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H M Wei

Publications and source records attributed to H M Wei.

33 records · Page 2Linked to original sources
PubMed1993

Diminished effect of inhibition of nitric oxide synthase on regional cerebral vascular resistance in conscious and in isoflurane anesthetized rats during hemorrhage.

Effects of a nitric oxide (NO) synthase inhibitor on regional cerebral vascular resistance (rCVR) and regional cerebral blood flow (rCBF) were studied during a severe hemorrhage in conscious and in isoflurane anesthetized groups of rats. Half of each group was infused with NG-nitro-L-arginine-methyl ester (L-NAME), a NO synthase inhibitor, at a rate of 2 mg.kg-1.min-1 for 30 min. Half of the L-NAME infused and half of the normal saline infused rats were bled to reduce the mean arterial blood pressure (MAP) to 44-49 mmHg. rCBF was measured using [14C]iodoantipyrine. rCVR was calculated as the ratio of MAP to rCBF. In the conscious non-hemorrhagic rats, L-NAME markedly increased rCVR in all the brain regions that we studied. In the conscious rats without L-NAME treatment, hemorrhage decreased rCVR in most of the brain regions. With L-NAME treatment in this group, hemorrhage increased rCVR only in the rostral part of the brain. Isoflurane decreased rCVR in most of the brain regions except the cortical area. L-NAME markedly increased rCVR in all the brain regions that we studied in the isoflurane anesthetized rats. In the isoflurane anesthetized rats, hemorrhage did not reduce rCVR in any of the brain regions. In the isoflurane anesthetized hemorrhagic rats, L-NAME did not significantly affect rCVR in any of the brain regions that we studied. We found that L-NAME increased rCVR to a greater extent in the non-hemorrhagic rats than in the hemorrhagic rats in both the conscious and in the isoflurane anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1993

Effect of cervical sympathectomy and hypoxia on the heterogeneity of O2 saturation of small cerebrocortical veins.

This study evaluated the hypothesis that the sympathetic nervous system was one of the factors increasing the heterogeneity of cerebrocortical venous O2 saturation and this heterogeneity would be greater during hypoxia when cervical sympathetic activity was elevated. Thirty-two male Long-Evans rats were either sham operated (n = 16) or received bilateral cervical sympathectomy (n = 16). One-half of the animals (n = 8) in each treatment were challenged by hypoxia (8% O2 in N2). Cerebral blood flow was determined in five brain regions with [14C]iodoantipyrine. Oxygen saturation was measured microspectrophotometrically in small cerebrocortical arteries and veins. The degree of hypoxic hyperemia was not significantly different between sham-operated and sympathectomized rats. Cortical venous O2 saturations, indicating the balance between O2 supply and consumption, were significantly more heterogeneous in the sham-operated group under both normoxic and hypoxic conditions. The coefficient of variation (CV = 100 x SD/mean) for the normoxic sham-operated animals was 24.9% and the average venous O2 saturation was 53.8%. During hypoxia, venous O2 saturation was significantly decreased to 43.1% without a change in CV (24.5%). Sympathectomy significantly reduced this heterogeneity through a reduction in the number of low O2 saturation veins (CV = 13.2%) under normoxic conditions and the effect was similar under hypoxic conditions (CV = 15.3%). In both sham-operated and sympathectomized groups, hypoxia elicited a significantly higher cerebrocortical O2 consumption. Thus, bilateral cervical sympathectomy improved the O2 supply in selective cerebrocortical regions with high O2 extraction. However, the effect of sympathetic innervation on the heterogeneity of cerebrocortical venous O2 saturation was not potentiated by hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of pentobarbital and isoflurane on regional cerebral oxygen extraction and consumption with middle cerebral artery occlusion in rats.

BACKGROUND: When compared with barbiturates, isoflurane may lack protective effects during focal cerebral ischemia. The reason for this difference is not clear. In this study, regional cerebral blood flow (rCBF), arterial and venous O2 saturation, and O2 extraction were compared in the ischemic cortex and in the nonischemic brain regions of rats anesthetized with isoflurane or pentobarbital using a microspectrophotometric technique that directly measures the O2 saturation of blood in the small arteries and veins. METHODS: Twenty-eight rats were anesthetized with 1.4% isoflurane or 50 mg/kg pentobarbital. One hour after a middle cerebral artery (MCA) occlusion, rCBF was measured in the ischemic cortex and in the nonischemic brain regions using 14C-iodoantipyrine in one-half of each group of animals. Regional arterial and venous O2 saturation were determined using microspectrophotometry in the other one-half of each group. RESULTS: The rCBF of the ischemic cortex (IC) and the non-ischemic contralateral cortex (CC) of the isoflurane group were significantly higher than those of the pentobarbital group. The venous O2 saturation was significantly less, and the O2 extraction was significantly higher, in the IC than in the nonischemic regions in both groups of animals (pentobarbital group, IC 10.5 +/- 1.1 ml O2.100 ml blood-1, CC 6.3 +/- 0.7; isoflurane group, IC 10.8 +/- 0.6, CC 5.9 +/- 0.2). There was no significant difference between the two groups. CONCLUSIONS: Because the rCBF was less and the O2 extraction was similar, O2 consumption in the focal ischemic area of the brain during pentobarbital anesthesia must have been less than that during isoflurane anesthesia.

Animals↗
PubMed1993

Cervical sympathectomy reduces the heterogeneity of oxygen saturation in small cerebrocortical veins.

This study evaluated the hypothesis that the peripheral sympathetic nervous system is one of the factors increasing the heterogeneity of venous O2 saturation in selective brain regions. Regional cerebral blood flow and O2 saturation were determined in the anterior cortex, posterior cortex, and medulla of either sham-operated or bilaterally sympathectomized Long-Evans rats. Cerebral venous O2 saturations, indicating the balance between local O2 supply and consumption, were found to be significantly more heterogeneous in the sham-operated group. In the anterior cortex, the coefficient of variation [100(SD/mean)] for the sham-operated animals was 22.4%. Sympathectomy significantly reduced this heterogeneity in the anterior cortex through a reduction in the number of low O2 saturation veins (coefficient of variation 11.7%). Blood flow and O2 consumption in the anterior cortex were not different between groups. The effects of sympathectomy in the posterior cortex were similar to those in the anterior cortex. However, sympathectomy did not alter any measured variables in the medulla. Thus, bilateral superior cervical ganglionectomy reduced the heterogeneity of cerebrocortical venous O2 saturation by reducing the number of low O2 saturation veins in the rostral part of the brain.

Animals↗
PubMed1993

Effects of nitric oxide synthase inhibition on regional cerebral blood flow and vascular resistance in conscious and isoflurane-anesthetized rats.

Nitric oxide is an important regulator of the regional cerebral vascular tone. We compared the magnitude of nitric oxide-related changes in the vascular tone by studying the regional cerebral blood flow (rCBF) and vascular resistance in conscious and isoflurane-anesthetized rats by using a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). In the conscious group (n = 12), after cannulation of a femoral artery and two veins under isoflurane anesthesia, rats were allowed to remain awake for 90 min. In the anesthetized group (n = 18), rats were anesthetized with 2% isoflurane and mechanically ventilated. Six rats in each group were treated with L-NAME (2 mg.kg-1 x min-1 for 30 min) or saline. For the remaining rats in the isoflurane-anesthetized group (n = 6), arterial blood pressure was increased by phenylephrine infusion to the same level as that in the L-NAME-treated, isoflurane-anesthetized rats. Regional vascular resistance was determined by the ratio of mean arterial blood pressure and rCBF which was measured by [14C]iodoantipyrine. L-NAME significantly increased mean arterial blood pressure in both the conscious (123 to 158 mm Hg) and anesthetized (82 to 144 mm Hg) rats. Regional vascular resistance increased significantly in all 12 brain regions studied with the average value increasing from 1.19 +/- 0.33 mm Hg.mL-1 x min x 100 g to 2.22 +/- 0.48 (P < 0.0001) in the conscious and from 0.78 +/- 0.27 to 1.61 +/- 0.48 (P < 0.0001) in the isoflurane-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1992

Effects of isoflurane on transport across the blood-brain barrier.

The blood-brain barrier (BBB) plays an important role in regulating and restricting transfer of molecules into the interstitial space of the brain. Anesthetic agents may affect the permeability of the BBB. In this investigation, the effect of isoflurane on the transport of small hydrophilic molecules across the BBB was studied in rats by measuring the blood-brain transfer coefficient (Ki) and the regional cerebral blood flow (rCBF) and by calculating the capillary permeability-surface area (PS) product. In the control group, after a femoral artery and vein were catheterized under isoflurane anesthesia, rats were allowed to remain awake for 2 h before measuring Ki (n = 6) or rCBF (n = 11). In the two experimental groups, rats were anesthetized with 1% and 2% isoflurane respectively, and their lungs were mechanically ventilated through a tracheal tube. Ki was measured (1% n = 6, 2% n = 7) using 14C-alpha-aminoisobutyric acid, and rCBF was measured (2% n = 7) using 14C-iodoantipyrine. Two percent isoflurane did not affect rCBF in 9 of 13 brain regions. Blood flow was less in the lateral and posterior cortex and greater in the medulla and pons when compared with the control group. Ki was less in 11 of 13 brain regions in both the 1% and 2% isoflurane groups than in the control group. There was no significant difference between 1 and 2% isoflurane in any brain region.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoisobutyric Acids↗
PubMed1992

Effects of fentanyl on alpha-aminoisobutyric acid transfer across the blood-brain barrier.

The effect of fentanyl on the transfer of small hydrophilic molecules across the blood-brain barrier was studied in rats by measuring the blood-brain transfer coefficient (Ki) and the regional cerebral blood flow (rCBF) and by calculating the capillary permeability-surface area product. In the control group (n = 14), after a femoral artery and vein were catheterized under isoflurane anesthesia, the rats were allowed to remain awake for 1.5 h before measuring Ki (n = 8) using intravenous 14C-alpha-aminoisobutyric acid or rCBF (n = 6) using 14C-iodoantipyrine. In the fentanyl groups, rats were injected with 25 micrograms/kg (low (n = 6) or 100 micrograms/kg (high dose) of fentanyl (n = 14), followed by a continuous infusion at a rate of 50 or 200 micrograms.kg-1.h-1, respectively. Their lungs were mechanically ventilated. The Ki (low dose, n = 6; high dose, n = 8) and rCBF (high dose, n = 6) were measured 1 h after fentanyl infusion. The Ki was lower in 9 of 13 brain regions in the low-dose fentanyl group and in 7 of 13 brain regions in the high-dose fentanyl group than in the control animals. The average value of Ki in all the brain regions was 8.6 +/- 4.6 microL.g-1.min-1 in the control group, 5.2 +/- 2.9 microL.g-1.min-1 in the low-dose fentanyl group, and 5.7 +/- 2.9 microL.g-1.min-1 in the high-dose fentanyl group. High-dose fentanyl did not significantly affect rCBF in any brain region studied. The value of the regional permeability-surface area product was similar to the corresponding regional Ki in the groups studied. In conclusion, fentanyl decreased the transfer of small hydrophilic molecules across the blood-brain barrier, as demonstrated by a decreased Ki and permeability-surface area product, without significant changes in rCBF.

Aminoisobutyric Acids↗
PubMed1990

Role of adenosine in catecholamine-induced global coronary functional hyperemia in isolated guinea pig hearts.

This study was designed to test the hypothesis that endogenous adenosine participates in the global coronary functional hyperemia accompanying intracoronary infusions of norepinephrine (NE) and isoproterenol (ISO). Intracoronary adenosine deaminase (ADA) was employed to test the hypothesis in isolated, perfused guinea pig hearts. We measured coronary perfusate flow (CPF) at a constant coronary perfusion pressure. Heart rate (HR), left ventricular pressure, and its rate of development were also measured. Global myocardial oxygen consumption (MVO2) and oxygen extraction were calculated, and blood gases and pH were measured routinely in inflow and outflow perfusate samples. In the absence of ADA, NE and ISO increased HR 67 +/- 6 and 106 +/- 11 beats.min-1, left ventricular pressure development 519 +/- 46 and 375 +/- 35 mm Hg.s-1, MVO2 22 +/- 2 and 28 +/- 3 microliters.min-1.g-1, and CPF 1.6 +/- 0.2 and 2.2 +/- 0.2 ml.min-1.g-1, respectively. With constant infusion of ADA (4.5 U.min-1.g-1, a dose which produces no direct effects on cardiac function) for 4 min, similar increments in HR and left ventricular pressure development were achieved with both catecholamines. Corresponding changes in MVO2 (9 +/- 2 and 6 +/- 3 microliters.min-1.g-1) were significantly less than those seen in the absence of ADA. Moreover, CPF did not increase in response to NE and ISO in the presence of ADA. These findings support an important role for adenosine in catecholamine-induced global coronary functional hyperemia in isolated, perfused guinea pig hearts.

Adenosine↗
PubMed1990

Coronary vasodilation caused by intravenous cocaine in the anesthetized beagle.

The aim of this study was to determine the effect of intravenous cocaine on the coronary circulation in the dog. Sixteen beagles separated into three groups were administered either cocaine (n = 8) or lidocaine (n = 4) at doses of 0.4, 2.0, and 10.0 mg/kg under conditions of constant coronary blood flow. A third group of beagles (n = 4) was administered cocaine under conditions of natural coronary blood flow. In the first group, the lowest dose of cocaine had no significant effect on coronary perfusion pressure, even though it increased mean systemic arterial pressure by 10% (p less than 0.05). The second two doses decreased coronary perfusion pressure by 13 (p less than 0.05) and 68% (p less than 0.05), respectively. In the second group, the lowest dose of lidocaine did not significantly affect coronary perfusion pressure. However, the second two doses significantly decreased coronary perfusion pressure by 22 (p less than 0.05) and 45% (p less than 0.05), respectively. Under conditions of natural coronary blood flow and coronary perfusion pressure, these same doses of cocaine increased coronary blood flow by 25, 63, and 175%, respectively. All coronary vascular responses occurred 60 s after administration of cocaine or lidocaine. We conclude that cocaine causes rapid, dose-dependent coronary vasodilation in the anesthetized beagle. The coronary vasodilation appears to be related to cocaine's known, local anesthetic properties.

Anesthesia↗
PubMed1989

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline.

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Adenosine↗
PubMed1988

Coronary vasodilation during global myocardial hypoxia: effects of adenosine deaminase.

Isolated, perfused guinea pig hearts were infused with intracoronary adenosine deaminase to investigate the contribution of endogenous adenosine to the coronary vasodilation of global myocardial hypoxia. Coronary perfusate pressure was held constant at 70 cmH2O throughout the experiment. We measured retrograde aortic inflow (assumed to equal total antegrade coronary flow) for 3-5 min of hypoxia before and 4 min after initiation of intracoronary adenosine deaminase infusion (4 U.g-1.min-1). In the absence of adenosine deaminase mild global hypoxia increased coronary perfusate flow 60%. In the presence of adenosine deaminase the response was limited to a 5% increment. Myocardial O2 consumption was significantly reduced during hypoxia in the presence of adenosine deaminase. In a second group of hearts, moderate global hypoxia increased coronary perfusate flow 125%. This was limited to a 53% increment in the presence of adenosine deaminase. Adenosine deaminase vehicle had no measurable effect on coronary perfusate flow responses to repeat mild hypoxia in a third group of hearts. We conclude that endogenous adenosine is singularly important in the coronary vasodilation of mild global myocardial hypoxia, but that other regulatory mechanisms might also contribute during moderate hypoxia.

Adenosine Deaminase↗
PubMed1987

Pressure-dependent vasoactive effects of histamine in the coronary circulation.

Twenty-one isolated, perfused, spontaneously rhythmic guinea pig hearts (Langendorff preparation) were used to investigate the effects of coronary perfusion pressure (CPP) on the coronary vasoactive response to a continuous infusion of histamine. Heart rate (HR), coronary perfusate flow (CPF), left ventricular pressure, dp/dtmax, oxygen extraction, and myocardial oxygen consumption (MVO2) were measured at constant CPP of 40 (n = 9), 53 (n = 6), and 65 cm H2O (n = 6) in the absence and presence of continuous intracoronary infusion of histamine [0.9 +/- 0.2 microgram/(min X g)]. At 40 cm H2O histamine caused significant coronary vasodilation. At 65 cm H2O histamine caused significant coronary vasoconstriction. At an intermediate pressure of 53 cm H2O histamine had no effect on CPF. At all three pressures HR, left ventricular pressure, dp/dtmax, and oxygen extraction increased significantly in response to histamine. MVO2 was unchanged by histamine at 65 cm H2O (flow was reduced but extraction increased. MVO2 increased modestly but significantly at 53 cm H2O (12% increase; flow unchanged but extraction increased), and increased prominently at 40 cm H2O (50% increase; flow and extraction increased). We conclude that the coronary vascular effects of continuously infused histamine are dependent on the preexisting, steady-state level of CPP in the isolated perfused guinea pig heart.

Animals↗
PubMed1987

Histamine-induced changes in coronary circulation and myocardial oxygen consumption: influences of histamine receptor antagonists.

The effects of histamine and selected H1 and H2 histamine receptor antagonists on cardiac inotropic and chronotropic activity, coronary perfusate flow (CPF), and myocardial oxygen consumption (MVO2) were studied in isolated guinea pig hearts perfused at constant pressure. Data were collected at the end of a 3-min infusion period at steady state. Cardiac performance increased significantly whereas CPF decreased during histamine infusion. MVO2 remained constant owing to a significant increase in myocardial oxygen extraction. Diphenhydramine attenuated the coronary vasoconstriction but potentiated the positive inotropic response. Cimetidine attenuated the inotropic and chronotropic responses but had no effect on coronary vasoconstriction. In combination, the histamine antagonists attenuated the changes in heart rate, contractility, and CPF. The histamine-induced increase in myocardial oxygen extraction was accompanied by a significant increase in MVO2 in the presence of diphenhydramine. The ratio of the change in oxygen extraction to the change in oxygen consumption caused by histamine was significantly increased by diphenhydramine. This compensated for a histamine-induced decrement in the ratio of the change of CPF to the change in oxygen consumption. Cimetidine had no effect on the changes in coronary flow, oxygen consumption, or the above ratios. Thus, histamine causes direct coronary vasoconstriction via an H1 receptor mechanism, cardiac positive inotropy by an H2 receptor mechanism, and cardiac positive chronotropy by combined H1 and H2 mechanisms. In the presence of a histamine-induced decrease in myocardial oxygen supply, increments in oxygen demand are met by increased oxygen extraction.

Animals↗
PubMedDate not supplied

Effects of hemorrhage on regional cerebral blood flow in awake and in isoflurane-anesthetized rats.

During hemorrhage, redistribution of cerebral blood flow may occur. We compared the effects of hemorrhage on regional cerebral blood flow in awake rats and in rats anesthetized with 1% or 2% isoflurane. In half of each group, regional cerebral blood flow was measured without hemorrhage. The other half was slowly bled to a mean arterial blood pressure of 40-45 mm Hg before measuring the regional cerebral blood flow. Without hemorrhage, the cortical regional blood flow was greater in the awake animals than that of the caudal part of the brain. In the 2% isoflurane group, however, the regional cerebral blood flow of the caudal part was greater than the cortical regional cerebral blood flow. After hemorrhage, a similar decrease (-45%) of the regional cerebral blood flow was observed in each brain region and the pattern of distribution of it remained unchanged in all experimental groups. However, the absolute value of the cortical flow was higher in the awake animals than in the isoflurane groups. Our experiment demonstrated that hemorrhage decreased the regional cerebral blood flow. However, it did not alter the redistribution of the cerebral blood flow in awake animals nor in the animals anesthetized with isoflurane.

Anesthesia↗