Biomedical subjects

H R Weiss

Publications and source records attributed to H R Weiss.

At least 145 records · Page 8Linked to original sources

PubMed1990

Effect of chemodenervation on the cerebral vascular and microvascular response to hypoxia.

This study evaluated the effect of bilateral carotid chemodenervation on the cerebrovascular response to hypoxia in conscious rats. Cerebral blood flow was measured using 4-iodo[N-methyl-14C]antipyrine, and the total and perfused microvasculature was studied by injection of fluorescein isothiocyanate dextran and alkaline phosphatase staining. To maintain constant PCO2, hypoxia was achieved in chemoreceptor-intact rats by the use of 4% CO2-8% O2-88% N2 and in chemodenervated rats by the administration of 8% O2-92% N2. Blood gas and hemodynamic parameters were similar in the two groups of rats. Chemodenervation had no significant effect on either resting blood flow or the perfused microvasculature during normoxia. A significant increase in cerebral blood flow (from 71 +/- 3 to 138 +/- 9 ml/min/100 g in control and from 91 +/- 5 to 127 +/- 7 ml/min/100 g in chemodenervated rats) and in the percent of cerebral arterioles and capillaries perfused occurred in both hypoxic control and chemodenervated rats. In chemoreceptor-intact rats, the greatest increase in blood flow and in perfused microvasculature occurred in caudal structures (medulla and pons) in comparison with rostral structures (cortex, thalamus, and hypothalamus). In chemodenervated rats, a similar increase in blood flow and perfused microvasculature occurred in all brain regions, with no regional differences. Thus, chemodenervation did not affect the overall cerebral blood flow or the microvascular response to hypoxia; however, rostral-to-caudal regional differences in the hypoxic response were lost after chemodenervation.

Animals↗

PubMed1990

Effect of thromboxane receptor blockade on oxygen supply/consumption variables during reperfusion in the anesthetized dog.

The thromboxane A2/PGH2 receptor antagonist SQ 30,741 has been previously shown to reduce infarct size and to improve subendocardial reflow. The purpose of this study was to determine the effect of SQ 30,741 on reperfusion O2 supply/consumption variables. Anesthetized open-chest dogs treated with vehicle or 1 mg/kg + 1 mg/kg/hr SQ 30,741, i.v. (starting 10 min after the onset of ischemia) were subjected to 90 min left circumflex coronary occlusion and 3 hr reperfusion. Regional myocardial blood flow (radioactive microspheres) and arterial and venous O2 saturations (microspectrophotometry) were determined. Animals treated with SQ 30,741 had significantly higher subendocardial reflow at 3 hr (48 +/- 6 ml/min/100 g) compared with vehicle (27 +/- 10 ml/min/100 g). At 3 hr postreperfusion, O2 extraction was significantly higher in the reperfused region compared with the nonischemic region, although extraction was not at maximal values. O2 extraction was similar in vehicle- and SQ 30,741-treated animals despite the near doubling of reflow into the subendocardial region with SQ 30,741. O2 consumption was significantly reduced in the reperfused subendocardial region (1.65 +/- 0.9 ml O2/min/100 g) in vehicle controls compared with the nonischemic subendocardial region (10.2 +/- 2.6 ml O2/min/100 g). SQ 30,741 significantly improved subendocardial reperfused regional O2 consumption (4.03 +/- 0.41 ml O2/min/100 g) compared with vehicle and this increase was proportional to the flow increment (no change in the O2 supply/consumption ratio). SQ 30,741 is thus increasing subendocardial reflow secondary to an increase in O2 consumption and the increased O2 consumption may be due to preservation of myocardial tissue.

Animals↗

PubMed1989

Effects of nitroglycerin on regional O2 supply and O2 consumption in reperfused dog myocardium.

This study was designed to assess whether nitroglycerin would improve the relationship between O2 supply and O2 consumption in the reperfused ischemic dog myocardium. In 16 dogs the left anterior descending coronary artery was occluded for 2 h, followed by a 4 h period of reperfusion. In 8 of the 16 dogs, an infusion of 10 micrograms/kg per min of nitroglycerin was begun 10 min prior and continued during 4 h of reperfusion. Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional blood flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. In both groups, 2 h of occlusion lowered the regional flow to a similar level. In the control group, 4 h of reperfusion returned the blood flow towards normal levels, from 15 +/- 20 ml/min per 100 g (mean +/- S.D.) at the end of occlusion to 57 +/- 39 in the affected area compared to 84 +/- 32 ml/min per 100 g in the nonischemic area. In nitroglycerin treated animals, the flow increase with reperfusion was similar to the control group (12 +/- 10 to 65 +/- 33 ml/min per 100 g). O2 extraction was greater in the reperfused than in the unaffected area in both groups. However, reperfused region O2 extraction was lower in the nitroglycerin treated than control group. There was a greater number of arteries and veins with reduced O2 saturations in the control group reperfused area compared to the nonischemic area. Nitroglycerin decreased the number of low O2 saturation vessels in the reperfusion area. Reperfusion alone does not restore the ratio of O2 supply to O2 consumption to control values, while nitroglycerin significantly improves this ratio. Thus nitroglycerin appears to better match the increased flow during reperfusion with microregional O2 consumption.

Animals↗

PubMed1989

The effect of acetylcholine on regional myocardial O2 consumption and coronary blood flow in the rabbit heart.

The effect of acetylcholine on the regional coronary perfusion and O2 consumption was determined in anesthetized open chest rabbits in order to compare its direct vasodilatory effects with the metabolic vasoconstriction it induces. Experiments were conducted in seven untreated controls and seven rabbits which were infused with acetylcholine (1 microgram/kg/min). Myocardial blood flow was determined before and during acetylcholine infusion using radioactive microspheres. Regional arterial and venous O2 saturation was analyzed microspectrophotometrically. Acetylcholine reduced heart rate by 30% and significantly depressed the arterial systolic and diastolic blood pressure. The mean O2 consumption was significantly reduced with acetylcholine from 9.6 +/- 2.0 to 6.1 +/- 3.6 ml O2/min/100 g. Coronary blood flow decreased uniformly across the left ventricular wall by about 50% and resistance to flow increased by 42% despite potential direct cholinergic vasodilation. O2 extraction was not affected during acetylcholine infusion. It is concluded that the acetylcholine infusion directly decreased myocardial O2 consumption which in turn lowered the coronary blood flow and increased the resistance. The decreased flow was related to a reduced metabolic demand rather than a direct result of lowered aortic blood pressure. Unaffected myocardial O2 extraction also suggests that blood flow and metabolism were matched. This indicates that direct cholinergic vasodilation of the coronary vasculature does not allow a greater reduction in metabolism than flow in the anesthetized open chest rabbit heart during acetylcholine infusion.

Acetylcholine↗

PubMed1989

Relationship between beta-adrenoceptors and coronary blood flow heterogeneity.

The purpose of this study was to investigate the hypothesis that the heterogeneous distribution of beta adrenoceptors contributes to the control of flow heterogeneity in the canine myocardium. beta adrenoceptor density and affinity were measured simultaneously with coronary blood flow in multiple sections of the left ventricle of 14 anesthetized open chest dogs. Radioactive microspheres were used for the measurement of blood flow. The left ventricle was cut into 15 subepicardial (EPI) and 15 subendocardial (ENDO) sections. Receptor density (Bmax) and dissociation constant (Kd) were measured using [125I]-iodopindolol. The average control myocardial blood flow (MBF) was 86 +/- 15 ml/min/100 g. Isoproterenol (0.5 micrograms/kg/min) increased MBF by 82%, whereas propranolol (2 mg/kg) reduced MBF by 13%. The mean value for Bmax was unaltered by either treatment. Under control conditions, a significant positive correlation (r = 0.26, p less than 0.0001) was observed between Bmax and blood flow. In the isoproterenol treatment group, this correlation was enhanced (r = 0.49, p less than 0.0001). Beta adrenoceptor blockade led to a negative correlation. Kd showed no overall correlation with blood flow. Kd but not Bmax was significantly higher in the EPI than in the ENDO and in the base compared to the apex. There appears to be a direct linear relationship between the distribution of beta adrenoceptors and MBF distribution which is enhanced under conditions of high beta adrenergic activity. There is a correlation between beta adrenoceptor activity and blood flow distribution in the canine myocardium.

Animals↗

PubMed1989

Increased myocardial microvascular utilisation and flow during atrial pacing.

To determine the influence of heart rate on regional coronary flow, the coronary vascular and microvascular responses to increased heart rate were examined in anaesthetised open chest New Zealand white rabbits. Coronary blood flow was measured with labelled microspheres. Fluorescein isothiocyanate (FITC)-dextran (150 mg.kg-1) was given to mark the perfused microvessels. The FITC-dextran was given at various intervals before removal of the heart. Alkaline phosphatase stain was used to locate the total microvasculature. Increase in heart rate from 272(SD23) to 339(13) beats.min-1 increased the coronary blood flow from 198(56) to 288(82) ml.min-1.100 g-1. The subendocardial/subepicardial flow ratio was not altered by pacing. Total capillary density averaged 2508(363).mm-2 and arteriolar density was 1.74(4.1).mm-2. There were no significant regional or treatment differences in these values. The increase in blood flow with pacing was accompanied by a uniform increase in the percentage of the microvasculature perfused in the subepicardial and the subendocardial layers of the left ventricular free wall, from 58(6)% to 75(10)% for capillaries and from 54(17)% to 81(19)% for arterioles. These results show that enhanced heart rate increases the coronary blood flow and the density of the perfused microvessels uniformly across the ventricular wall. Thus both the coronary vascular and microvascular reserves are used in the rabbit heart during tachycardia.

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PubMed1989

Relationship between local oxygen consumption and local and external cardiac work: effect of tachycardia.

This study was designed to determine the extent of coupling between regional myocardial segment work and corresponding regional oxygen consumption, and to examine whether tachycardia induced changes in regional work are translated into corresponding changes in external cardiac work. In the open chest anaesthetised dog, the heart was paced at frequencies of 120-270 beats.min-1. Global and regional myocardial O2 supply, consumption, and balance were evaluated at each heart rate, and correlated with corresponding functional changes. Global cardiac function was evaluated from aortic flow, blood pressure, and left ventricular pressure. Coronary sinus flow and O2 saturation were used to calculate O2 consumption. The integrated multiple of myocardial shortening (ultrasonic dimension crystals) by corresponding force (strain gauge arch) during an averaged beat was used to express regional segment work. Regional coronary blood flow was measured with radioactive microspheres, and microspectrophotometry was used to evaluate O2 saturation in small arteries and veins. These indices were used to calculate regional myocardial oxygen consumption. NADH redox levels were recorded by surface fluorometry, and were found to increase with heart rate by up to 67%. Increasing heart rate from 120 to 180 beats.min-1 increased regional work from 3040(SEM 220) to a peak of 4290(280) mm.g-1.min-1, whereas external cardiac work did not increase [67.0(2.6) to 65.3(4.4) mm Hg.litre-1.min-1] and fell further at the highest rates. Regional oxygen consumption increased from 6.16(0.47) to 8.29(0.53) ml O2.min-1.100 g-1 and was linearly related to regional work at all heart rates (r = 0.971, p less than 0.05). External cardiac work fell by about 26% whereas global myocardial oxygen consumption increased by 49% during tachycardia. It is concluded that myocardial oxygen consumption is more closely related to regional segment work than to external work, and that tachycardia significantly raises the oxygen cost of external work of the heart.

Animals↗

PubMed1989

Role of beta adrenoceptors in the hypertrophic response to thyroxine.

The ability of beta-adrenoceptor blockade to reduce the hypertrophic response to thyroxine (T4, 0.5 mg/kg per day, s.c.) was tested in New Zealand white rabbits. Two beta-adrenergic blocking agents, one a full antagonist (propranolol, 9.6 mg/kg per day) and the other a partial agonist (pindolol, 0.96 mg/kg per day) were administered in combination with T4 in an effort to reduce myocardial hypertrophy. A 3 and 16 day group were generated to test the time course of the hypertrophic and receptor responses. Coronary blood flow was measured using radioactive microspheres, and beta-adrenoceptor number and affinity were measured using 125I(-) pindolol as the radioligand. T4 increased coronary blood flow to 1.95 times control values in the 3 day group and 2.2 times control levels in the 16 day group; beta-adrenoceptor number was increased similarly in 3 and 16 day groups to 1.9 times control Bmax levels. Heart weight (HW) to body weight (BW) ratios were significantly increased in only the 16 day group to 1.22 and 1.61 times control, respectively. Treatment with propranolol + T4 blunted the coronary blood flow increase, but receptor upregulation occurred to the same extent as with either substance alone. The HW/BW was increased to 1.49 times control. Pindolol + T4 did not decrease coronary blood flow but blocked beta-adrenoceptor upregulation. The HW was reduced to control levels and the HW/BW ratio was 1.40 times control and significantly decreased from T4 alone. Thus, pindolol was effective in reducing the hypertrophic response to T4, whereas propranolol was only moderately effective in doing so.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Cervical sympathectomy and cerebral microvascular and blood flow responses to hypocapnic hypoxia.

This study evaluated the effects of bilateral superior cervical ganglionectomy on cerebral blood flow (CBF) and utilization of brain capillary reserve in conscious rats during normoxia and hypoxia (8% O2 in N2). Regional CBF was determined in sham-lesioned and ganglionectomized rats with [14C]iodoantipyrine. The percentage of the total volume fraction and number of perfused capillaries was determined by comparing the perfused microvessels, identified by the presence of fluorescein isothiocyanate dextran, with the total microvascular bed, identified by alkaline phosphatase stain. There were no significant differences in regional CBF between control and ganglionectomized rats under normoxic conditions. CBF increased significantly during hypoxia in both control and control ganglionectomized rats. In control, hypoxic flow to caudal structures was significantly higher than to rostral structures and that differential response was prevented by ganglionectomy. There was no significant difference in the number of perfused microvessels between sham-lesioned and ganglionectomized rats during normoxia. The number of perfused arterioles and capillaries was significantly higher under hypoxic conditions than under normoxic conditions in sham and ganglionectomized animals. During hypoxia, the percent of arterioles per squared millimeter perfused increased to 63 +/- 5% in sham-lesioned rats and to a significantly greater extent, 80 +/- 6%, in ganglionectomized rats. The percentage of capillaries per squared millimeter perfused changed similarly. The peripheral sympathetic nervous system appeared to play an important role in the control of cerebral microvascular response to hypoxia.

Animals↗

PubMed1989

Adenosine and cerebral capillary perfusion and blood flow during middle cerebral artery occlusion.

The effects of adenosine on regional cerebral blood flow and indexes of the total and perfused microvascular bed were studied after 1 h of middle cerebral artery occlusion in the anesthetized rat. Iodo[14C]antipyrine was used to determine cerebral blood flow. Fluorescein isothiocyanate-dextran was used to study the perfused microvasculature, and an alkaline phosphatase stain was used to identify the total bed. Mean arterial blood pressure was significantly reduced by adenosine. Cerebral blood flow increased significantly by 75%, except in the flow-restricted cortex where flow averaged 28 +/- 15 (SD) ml.min-1.100 g-1 in control and 34 +/- 33 ml.min-1.100 g-1 in adenosine-treated animals. No significant regional structural differences were observed within the microvascular beds of the two groups. The percentage of the microvascular volume perfused increased significantly in all brain regions in the adenosine-treated rats, including the flow-restricted cortex. The percent perfused arteriolar volume in the flow-restricted cortex was 30 +/- 12% in control and 95 +/- 3% in adenosine-treated animals. Similar values for the capillary bed were 22 +/- 10% in control and 54 +/- 3% in adenosine-treated rats. These results indicate a maintenance of flow with a reduction in diffusion distances in the flow-restricted cortex after treatment with adenosine.

Adenosine↗

PubMed1989

Effect of carbon dioxide on the utilization of brain capillary reserve and flow.

This study investigated effects of increased arterial carbon dioxide on the brain capillary perfusion pattern. Conscious rats were exposed to a 0%, 8% or 12% CO2 in air gas mixture. Arterial blood pressure, heart rate, arterial blood gases and pH were recorded, and either regional cerebral blood flow or the percent of capillary volume/mm3 or number/mm2 perfused were determined in cortical, hypothalamic, pontine or medullary regions of the brain. Arterial PCO2 increased from 37 +/- 1 in control to 74 +/- 1 torr in the high CO2 group. A position linear relationship was found between cerebral blood flow and arterial PCO2 in all examined regions. Approximately half of the capillaries in the examined regions were perfused under normocapnic conditions. Increasing arterial PCO2 had no effect on the percent of the capillary bed perfused in the cortex or hypothalamus. However, there was a significant linear relationship between carbon dioxide tension and the percent of the microvasculature perfused in the hindbrain. The percent of capillaries/mm2 perfused increased significantly in the medulla (to 60 +/- 5%) and pons (70 +/- 4%) with 12% CO2 in air. These data suggest that carbon dioxide may have differential effects on diffusion distances affecting the hindbrain to a greater extent than the forebrain.

Animals↗

PubMed1989

Microvascular perfusion during atrial pacing in renal hypertension induced cardiac hypertrophy.

The purpose of this study was to determine if microvascular reserve was recruited during atrial pacing in the hypertrophied myocardium. Hypertrophy was induced by one-kidney, one-clip (1K1C) renal hypertension and compared to uninephrectomized control rabbits 30 days after surgery. Coronary flow was determined by radioactive microspheres. Microvascular perfusion was determined by comparison of fluorescein isothiocyanate-dextran labeled vessels with an alkaline phosphatase stain. Heart rates were not different between groups and all animals were paced 35% above baseline. Baseline coronary flow (176 +/- 44 and 207 +/- 61 ml/min/100 g, control and 1K1C animals) was not altered by pacing in either group. The baseline percent of capillaries perfused was not different between groups (56 +/- 2 and 61 +/- 3%, sham and 1K1C) and the percent perfused increased significantly during pacing for both the non-hypertrophied and 1K1C myocardium (76 +/- 6 and 78 +/- 10%). The baseline percent of the arteriolar bed perfused, was higher in the 1K1C (86 +/- 5%) compared to non-hypertrophied (63 +/- 6%) myocardium. During pacing, the percent of the arteriolar bed perfused increased in non-hypertrophied (89 +/- 14%) but not in the 1K1C myocardium. Although the percent of arterioles perfused did not increase with pacing in the 1K1C myocardium, the capillary reserve was recruited, facilitating the transport of O2 in both the hypertrophied and non-hypertrophied myocardium.

Animals↗

PubMed1989

Effect of diltiazem on regional oxygenation of reperfused myocardium.

Reperfusion after 2 hr of experimental ischemia results in reduced blood flow to the reperfused region, as well as elevated regional O2 extraction in that region. The aim of the present study was to determine whether diltiazem, administered during reperfusion, can improve regional blood flow and lower O2 extraction in the previously occluded region. In open-chest anesthetized dogs, 2-hr occlusion of the left anterior descending coronary artery was followed by a 4-hr period of reperfusion. In 7 of the 15 animals, diltiazem (0.45 micrograms/kg/min) was infused i.v. during the reperfusion period; this was preceded by a loading dose of 0.18 micrograms/kg 10 min before release. Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional blood flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. In both groups, coronary occlusion lowered regional flow to a similar level. After a 4-hr reperfusion, flow to the subendocardial region of treated hearts was significantly greater than that to the untreated reperfused myocardium (75.6 +/- 46.4 vs. 40.3 +/- 25.8 ml/min/100 g), and did not differ from the preocclusion level. The subendocardium/subepicardium flow ratio was reversed in occluded and untreated reperfused myocardium (subendocardium flow less than subepicardium flow), but was not reversed in treated reperfused regions. Myocardial oxygen extraction was 11.0 +/- 2.4 ml of O2/100 ml of blood in the untreated reperfused subendocardium, and was significantly decreased to 8.5 +/- 0.9 ml of O2/100 ml in the treated subendocardium. The proportion of individual veins having O2 saturations below 25% was significantly reduced by diltiazem treatment from 45.2 to 22.7%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Regional O2 consumption and coronary flow during beta adrenoceptor stimulation in reperfused canine myocardium.

This study was performed to assess the ability of a reperfused region to increase its flow and O2 consumption upon inotropic stimulation. Isoproterenol (5 micrograms/kg/min) was infused i.v. during the reperfusion phase (4 hr) after 2 hr of the left anterior descending coronary artery occlusion in anesthetized open chest dogs (n = 7). The response was compared to a similar untreated reperfused group (n = 8). Coronary blood flow was obtained with labeled microspheres. Arterial and venous O2 saturations were determined microspectrophotometrically. During reperfusion and isoproterenol infusion, significantly higher heart rate (226 +/- 48 beats/min), maximum positive derivative of left ventricular pressure (3132 +/- 838 mm Hg/sec) and systolic aortic blood pressure (162 +/- 16 mm Hg) were recorded compared to reperfusion in the control group (133 +/- 22, 1615 +/- 184 and 124 +/- 30, respectively). In the control group, coronary blood flow to the reperfused areas decreased from preocclusion values of 85 +/- 22 and 95 +/- 43 to 63 +/- 45 and 47 +/- 31 ml/min/100 g for the subepicardium and subendocardium, respectively. O2 extraction was increased significantly in the reperfused region and O2 consumption was similar to that in the nonoccluded area. The corresponding flow values in the treated group at the end of the reperfusion period were 272 +/- 142 and 183 +/- 150 ml/min/100 g, respectively. With isoproterenol, the O2 extraction was not greater than in the nonoccluded area and the O2 consumption increased about 3-fold in comparison to the control group, although the increase in the reperfused subendocardium was less.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Role of alpha-adrenoceptors in the control of the cerebral blood flow response to hypoxia.

This study assessed the role of vascular and central alpha-adrenoceptors in the regional cerebral blood flow response to moderate hypoxia. Studies were conducted in 21 rabbits using radioactive microspheres under normoxic and hypoxic (10% O2 in N2) conditions. Animals were divided into three groups and administered either saline, N-methyl chlorpromazine, or phenoxybenzamine. During normoxia, there were regional differences in cerebral blood flow distribution in the saline- and N-methyl chlorpromazine-treated rabbits which were eliminated by phenoxybenzamine. In control, hypoxia significantly increased average cerebral blood flow from 57 +/- 22 to 132 +/- 52 ml/min per 100 g. Flow to the hindbrain increased to a significantly greater extent than to the mid- or forebrain during hypoxia. The increase in average cerebral blood flow during hypoxia was significantly reduced to 97 +/- 34 ml/min per 100 g by phenoxybenzamine. Both alpha-adrenoceptor antagonists prevented the significantly greater increase in hindbrain flow during hypoxia. The greater flow responsiveness of the hindbrain to hypoxia appears to be related at least in part to alpha-adrenoceptors found in the cerebral vasculature.

Animals↗

PubMed1988

Effect of reperfusion on O2 supply/consumption balance in ischemic canine left ventricle.

This study was designed to assess the effects of reperfusion on regional O2 supply and O2 consumption of ischemic areas of the myocardium in 15 anesthetized open-chested dogs. The left anterior descending coronary artery (LAD) was occluded for 6 h (n = 8), 2 h (n = 5), 2-h occlusion followed by 4-h period of reperfusion (n = 7), and 10-min occlusion followed by 90-min period of reperfusion (n = 3). Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. Coronary occlusion for 2 or 6 h significantly reduced mean flow to 15 +/- 8 and 13 +/- 14 ml/min/100 g (mean +/- SD), respectively, in the affected LAD areas as compared to 128 +/- 26 and 113 +/- 46 ml/min/100 g in the non-ischemic areas. In the 4-h reperfusion group, reperfusion increased the average flow (60 +/- 42 ml/min/100 g). O2 extraction was greater in the ischemic area than in the unaffected area after both occlusion and 4-h reperfusion. In the affected area, O2 consumption was reduced by 84% after 6-h occlusion. Reperfusion for 4 h increased O2 consumption toward normal values. Coronary artery occlusion produced an increase in the number of arteries and veins with reduced O2 saturations and this was not affected by reperfusion. Short-term occlusion had no significant O2 supply effects after 90 min of reperfusion. It can be concluded that even though there was an increased O2 consumption as a consequence of reperfusion, O2 consumption still appeared to be flow-limited as indicated by the microregions of low O2 supply and/or high O2 extraction.

Animals↗

PubMed1988

Measurement of cerebral capillary perfusion with a fluorescent label.

The aim of this study was to evaluate methods of labeling the perfused cerebral capillary bed using fluorescein isothiocyanate (FITC)-dextran or FITC-globulin. An alkaline phosphatase stain was used to identify the total capillary bed. All experiments were conducted on anesthetized rats. FITC labels were injected and the rats were sacrificed either 20 sec or 6 min after injection. Heads were frozen in liquid N2 or dry ice-cooled methanol. An additional group was perfused with India ink. Comparisons were made between FITC labels and methods of slide analysis. No significant differences in cerebral capillary number per square millimeter or volume per cubic millimeter were found in animals in which the heads were frozen in liquid N2 or dry ice-cooled methanol. in FITC labels, or in light sources. When sections were air dried, 56 +/- 4% of the alkaline phosphatase stained vessels were marked with FITC label in brains frozen 20 sec after FITC injection. India ink labeled 89 +/- 7% of the alkaline phosphatase stained capillaries. When sections were air dried, 86 +/- 7% of the alkaline phosphatase stained vessels were labeled in brains frozen 6 min after injection of the FITC label. Using a technique of absolute alcohol impregnation of the sections, 130 +/- 25% and 144 +/- 28% of the alkaline phosphatase stained sections were FITC labeled. It can be concluded that the absolute alcohol impregnation technique significantly overestimates the number of perfused cerebral capillaries.

Alkaline Phosphatase↗

PubMed1988

Chemical sympathectomy and utilization of coronary capillary reserve in rabbits.

The effect of chemical sympathectomy with 6-hydroxydopamine (60 mg/kg, 5 days prior to the experiment) on coronary blood flow and the percentage of perfused myocardial arterioles and capillaries was investigated in anesthetized open-chest rabbits and compared to a control group. In half of the animals, coronary flow was determined using radioactive microspheres. The others were given fluorescein isothiocyanate-dextran to mark the perfused microvessels. Alkaline phosphatase stain was employed to locate the total microvasculature. A group of control and sympathectomized rabbits were administered 2 mg/kg of propranolol. Myocardial norepinephrine content was significantly decreased from 1108 +/- 161 (mean +/- SEM) in the control group to 162 +/- 31 ng/g wet weight in the denervated group as determined by HPLC technique and electrochemical analysis. However, the decrease in arterial blood pressure, heart rate, and coronary blood flow of the denervated group as compared to the control was not significant. Chemical sympathectomy significantly increased the number (Na) of the perfused capillaries from 57 +/- 3 to 66 +/- 3% and arterioles from 57 +/- 5 to 76 +/- 9%. A similar increase in the percentage of microvessels perfused with denervation was observed after propranolol. It is concluded that although denervation had no significant effect on the hemodynamic conditions or average coronary blood flow, it significantly increased the utilization of the myocardial microvessels. We suggest that the sympathetic nervous system and alpha adrenoceptors exert significant control of the utilization of coronary microvascular reserve.

Animals↗