effects of fenoldopam on renal blood flow and systemic hemodynamics during isoflurane anesthesia.

The authors compared the systemic hemodynamic and renal vascular effects of hypotension induced by fenoldopam with those produced by the most commonly used hypotensive agent, sodium nitroprusside, in 10 dogs. Mean arterial pressure decreased 26% +/- 3% from control following infusion with fenoldopam, and 30% +/- 2% following infusion with sodium nitroprusside (these decreases were not significantly different between the groups). Renal blood flow (RBF) was preserved during fenoldopam-induced hypotension (214 +/- 16 mL/min at baseline and 197 +/- 16 mL/min after fenoldopam-induced hypotension). In contrast, RBF decreased from 223 +/- 17 mL/min to 167 +/- 12 mL/min during sodium nitroprusside-induced hypotension (P less than 0.02). The differences in RBF between the two groups occurred in spite of the fact that cardiac output and pulmonary capillary wedge pressure were kept similar between the two groups. The authors conclude that fenoldopam, a selective dopamine1 (DA1) receptor agonist, preserves blood flow to the kidney during induced hypotension. On the other hand, sodium nitroprusside is a nonselective arteriolar and venous vasodilator that redistributes blood flow away from the kidneys during induced hypotension.     

Effect of small-dose dopamine on mesenteric blood flow and renal function in a pig model of cardiopulmonary resuscitation with vasopressin

Vasopressin (antidiuretic hormone) seems a promising alternative to epinephrine for cardiopulmonary resuscitation (CPR) in cardiac arrest victims, mediating a pronounced blood flow shift toward vital organs. We evaluated the effects of small-dose dopamine on splanchnic blood flow and renal function after successful resuscitation with this potent vasoconstrictor in an established porcine CPR model. After 4 min of cardiac arrest and 3 min of CPR, animals received 0.4 U/kg vasopressin and were continuously infused with either dopamine 4 microg x kg(-1) x min(-1) (n = 6), or saline placebo (n = 6). Defibrillation was performed 5 min after drug administration; all animals were observed for 6 h after return of spontaneous circulation. During the postresuscitation phase, average mean +/- SD superior mesenteric artery blood flow was significantly (P = 0.002) higher in the dopamine group compared with the placebo group (1185+/-130 vs 740+/-235 mL/min), whereas renal blood flow was comparable between groups (255+/-40 vs 250+/-85 mL/min). The median calculated glomerular filtration rate had higher values in the dopamine group (70-120 mL/min) than in the placebo group (40-70 mL/min; P = 0.1 at 0 min and P = 0.08 at 360 min). We conclude that small-dose dopamine administration may be useful in improving superior mesenteric artery blood flow and renal function after successful resuscitation with vasopressin. IMPLICATIONS: Long-term survival after cardiac arrest may be determined by the ability to ensure adequate organ perfusion during cardiopulmonary resuscitation and in the postresuscitation phase. In this regard, small-dose dopamine improved postresuscitation blood flow to the mesenteric bed when vasopressin was used as an alternative vasopressor in an animal model of cardiac arrest.     

Effect of inspired oxygen on portal and hepatic oxygenation: effective arterialization of portal blood by hyperoxia

Because hypoxia may compromise the survival of intraportally transplanted pancreatic islets, we have measured portal blood flow and both portal and hepatic oxygenation in normal and diabetic rats breathing graded inspired oxygen concentrations. Portal blood flow and hepatic tissue oxygenation were measured using a transonic flowmeter and near infrared spectroscopy while gas analysis was carried out on portal venous blood samples. The effects of breathing 13%, 21%, 50%, or 100% oxygen were compared in animals with steptozotocin-induced diabetes and in controls. In diabetic rats breathing 21% oxygen, portal blood flow was significantly lower than in controls (7.2+/-0.7 vs. 9.1+/-0.8 ml/min, p < 0.05). In both groups, breathing 100% oxygen significantly increased portal flow (to 8.4+/-1.0 and 12.2+/-0.7 ml/min, respectively). This effect was not secondary to hepatic arterial vasoconstriction because it was not prevented by hepatic artery ligation. In controls, breathing 100% oxygen increased portal pO2 from 5.0+/-0.9 to 14.4+/-1.4 kPa (p < 0.05) and portal venous oxygen saturation (PSaO2) from 53.9+/-12.1% to 92.9+/-1.4% (p < 0.05), a value not significantly different from peripheral (arterial) saturation. Similarly, in diabetic animals pO2 rose from 5.6+/-0.3 to 11.7+/-0.4 kPa (p < 0.01) and SO2 from 55.5+/-5.2% to 88.5+/-0.6% (p < 0.05). Hepatic oxyhemoglobin rose and deoxyhemoglobin fell reciprocally as a function of the inspired oxygen concentration. Improved hepatic oxygenation observed in animals breathing oxygen-enriched gas mixtures results from an increase in splanchnic blood flow coupled with a marked increase in portal oxygen saturation. This effective arterialization of portal blood may have important consequences for the success of intraportal transplantation of pancreatic islets.     

肝硬变时肝内门静脉系统血管顺应性的研究

目的用隔离灌流的鼠肝硬变模型（ＩＰＣＭ）观测肝内血管的顺应性。方法８０只四氯化碳（ＣＣｌ４）诱导肝硬变大鼠,按门静脉单纯灌流和门静脉肝动脉联合灌流分为Ａ、Ｂ两组,通过递增灌流速度观察模型血流动力学变化。结果Ａ组中,对照组基础压力为１６５±０２８ｋＰａ,与此相比,每分钟灌流速分别为３５ｍｌ,４５ｍｌ,５５ｍｌ的３个实验组灌注压随着灌流速度的梯度增加而迅速升高,二者间有高度相关性（ｒ＝０９８５,Ｐ＜００１）,肝内阻力变化不大（Ｐ＞００５）;每分钟灌流速为１５ｍｌ的Ｑ１５组则由于低灌流造成了模型的不可逆损伤。ＩＰＣＭ最大灌流速度范围小于文献报告的正常肝脏灌流的相应范围。Ｂ组中,Ｑ３５～Ｑ５５组的灌注压力也呈迅速升高趋势（Ｐ＜００５）,但未发生Ｑ１５组的低灌流现象;与Ａ组相比,Ｂ组由于开放了肝动脉灌流而部分地缓解了门静脉的压力升高。结论（１）肝硬变门静脉高压症时肝内循环顺应性下降而向肝血流量增加;（２）肝动脉与门静脉两系统间可能存在血流动力学功能的相互代偿     

Comparative effects of halothane, isoflurane, and sevoflurane on the liver with hepatic artery ligation in the beagle.

Recently, there has been increasing interest in the alterations in splanchnic and hepatic circulation and preservation of hepatic oxygenation and function during anesthesia and surgery. However, the effects of volatile anesthetics under a condition of marginal hepatic oxygen supply are not well understood. Using a crossover design, we therefore studied the effects of equianesthetic concentrations (1.5 MAC) of halothane, isoflurane, and sevoflurane on hepatic oxygenation and function in nine beagles in which the hepatic artery had been ligated. Portal blood flow was measured by an electro-magnetic flow meter. Hepatic function was assessed by indocyanine green elimination kinetics. While cardiac output and mean arterial pressure were greater during halothane anesthesia than during isoflurane and sevoflurane anesthesia, portal blood flow and hepatic oxygen supply were significantly less during halothane and sevoflurane anesthesia than during isoflurane anesthesia. With regard to hepatic oxygen uptake, there was a significant difference between halothane (2.7 +/- 1.2 ml.min-1 x 100 g-1) and sevoflurane (3.7 +/- 2.0 ml.min-1 x 100 g-1; P less than 0.05). Consequently, the hepatic oxygen supply/uptake ratio and the hemoglobin oxygen saturation and oxygen partial pressure in hepatic venous blood during sevoflurane anesthesia were significantly less than they were with the other anesthetics. Indocyanine green clearance was better preserved during sevoflurane anesthesia (39.7 +/- 12.0 ml.min-1) than during halothane anesthesia (30.9 +/- 8.4 ml.min-1; P less than 0.05). We conclude that sevoflurane is accompanied by a smaller oxygen supply/uptake ratio than is halothane and isoflurane, while it preserves hepatic function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Overcoming reduced hepatic and renal perfusion caused by positive-pressure pneumoperitoneum

HYPOTHESIS: Use of the intermittent sequential pneumatic compression (ISPC) device may improve splanchnic and renal perfusion caused by positive-pressure pneumoperitoneum (PPP) in patients undergoing laparoscopic cholecystectomy. DESIGN: Prospective controlled study. SETTING: University hospital. PATIENTS: Twenty-two consecutive patients undergoing elective laparoscopic cholecystectomy whose cardiac output decreased at least 10% on induction of PPP. INTERVENTION: The ISPC device was activated over the lower limbs 15 minutes after PPP was established for the remainder of surgery. MAIN OUTCOME MEASURES: Urine output, cardiovascular functions, and hepatic and renal perfusion were measured during the surgical phases; urine output was quantified in a matched control group (n = 30). RESULTS: Induction of PPP significantly decreased cardiac output and stroke volume, while ISPC significantly reversed these changes. Increased systemic vascular resistance during PPP was reversed by ISPC. Activation of the pneumatic sleeves during PPP increased the mean +/- SD portal venous and hepatic arterial blood flows from 0.86 +/- 0.30 to 1.33 +/- 0.44 L/min (P<.001) and from 0.26 +/- 0.10 to 0.38 +/- 0.19 L/min (P = .002), respectively; the mean renal segmental arterial index decreased with ISPC from 0.68 +/- 0.05 to 0.63 +/- 0.08 (P = .003). During PPP, urine output decreased from 1.10 to 0.28 mL/min per meter squared (P = .001) but improved markedly with ISPC to 0.61 mL/min per meter squared (P = .01). Such improvement was absent in the control group. CONCLUSIONS: Use of ISPC significantly improves hepatic and renal blood flows during PPP. Its application is recommended during prolonged laparoscopic procedures, including laparoscopic live donor nephrectomy.     

A comparison of nitroglycerin and nitroprusside: I. Treatment of postoperative hypertension

Nitroglycerin improves perfusion to ischemic myocardial regions and therefore has theoretical advantages over sodium nitroprusside to treat hypertension (mean arterial pressure [MAP] greater than 95 mm Hg) following coronary bypass operation. Thirty-three hypertensive patients were randomized to an initial infusion of either nitroglycerin or nitroprusside in a crossover trial designed to reduce MAP to 85 mm Hg. Thermodilution cardiac output measurements permitted calculation of left ventricular stroke work index (LVSWI), and nuclear ventriculograms permitted estimation of left ventricular ejection fraction, left ventricular end-diastolic volume index (LVEDVI), and left ventricular end-systolic volume index (LVESVI). Coronary sinus blood flow was measured by the continuous thermodilution technique, and arterial and coronary sinus lactate measurements permitted calculation of myocardial lactate flux (MVL). Both nitroglycerin and nitroprusside reduced MAP (-25 +/- 12 mm Hg and -20 +/- 10 mm Hg, respectively; not significant [NS]). Nitroglycerin reduced LVSWI more than did nitroprusside (-15 +/- 13 gm-m/m2 and -7 +/- 9 gm-m/m2, respectively; p less than 0.01). Both agents increased left ventricular ejection fraction (nitroglycerin, +8 +/- 8%, and nitroprusside, +10 +/- 7%; NS), and decreased LVEDVI (-20 +/- 22 ml/m2 and -11 +/- 17 ml/m2, respectively; NS) and LVESVI (-13 +/- 14 ml/m2 and -10 +/- 12 ml/m2, respectively; NS). Coronary sinus blood flow decreased with both drugs (NS), but MVL increased with nitroglycerin (+0.02 +/- 0.14 mmol/min) and decreased with nitroprusside (-0.02 +/- 0.02 mmol/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hyperperfusion syndrome in small-for-size livers

BACKGROUND: Portal hyperperfusion in small-for-size livers might seriously impair postoperative liver regeneration. Using an experimental model, we investigated splenectomy as a measure to reduce portal blood flow and its impact on postoperative recovery following extended liver resection. METHOD: Wistar rats underwent partial (90%) hepatectomy with or without splenectomy under temporary inflow occlusion (30 min). In addition to 10-day survival rate, laser Doppler flowmetry of hepatic blood flow and fluorescence microscopic analysis of hepatic microcirculation were performed to assess the effect of splenectomy on initial microvascular reperfusion of liver remnants. RESULTS: While postischemic perfusion failure was comparable between both groups, portal blood flow was significantly reduced after simultaneous splenectomy (3.5+/-0.4 vs. 5.4+/-0.4 ml/min). Moreover, red blood cell velocity and volumetric blood flow were reduced in splenectomized animals. These animals experienced lower AST levels (421+/-36 vs. 574+/-73 U/l) and a significantly increased survival rate, reaching 6.6+/-1.3 vs 2.6+/-0.8 days. CONCLUSION: Simultaneous splenectomy significantly reduced the risk for postoperative hyperperfusion syndrome in small-for-size livers. Shear-stress-induced liver injury was diminished due to a significant reduction of portal venous blood flow, which positively influenced postoperative regeneration resulting in significantly higher survival.     

Effects of Ephedrine on Haemodynamics and Oxygen Consumption in the Dog During High Epidural Block with Special Reference to the Splanchnic Region

High lumbar epidural block was induced in seven dogs with 0.5% bupivacaine, causing a fall in mean arterial blood pressure (AP) from 19.2 +/- 3.2 to 10.5 +/- 3.2 kPa, owing to equal reductions in cardiac output (QT) and systemic vascular resistance (SVR). After the administration of ephedrine (a single injection of 200-300 micrograms X kg-1 b.w. followed by a continuous infusion of 10-20 micrograms X kg-1 b.w. X min-1) AP, QT and SVR rose to pre-epidural values. Furthermore, the hypokinetic circulation following the epidural block returned to normokinetic levels. Portal venous blood flow was increased from 16.5 +/- 6.2 to 25.5 +/- 4.3 ml X kg-1 b.w. X min-1 by ephedrine, while the hepatic arterial blood flow was unchanged and remained at its pre-epidural level. In spite of a slight rise in hepatic oxygen consumption from 1.2 +/- 0.4 to 1.6 +/- 0.6 ml X kg-1 b.w. X min-1, the percentages of oxygen extracted from the portal vein and the hepatic artery decreased significantly. It is concluded that ephedrine restores central and splanchnic haemodynamics in a desirable manner during high epidural anaesthesia.     

Water diuresis during methohexitone anaesthesia. Studies in chronically instrumented dogs (author's transl)

Seven chronically prepared dogs (electromagnetic flow transducers around the pulmonary and left renal artery, left atrial catheter) maintained on a controlled sodium and water intake were studied. About 20 h after the last intake of food and water, the effects of i.v. methohexitone (initial dose: 6.10 +/- 0.84 mg/kg bw; sustaining infusion: 0.34 +/- 0.10 mg/min.kg bw) on renal excretion of sodium, potassium, urea and water as well as on several haemodynamic values were investigated over a period of 60 min (MP) after a control period (CP) of 60 min in the unanaesthetized state. In 18 of 19 experiments water diuresis (U/Posm less than 1) was observed between 20 and 40 min after starting the administration of methohexitone. Urine volume increased from 44 +/- 21 microliter/min.kg bw (CP) to 104 +/- 62 microliter/min.kg bw (MP).I.v. administration of arginine-vasopressin (ADH) completely abolished water diuresis. During MP, there was a decrease in cardiac output (-11%), stroke volume (-36%) and left atrial pressure (-27%), heart rate increased (+ 43%). Mean arterial blood pressure and renal blood flow did not change. It is assumed-as plasma osmolality did not change-that the central release of antidiuretic hormone is suppressed by methohexitone.