Changes in blood flow and metabolism in a neurovascular island skin flap after a burn

In 8 male white Yorkshire pigs weighing approximately 42 kg each, 12 buttock neurovascular island skin flaps were dissected. Baseline recordings were made of blood flow and O2 consumption in the flap. Two series of experiments were carried out. In control animals (5), the flap was dissected and the "cold" aluminum plate was applied for 10 seconds. In the burned flaps (7) a contact burn of 2.68 calories/cm2 was created with a heated aluminium plate applied to the skin for 10 seconds. After this the flaps were studied for 4 hours. In the control flaps, blood flow and O2 consumption did not change. The burned flaps showed no change in blood flow, while O2 consumption increased significantly from .07 +/- .01 (SE) ml/100 g/min to .18 +/- .08 (SE) ml/100 g/min (p less than .05).     

Method for skin blood flow studies in the pig

In this methodological paper a quantitative blood flow measuring technique in porcine skin is described. The anatomy, technical preparation and surgical technique is emphasized. Baseline recordings yielded a total blood flow of 6.6 +/- 0.9 (S.E.) cc/100 g/min and an oxygen consumption of 0.16 +/- 0.02 cc/100 g/min at a dermal temperature of 35 degrees C. Approximately 75% of the experiments were successful and unsuccessful experiments were mainly due to malignant hyperthermia in the pig or inability to cannulate the vessels.     

Optimal perfusion flow rate for the brain during deep hypothermic cardiopulmonary bypass at 20 degrees C. An experimental study

The relationship between the perfusion flow rate and cerebral oxygen consumption during deep hypothermic cardiopulmonary bypass at 20 degrees C was investigated in dogs. In 10 dogs the perfusion flow rate was decreased in steps from 100 to 60, 30, and 15 ml/kg/min every 30 minutes. Although cerebral blood flow decreased as perfusion flow rate decreased, the ratio of cerebral blood flow to the perfusion flow rate increased significantly (p less than 0.05) at a perfusion flow rate of 15 ml/kg/min compared to that at a perfusion flow rate of 100 or 60 ml/kg/min. The arterial-sagittal sinus blood oxygen content difference increased as perfusion flow rate decreased. Consequently, cerebral oxygen consumption did not vary significantly at perfusion flow rates of 100 (0.48 +/- 0.10), 60 (0.43 +/- 0.14), and 30 ml/kg/min (0.44 +/- 0.12 ml/100 gm/min), and it decreased significantly to 0.31 +/- 0.22 ml/100 gm/min at a perfusion flow rate of 15 ml/kg/min. In five dogs the perfusion flow rate was decreased in one step from 100 to 15 ml/kg/min, and after 60 minutes' perfusion at a perfusion flow rate of 15 ml/kg/min, the perfusion flow rate was returned to 100 ml/kg/min. Cerebral oxygen consumption decreased significantly during 60 minutes' perfusion at a perfusion flow rate of 15 ml/kg/min and did not return to its initial value after the perfusion flow rate was returned to 100 ml/kg/min. These data indicate that the optimal perfusion flow rate for the brain during deep hypothermic cardiopulmonary bypass at 20 degrees C appears to be 30 ml/kg/min, with a possible oxygen debt in the brain resulting in anaerobic metabolism if the perfusion flow rate is kept at 15 ml/kg/min or less.     

Kidney function parameters following ischemia stress using the Euro-Collins solution or the Bretschneider cardioplegic HTK solution

Protection-methods, for an improvement of ischemic tolerance of the kidney, can be investigated by intraischemic analysis of metabolism and structure. A definite proof for the effectiveness of a protection method is only postischemic function in combination with postischemic structure-regeneration. For this reason postischemic function was chosen for examination of the protective ability of the Euro-Collins-solution and the HTK-solution during a two-hour reperfusion period. We perfused 57 dog kidneys either with the Euro-Collins- or with the HTK-solution prior to ischemia. Ischemia was 7, 60, 90 and 120 min after Euro-Collins-perfusion and 7, 120, 150 and 180 min after HTK-protection. The protected and ischemic kidneys were left in-situ; the mean ischemic temperature was therefore 20-25 degrees C for the shorter ischemic times and 30-34 degrees C for the longer ischemic times. We compared the protected and ischemic kidneys with 14 untreated kidneys (control). Postischemic renal blood flow (RBF) was measured by an electromagnetic flow probe; renal oxygen consumption (V02/min) was calculated by arterio-venous oxygen content difference and the renal blood flow. If urine could be collected, the glomerular filtration rate (GFR) was measured by an endogenous creatinine clearance. In Euro-Collins-protected kidneys after 60-120 min ischemia the RBF was after 15 min of reperfusion between 20 and 100 ml/min/100 g. After 30 min we got values of 100-200 ml/min/100 g. The V02/min, which was in the control kidneys between 5-6 ml/min/100 g, was about 2 ml/min/100 g.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow rate during cardiopulmonary bypass and optimal cerebral perfusion flow rate during separated brain perfusion--a clinical study

There is no established theory to determine the cerebral blood flow rate (CBF) during not only the standard cardiopulmonary bypass but during the cardiopulmonary bypass with separated brain perfusion. This study was carried out to answer the following questions. (1) what is the relationship during the cardiopulmonary bypass between CBF and systemic flow rate or blood pressure?. (2) what is the optimal flow rate to the innominate artery during the separated brain perfusion? Twenty-one patients were selected for this study, who were operated under the cardiopulmonary bypass with a standard roller pump and a membrane oxygenator under moderate hypothermia (nasopharyngeal temperature of 26-28 degrees C). Systemic flow rate was maintained between 40 and 70 ml/kg/min. CBF before the cardiopulmonary bypass was 30.6 +/- 5.5 ml/100 g brain/min, and increased to 33.8 +/- 8.9 ml/100 g brain/min during the cardiopulmonary bypass. CBF was proportional to systemic flow rate (r = 0.62, p less than 0.01) and showed poor association with blood pressure ranged from 35 to 94 mmHg. As for the relationship between innominate arterial and cerebral blood flow rate, CBF linearly followed the decrease of innominate arterial flow rate to below about 9 ml/kg/min, but showed almost no changes when innominate arterial flow rate was over 9 ml/kg/min. It was observed that cerebral oxygen consumption did not decrease significantly under moderate hypothermia (26-28 degrees C), as far as CBF of 25 ml/100 g brain/min was maintained. Based on the relationship between innominate arterial and cerebral blood flow rate, it was shown that the innominate arterial flow rate to provide CBF of 25 ml/100 g brain/min was 5.5 ml/kg/min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen tension and consumption measured by a tc-Po2 electrode on heated skin before and after epidermal stripping

Oxygen tensions, cutaneous blood flow rate, and skin oxygen consumption rate were determined by tc-PO2 measurements at an electrode temperature of 45 degrees C. The epidermal surface was stripped by 50 applications of adhesive plaster to the surface. Ten healthy, normotensive adults were examined. Cutaneous blood flow rate was 41.2 +/- 8.6 ml X (100 g)-1 X min-1 before and 42.8 +/- 5.9 ml X (100 g)-1 X min-1 after epidermal stripping. Oxygen consumption before stripping was 0.327 +/- 0.065 ml O2 X (100 g)-1 X min-1, and after stripping it was determined at two different saturation levels to be 0.208 +/- 0.072 ml O2 X (100 g)-1 X min-1 and 0.251 +/- 0.096 ml O2 X (100 g)-1 X min-1. Capillary temperature was estimated to be approximately 43 degrees C before and after stripping. At this temperature mean arterial PO2 was estimated to be 18.1 kPa (136 mmHg), which would be reduced by the computed local metabolism to a mean capillary PO2 of 14.4 kPa (108 mmHg) before stripping and 15.2 kPa (114 mmHg) after. Stripping increased mean skin PO2 from 10.9 +/- 0.6 kPa (82.3 +/- 4.7 mmHg) to 14.6 +/- 1.0 kPa (109.4 +/- 7.7 mmHg). Thus, stripping eliminated 82% of the gradient between the capillaries and electrode while reducing the computed oxygen consumption by 23-36%. It is concluded that the epidermal membrane is a significant barrier to oxygen diffusion and that the transcutaneous oxygen electrode has a significant effect on skin PO2 owing to its own even low oxygen consumption. This will reduce the observed skin PO2 significantly.     

Cerebrovascular and cerebral metabolic effects of N2O in unrestrained rats

There is controversy about whether N2O increases cerebral blood flow and cortical oxygen consumption (CMRO2) in rats. Cortical and subcortical blood flow and CMRO2 were measured in awake, unrestrained rats while awake and during 70% N2O administration using radioactive microspheres. In the awake state, cortical and subcortical blood flow were 126 +/- 10 and 98 +/- 7 ml.100 g-1.min-1, respectively, and CMRO2 (cortical) was 10.0 +/- 0.6 ml O2.100 g-1.min-1 (mean +/- SE). After 15 min of 70% N2O, cortical and subcortical blood flow increased 100% and 40%, respectively, while CMRO2 did not increase significantly. Cerebral blood flow remained increased after 60 min of N2O exposure, and CMRO2 did not change. These results show that N2O produces cerebrovasodilation in rats that is not related to a change in metabolic demand. Plasma catecholamines do not change during N2O administration, indicating that the increase in blood flow is not due to a general stress response.     

Evaluation of blood flow in free microvascular flaps

Free flap surgery is routine today, yet little is known of its pathophysiology. In this study, the authors evaluated the hemodynamics in different types of free microvascular flaps, by measuring intraoperative transit-time flow. Eighty-six free transplants--21 free TRAM flaps for breast reconstruction, 18 radial forearm flaps for head and neck reconstructions, and 47 muscle flaps for head and neck, trunk and lower extremity reconstructions--were studied. Donor artery flow was highest in the radial artery (mean: 57.5 +/- 50 (SD) ml/min) but dropped (p < 0.001) to one tenth (6.1 +/- 2 ml/min) after anastomosis. The flow was lowest (4.9 +/- 3 ml/min) in the recipient artery of the TRAM flap but, after anastomosis, increased significantly (13.7 +/- 5 ml/min) to the level of the flow in the donor artery. The donor-artery flow in muscle flaps had a mean of 15.9 +/- 11 ml/min, and it significantly increased after anastomosing (23.9 +/- 12 ml/min). Weight-related intake of blood was highest in the radial forearm flap (18.5 +/- 6 ml/ min/100g) and lowest in the TRAM flap (2.5 +/- 1 ml/min/100g). The study showed that blood flow through a free microvascular flap does not depend on recipient artery flow. Even low-flow arteries can be used as recipients, because the flow increases according to free-flap requirements. The blood flow through a free microvascular flap depends on the specific tissue components of the flap.     

Cerebral Blood Flow and Oxygen Metabolism During Mild Hypothermia in Patients with Subarachnoid Haemorrhage

Cerebral blood flow and O2 metabolism during hypothermia (33-34 degrees C) was evaluated in 5 patients with aneurysmal subarachnoid haemorrhage by positron emission tomography (PET). Their preoperative clinical condition was WFNS scale IV or V. The patients received surface cooling postoperatively, and were maintained in a hypothermic state during transfer for radiological examination. Positron emission tomography revealed a decrease in cerebral blood flow and O2 metabolic rate. Cerebral blood flow was 34.8+/-15.1 ml/100 ml/min and the O2 metabolic rate was 1.85+/-0.61 ml/100 ml/min in areas of the middle cerebral artery ipsilateral to the ruptured aneurysms, whereas these values were 30.8+/-7.1 and 2.21+/-0.45 ml/100 ml/min, respectively, on the contralateral side. This represents a decrease of 37+/-27% compared to normal cerebral blood flow and 52+/-16% compared to normal O2 metabolic rate (p < 0.02) in the ipsilateral areas, and decreases of 44+/-13% and 43+/-12%, respectively, on the contralateral side. The present results reflected the luxury perfusion state in almost all cases and provide the first PET evidence of decreased cerebral blood flow and metabolic rate of O2 during hypothermia in humans.     

The effects of hypothermia on myocardial oxygen consumption and transmural coronary blood flow in the potassium-arrested heart.

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.     

Relation between spinal cord blood flow and functional recovery after blocking weight-induced spinal cord injury in rats

Spinal cord blood flow (SCBF) and motor performance on the inclined plane were measured up to 9 days after a reversible spinal cord compression injury in 49 Sprague-Dawley rats. A load of 35 g on 11 mm2 of the thoracic spinal cord for 5 minutes caused transient paraparesis with a decrease in the capacity angle on the inclined plane from 62 +/- 1 degree (mean +/- SEM) before injury to 33 +/- 1 degree on Day 1, 45 +/- 2 degrees on Day 4, d and 54 +/- 3 degrees on Day 9. SCBF was measured by the [14C]iodoantipyrine method, and in gray matter there was a decrease from 78.4 +/- 2.3 ml/min/100 g of tissue in uninjured animals to 33.7 +/- 1.5 ml/min/100 g of tissue on Day 1 after injury, increasing to 50.1 +/- 2.0 on Day 4 and to 70.5 +/- 2.7 ml/min/100 g of tissue on Day 9. At the corresponding times, the SCBF values in white matter were 14.5 +/- 0.5, 6.7 +/- 0.5, 10.2 +/- 0.6, and 13.4 +/- 0.6 ml/min/100 g of tissue, respectively. The animals in another group were loaded with 25 g for 5 minutes and on Day 1 exhibited a capacity angle of 43 +/- 2 degrees while the SCBF values for gray and white matter were 55.1 +/- 2.0 and 11.1 +/- 0.4 ml/min/100 g of tissue, respectively; thus, the results in this group were similar to the values on Day 4 in the animals loaded with 35 g.(ABSTRACT TRUNCATED AT 250 WORDS)     

Liver circulation and oxygen metabolism during short time ligation and the hepatic artery in the dog

The changes of liver circulation and liver oxygen metabolism during and after one hour hepatic artery ligation (HAL) were studied in eight mongrel dogs. At the end of the HAL period total hepatic blood flow (THBF) was reduced from 115.6 +/- 5.5 ml/min . 100 g liver tissue to 68.0 +/- 3.7 ml/min . 100 g or 59% of the initial value. The portal venous blood flow was reduced from 83.1 +/- 3.4 to 58.8 +/- 3.7 ml/min . 100 or 82% of the initial value and the liver oxygen consumption was reduced from 4.1 +/- 0.2 ml/min . 100 g to 3.1 +/- 0.3 ml/min . 100 g or 76% of the initial value. The changes in portal venous blood flow and liver oxygen consumption were reversible following reopening of the hepatic artery. The clinical importance of a reduced portal venous blood flow and liver oxygen consumption following HAL and the possibilities to increase the portal venous blood flow are discussed.     

Relationship between adenylate cyclase activity and regional myocardial energetics in experimental left ventricular hypertrophy

The aim of this study was to examine the responsiveness of the hypertrophied left ventricle to beta-adrenergic stimulation in a pressure overload model produced by valvular aortic stenosis and characterized by reduced beta-adrenoceptor number. The study was designed to correlate changes in global and regional cardiac work and energetics in response to isoproterenol with adenylate cyclase activity. Eleven anesthetized dogs with left ventricular hypertrophy and 11 controls were studied at rest and during 0.5 and 1.0 micrograms/kg/min isoproterenol infusion. We measured regional work from segment length and force changes with ultrasonic dimension crystals and miniature force gauges in addition to arterial and left ventricular blood pressure and cardiac output. Regional myocardial oxygen consumption was calculated from O2 extraction using microspectrophotometry and blood flow using radioactively labeled microspheres. Adenylate cyclase activity was assayed at baseline and after stimulation with forskolin. Isoproterenol significantly increased heart rate, dP/dtmax, cardiac output, and external work to similar levels in control and hypertrophied animals. Similarly, regional work increased from 463 +/- 115 to 995 +/- 584 g x mm/min for controls and from 392 +/- 156 to 1175 +/- 577 for hypertrophied dogs with high dose isoproterenol. Regional O2 consumption also increased to similar levels (20.3 +/- 14.7 vs 16.2 +/- 6.3 ml O2/min/100 g) in both groups. Adenylate cyclase activity was lower in hypertrophy at baseline (23.9 +/- 7.3 vs 62.9 +/- 14.2 pM/min/mg protein for controls), but was the same as for controls with forskolin stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Palmar hyperhidrosis: intraoperative monitoring with laser Doppler blood flow as a guide for success after endoscopic thoracic sympathectomy

OBJECTIVE: Video-assisted endoscopic thoracic sympathectomy is an effective surgical procedure for treating patients with palmar hyperhidrosis. An increase by more than 1 degrees C in palmar temperature has been observed to be predictive of good outcome. In this study, we investigated the use of palmar laser Doppler flowmetry as an intraoperative assessment of the efficacy of the operation. METHODS: One hundred sixty-six patients underwent a total of 330 endoscopic thoracic sympathectomy procedures from March 1996 to June 2001. We studied 17 patients (15 men, 2 women) who underwent a total of 33 procedures. The patients' mean age was 27.07 +/- 7.92 years, and the mean hospital stay was 2.23 +/- 0.66 days. RESULTS: Mean baseline laser Doppler blood flow was 2.63 +/- 2.56 ml/min/100 g. After the procedure, mean blood flow increased significantly to 7.24 +/- 5.88 ml/min/100 g (r = 0.768, P < 0.000, 95% confidence limit, -6.1060, -3.0946), a 232.18 +/- 219.12% increase. Mean palmar temperature increased to 1.44 +/- 1.44 degrees C. All patients experienced relief after the operation. Compensatory hyperhidrosis occurred in 10 (58.8%) of 17 patients. CONCLUSION: Monitoring of palmar laser Doppler blood flow changes is a useful adjunct during endoscopic thoracic sympathectomy surgery, and, when coupled with the established methods of endoscopic visualization and palmar temperature, it can predict the success of the procedure accurately.     

Rapid Rewarming Causes an Increase in the Cerebral Metabolic Rate for Oxygen that Is Temporarily Unmatched by Cerebral Blood Flow: A Study during Cardiopulmonary Bypass in Rabbits

Background: Jugular venous hemoglobin desaturation during the rewarming phase of cardiopulmonary bypass is associated with adverse neuropsychologic outcome and may indicate a pathologic mismatch between cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). In some studies, rapid rewarming from hypothermic cardiopulmonary bypass results in greater jugular venous hemoglobin desaturation. The authors wished to determine if rewarming rate influences the temperature dependence of CBF and CMRO2.

Methods: Anesthetized New Zealand white rabbits, cooled to 25 degrees Celsius on cardiopulmonary bypass, were randomized to one of two rewarming groups. In the fast group (n = 9), aortic blood temperature was made normothermic over 25 min. Cerebral blood flow (microspheres) and CMRO2 (Fick) were determined at baseline (25 degrees C), and at brain temperatures of 28 degrees, 31 degrees, 34 degrees, and 37 degrees Celsius during rewarming.

Results: Systemic physiologic variables appeared similar between groups. At a brain temperature of 28 degrees C, CMRO2 was 47% greater in the fast rewarming group than in the slow group (2.2 +/-0.5 vs. 1.5+/-0.2 ml O2 *symbol* 100 g sup -1 *symbol* min sup -1, respectively; P = 0.01), whereas CBF did not differ (48+/-18 vs. 49+/-8 ml *symbol* 100 g sup -1 *symbol* min sup -1, respectively; P = 0.47). Throughout rewarming, CBF increased as a function of brain temperature but was indistinguishable between groups. Cerebral metabolic rate for oxygen differences between groups decreased as brain temperatures increased.     

Hemodynamic and microcirculatory changes in the liver in experimental acute pancreatitis of dogs

To investigate the hemodynamic changes of the liver in acute pancreatitis the microcirculation of the liver, portal venous flow, hepatic artery blood flow, cardiac index were measured in 15 dogs with acute pancreatitis induced by autologous bile and trypsin injection into the main pancreatic duct during the experimental period for 5 hrs. The effect of protease inhibitor (PATM) in a dose of 3 mg/kg/kg/hr on those hemodynamic changes was investigated in another series of acute pancreatitis in dogs. In acute pancreatitis hepatic microcirculation decreased to 26 +/- 15 ml/min/100g at 5 hrs after onset of pancreatitis, portal venous flow and hepatic artery flow decreased to 86 +/- 16 ml/min and 66 +/- 30 ml/min at 5 hrs, respectively. The administration of PATM maintained the portal blood flow during the first 2 hrs and showed a trend of decreasing to 219 +/- 93 ml/min at 5 hrs. The hepatic microcirculation showed 77 +/- 25 ml/min/100g and 72 +/- 14 ml/min/100g at 1 and 2 hrs respectively and then decreased to 47 +/- 21 ml/min/100g at 5 hrs. We concluded hemodynamic and microcirculatory changes of the liver in acute pancreatitis was disturbed due to the decreased portal and hepatic artery flow, however, the administration of PATM has an effect of improvement of liver microcirculation.     

Effect of hypothermia and cardioplegia on intramyocardial voltage and myocardial oxygen consumption

Intramyocardial voltage and myocardial oxygen consumption were measured in the fibrillating heart between the temperatures of 37 degrees C and 25 degrees C and in the arrested heart after infusion of potassium cardioplegic solution in 10 adult mongrel dogs. Electrical activity from the myocardium was recorded using specially designed plunge electrodes, and intramyocardial voltage was monitored by an in-line voltmeter. Myocardial oxygen consumption gradually decreased from 5.8 +/- 0.6 ml O2/min at 37 degrees C to 2.3 +/- 0.5 ml O2/min at 25 degrees C. In contrast, hypothermia did not cause a similar decrease in intramyocardial voltage which remained within a range of 1.8 +/- 0.5 mV to 2.4 +/- 0.5 mV between the temperatures of 37 degrees C and 25 degrees C. The infusion of potassium cardioplegic solution resulted in a dramatic decrease in voltage to 43 +/- 5 microV, and myocardial oxygen consumption fell to 0.5 +/- 0.3 ml O2/min. Our data demonstrated that the mean voltage of the fibrillating heart remains constant between the temperatures 37 degrees C and 25 degrees C and myocardial oxygen consumption decreases with hypothermia, which suggests that voltage does not correlate with the level of myocardial oxygen consumption. Myocardial oxygen consumption and intramyocardial voltage, however, decrease dramatically when cardioplegia is instituted.     

Spinal cord blood flow in the rat under normal physiological conditions

Regional spinal cord blood flow (SCBF) was measured in a group of rats under conditions of normothermia, normocarbia, normoxia, and normal blood pressure, using the hydrogen clearance technique. Regional SCBF in the cervical white matter was 26.8 +/- 1 (SE) ml/100 g/min and in the cervical gray matter 53.6 +/- 2.5; in the thoracic white matter it was 22.2 +/- 2.4 ml/100 g/min and in the thoracic gray matter 41.2 +/- 12/6 ml/100 g/min; and in the lumbar gray matter it was 52.3 +/- 1.9 ml/100 g/min. The effect of changes in blood pressure on SCBF (autoregulation) was investigated in nine rats. We have observed that SCBF remains relatively constant in the blood pressure range of 45 to 165 mm Hg and assumes a passive flow below or above this range.     

The effect of blood supply in muscle and an elevated muscle flap on endogenous tissue-engineered bone by rhBMP-2 in the rat

Metabolism and remodeling of bony tissue are maintained and controlled by blood supply. In this study, bony tissue osteoinduced heterotopically by recombinant human bone morphogenetic protein-2 (rhBMP-2) in rat muscles with different amounts of blood supply was investigated. The implant beds were in the latissimus dorsi muscle (LDM) and in the space wrapped with an elevated latissimus dorsi muscle flap (LDMF). The blood flow was preestimated at two muscle sites using a laser Doppler blood flowmeter. The flow value of the LDM was 2.23 +/- 0.17 ml/min/100 g (mean +/- standard deviation). The flow values of the LDMF were 1.71 +/- 0.22 ml/min/100 g 30 minutes after elevating the LDMF, 1.75 +/- 0.20 ml/min/100 g after 1 week, 1.83 +/- 0.19 ml/min/100 g after 2 weeks, and 1.99 +/- 0.18 ml/min/100 g after 3 weeks. Bony tissues induced heterotopically by rhBMP-2 were examined radiographically and histologically. On radiographs, radiopaque shadows in the LDM were almost as large as those in the LDMF. The radiopacity in the LDM was a little higher than that of the LDMF. The microscopic findings showed increased trabeculae and more hematopoietic marrow in the LDM than lamellalike bone in the LDMF. Mean bony area in the implant was 1.05 +/- 0.26 mm2 in the LDM, and was 0.70 +/- 0.11 mm2 in the LDMF. Bony proportions in the overall implant area were 18.3 +/- 3.46% in the LDF and 12.1 +/- 2.18% in the LDMF. The current study indicates that blood supply is an important factor for promoting heterotopic osteoinduction by rhBMP-2 to produce massive bony tissue as an endogenous method of tissue engineering.     

Postischemic [Ca2+] repletion improves cardiac performance without altering oxygen demands

The positive inotropism expected with correction of postischemic hypocalcemia might be counterbalanced by potential aggravation of reperfusion injury, in particular by calcium overload. We evaluated the effect of normalizing blood calcium concentration ([Ca2+]) on postischemic left ventricular systolic and diastolic mechanics using oxygen consumption and indices derived from pressure-diameter relations. In 10 open-chest dogs on cardiopulmonary bypass, the hearts underwent 30 minutes of normothermic global ischemia followed by one hour of multidose hypothermic (4 degrees C), hypocalcemic (0.3 mmol/L) blood cardioplegia. After reperfusion, systemic [Ca2+] had decreased to 70% of control (p = 0.017). The left ventricular inotropic state was significantly depressed from baseline (control) values, but was restored to baseline levels by resumption of normocalcemia after one hour of reperfusion. Chamber stiffness increased by 308% (p = 0.006) after hypocalcemic reperfusion but decreased significantly after [Ca2+] correction. Recovery of left ventricular performance with [Ca2+] correction did not augment myocardial oxygen consumption from the postischemic uncorrected state (5.0 +/- 0.3 mL O2/min/100 g versus 5.3 +/- 0.3 mL O2/min/100 g). We conclude that normalizing [Ca2+] after blood cardioplegia improves postischemic left ventricular performance without adversely affecting compliance or oxygen consumption.