Biomedical subjects

B A Acad

Publications and source records attributed to B A Acad.

At least 19 recordsLinked to original sources

PubMed1990

Pacing during reperfusion elevates regional myocardial oxygen consumption.

Reperfusion after 2 h of coronary artery occlusion has been shown to result in depressed coronary blood flow to the reperfused region and elevated regional myocardial extraction. This suggests that reperfused myocardium, even after 4 h of reperfusion, possesses limited flow and O2 consumption reserves. We studied the capacity of reperfused myocardium to elevate regional blood flow and regional O2 consumption in response to sustained increased O2 demand, produced by atrial pacing. Two groups of anesthetized open-chest dogs were subjected to 2 h of left anterior descending coronary artery occlusion followed by 4 h of reperfusion. One group was subjected to atrial pacing (40% increase in heart rate) during the entire 4-h reperfusion period. Regional O2 saturation was measured by microspectrophotometry in samples of reperfused and nonoccluded subepicardium and subendocardium, which were taken at the end of the reperfusion period. In the paced group, regional blood flow (radiolabeled microspheres) to reperfused myocardium was significantly higher than to corresponding regions of unpaced hearts (110 +/- 22 vs. 40 +/- 9 ml.min-1 x 100 g-1 in the subendocardium). In the control group, O2 extraction of reperfused subendocardium was significantly higher than that measured in the corresponding nonoccluded region (11.0 +/- 0.9 vs. 8.0 +/- 0.6 ml O2/100 ml). Pacing did not elevate O2 extraction of reperfused myocardium (8.7 +/- 0.6 vs. 8.3 +/- 0.7 ml O2/100 ml). Myocardial O2 consumption was significantly elevated in all regions of the paced heart. It is concluded that reperfused myocardium possesses significant unutilized O2 supply and consumption reserves.

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

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.

Animals↗

PubMed1989

Regional myocardial O2 consumption and coronary blood flow responses to acetylcholine in rabbit heart.

The effect of acetylcholine on regional coronary blood flow and myocardial O2 consumption was determined in order to compare its direct vasodilatory effects with the metabolic vasoconstriction it induces. Experiments were conducted in seven untreated control anaesthetized open chest rabbits 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 by 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 blood pressure. Unaffected myocardial O2 extraction also suggested 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 anaesthetized open chest rabbit heart during acetylcholine infusion.

Acetylcholine↗

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

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↗

PubMed1988

Effect of prolonged propranolol administration and withdrawal on perfusion of the myocardial capillary bed.

The effect of chronic propranolol administration (2 mg.kg-1.d-1 for 14d) and withdrawal on microvascular perfusion was studied in rabbit myocardium. Fluorescein isothiocyanate-dextran was injected into four groups of anaesthetised open chest rabbits. Fluorescent microscopy was used to identify the perfused vessels and alkaline phosphatase stain was employed to locate the total microvasculature. Beta adrenoceptor density (Bmax), measured using 125I-iodopindolol, increased from 20.3(SD 6.3) fmol.mg-1 protein in control to 52.4(8.9) in chronically treated rabbits. The proportion of the capillary bed which was perfused, 61.4(4.3)% was significantly decreased by acute injection of propranolol to 51.1(5.1)%, but not affected by chronic administration, remaining at 57.0(4.0)%. The percentage of the capillary bed perfused increased significantly after cessation of chronic propranolol treatment to 69.1(6.5)%. Similar results were seen for myocardial arterioles. Thus, while diffusion distances are increased by acute adrenoceptor blockade, this effect is not seen in the chronic condition. Diffusion distance decreased significantly after withdrawal of chronic propranolol treatment. We conclude that the percentage of perfused capillaries is strongly influenced by the number of beta adrenoceptors or their effect.

Animals↗

PubMed1988

Improved distribution of regional oxygenation in denervated ischemic dog myocardium.

The role of the adrenergic nervous system in the response to coronary artery occlusion has been examined using surgical and chemical denervation techniques. Experiments were conducted on four groups of dogs (n = 18): 1) untreated controls; 2) intrapericardial denervation immediately prior to coronary ligation; 3) surgical denervation 2 weeks prior to the experiment; and 4) chemical sympathectomy 5 days prior to the experiment with 6-hydroxydopamine (50 mg/kg). Small artery and vein O2 saturations were obtained microspectrophotometrically and combined with radioactive microsphere blood flow determinations to calculate regional myocardial O2 consumption in open chest dogs. Denervation significantly reduced the preocclusion heart rate from 165 +/- 16 beats/min in the control to 114 +/- 13 in the chronic surgically denervated and to 137 +/- 15 in the chemically sympathectomized groups. After 2 hours of occlusion, the O2 consumption and flow were similar in the nonischemic area except for lower values in the surgically denervated group. Total coronary blood flow and O2 consumption in the occluded regions were not significantly affected by chronic denervation. However, significant elimination of areas with low venous O2 saturation (less than 20%) were found in the ischemic myocardium of the chronically denervated groups as compared with the control or with the acutely denervated dogs. The mean venous O2 saturation was found to be significantly higher in all regions of these two groups as compared with the control. The O2 extraction was also lowered. Thus, chronic denervation reduced microregional heterogeneity of oxygenation in the ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Relation between myocardial substrate utilization, oxygen consumption and regional oxygen balance in the dog heart in vivo.

The interaction between myocardial function, oxygen consumption and energy production was examined in the left ventricular myocardium during various physiological conditions. Myocardial function was measured by both LV dP/dTmax and by local contractile tension. Coronary blood flow was measured from the coronary sinus; regional coronary blood supply was recorded using a thermistor placed on the epicardial surface. Intracellular oxygen balance was estimated using NADH fluorescence. Myocardial oxygen consumption and utilization of glucose, pyruvate, lactate and free fatty acids were calculated from their concentrations in the arterial and coronary sinus blood. The effects of tachycardia at 180 and 240 bpm, noradrenaline infusion (25 micrograms kg-1 min-1), and increased coronary blood flow caused by hypopneic respiration were examined. During pacing, contractile force, coronary flow and NADH fluorescence increased. At 240 bpm, the lactate/pyruvate ratio increased from 5.98 +/- 0.92 to 8.76 +/- 1.41 and NADH fluorescence increased from 50 to 71.7 +/- 3.73 (as compared to control), indicating impairment of myocardial oxygenation. Hypopneic respiration produced a marked elevation of coronary blood flow. Both noradrenaline infusion and hypopnea produced a decrease in both NADH fluorescence and the lactate/pyruvate ratio. No significant difference was found between the FORCE/ATP, FORCE/MVO2 and ATP/MVO2 ratios during pacing and noradrenaline. However, during hypopnea, the amount of ATP apparently formed (as calculated by substrate utilization assuming the formation of 3 ATP molecules per oxygen) was disproportionately greater than contractile force and oxygen consumption. It is suggested that this discrepancy may be due to the uncoupling of oxidative phosphorylation.

Adenosine Triphosphate↗

PubMed1985

Effect of global vs regional ischaemia upon myocardial contractility and oxygen balance.

The possible role of catecholamines upon the nature of myocardial response to regional and global left ventricular ischaemia was investigated. Global ischaemia was accomplished by temporary occlusion of the left main coronary artery and regional ischaemia by temporary ligation of the left anterior descending coronary artery. Isometric force of contraction was measured with strain gauge arches, regional blood flow by a thermistor technique and intracellular NADH redox level by a fluorometric technique. These measurements were made simultaneously in two areas on the left ventricular myocardium: one immediately below the bifurcation of the LAD and the other immediately below the circumflex coronary artery. Following LAD occlusion a variable inotropic response was observed in the ischaemic area. A decrease in contractile tension was found in 19 of the dogs (44%), no change in 23% and an increase was found in 33%. Global ischaemia invariably resulted in a decrease in contractile tension. NADH redox state was markedly higher during global than during regional ischaemia. Propranolol administration blocked the positive inotropic response to regional ischaemia. It is concluded that endogenous catecholamine release may be responsible for increased contractile force during regional ischaemia. This response is apparently limited by the oxygen availability to the tissue.

Animals↗

PubMed1985

Preservation of myocardial oxygen balance and functional reserve by coronary vasodilators.

Reduced myocardial function at very high heart rates may be due to limited coronary blood supply. The effects of the vasodilators nitroglycerin (10 micrograms kg-1 min-1) and elevated CO2 upon regional function during tachycardia were studied. In open-chest anaesthetized dogs, regional contractile force, epicardial tissue blood flow and local NADH redox level were recorded during graded ventricular pacing. It was found that the vasodilating action of nitroglycerin in the unpaced heart was much lower than produced by CO2 (23.6 +/- 5.8% vs. 137.6 +/- 33.5%). Maximal pacing at 275 bpm caused only a moderate flow elevation in control (20 +/- 6.8%) and CO2 conditions (20.3 +/- 4.03%), but marked vasodilation during nitroglycerin infusion (85.2 +/- 14.6%). Regional function during tachycardia was improved similarly by both vasodilators. NADH levels increased with heart rates under all experimental conditions, but the absolute NADH levels were consistently lower following vasodilator treatments. The lowest NADH levels were observed during nitroglycerin treatment at all heart rates. It is suggested that nitroglycerin augments myocardial functional reserve by preserving oxygen balance more than predicted by its vasodilatory effect alone.

Animals↗

PubMed1981

Dynamic redistribution of coronary blood flow in the dog as measured by a thermistor technique.

The effect of heart rate upon the coronary blood supply to the right and left ventricles was studied in anaesthetized, open-chest dogs. Indirect recording of coronary supply was obtained using thermistors placed locally on the surface or in the wall of the ventricles. The validity of the thermistor technique was examined in vivo as well as by using an in vitro laboratory model. Myocardial perfusion was also measured using electromagnetic flowmeters placed around the anterior descending and circumflex arteries, as well as the coronary sinus and Thebesian drainage. It was found that at heart rates lower than about 150/min, coronary perfusion to all areas increased equally as rate was elevated. At higher heart rates, coronary flow to the right ventricle continued to increase linearly with rate, whereas perfusion to the left ventricle either increased much less or declined. It is concluded that tachycardia causes coronary flow to be dynamically redistributed in favour of the right ventricle.

Animals↗

PubMed1981

An experimental approach for evaluation of the O2 balance in local myocardial regions in vivo.

Quantitative evaluation of myocardial oxygen balance can be accomplished by measurement of oxygen supply, demand, and intracellular oxygen concentration. Experimentally, these parameters are often related to coronary blood flow, cardiac contractility, and mitochondrial NADH redox level, respectively. Methods were developed to measure these three parameters in a local region on the myocardial surface in open-chest dogs. Local coronary blood supply was measured with the aid of a small surface thermistor, and cardiac work with a miniature strain gauge arch. NADH oxidation--reduction state was recorded using surface fluorometry through a fibre optic light guide. Transient anoxia produced by nitrogen breathing caused a rapid but reversible elevation in NADH levels, which was not always accompanied by a concomitant change in contractile force. Elevation of heart rate resulted in a rise in intramitochondrial NADH followed by an increase in coronary flow. In spite of the increased flow, NADH levels remained elevated, indicating a change in the O2 balance; this may indicate that autoregulation does not necessarily result in total compensation.

Animals↗

PubMed1981

Coronary vasodilation produced by tachycardia under various basal flow conditions.

Some properties of coronary vasodilation produced by heart rate elevation under various basal coronary flow levels was studied. Coronary sinus blood flow, myocardial oxygen consumption and left ventricular contractile force were measured in anaesthetized, open-chest dogs. Heart rate was progressively increased by electrical stimulation at rates ranging from 60/min to 210/min. This was repeated during control, noradrenaline infusion (0.2 microgram kg-1 min-1), in the presence of propranolol (0.25 mg/kg), and during hypopneic positive pressure respiration. It was found that under all experimental conditions, coronary perfusion increased linearly with heart rate. At each rate, coronary flow was greater during noradrenaline infusion and hypopneic respiration than that observed during control or following beta-blockade. Myocardial oxygen consumption behaved similarly to flow, and MVO2 was lowest in the presence of propranolol, and highest during hypopneic ventilation and catecholamine infusion. Contractile force per min (heart rate x tension) also increased with increasing heart rate, but was greatest during noradrenaline infusion, lowest during beta-blockade, and similar during both control and hypopneic respiration. These results indicate that the oxygen cost of contraction was different under the various conditions, and was particularly wasteful during hypopneic respiration. It is concluded that autoregulation caused by heart rate elevation is not dependent on the initial state of coronary blood flow, and that endogenous catecholamine release cannot account for this phenomenon.

Animals↗

PubMedDate not supplied

Differential effects of various inotropic agents on the intracellular NADH redox level in the in vivo dog heart.

A similar inotropic response was elicited by either increasing heart rate or infusing noradrenaline or ouabain in the open-chest dog preparation. Changes in local coronary blood supply and intracellular NADH redox level produced by these inotropic interactions were examined. Contractile tension was measured using a strain gauge arch; coronary flow, using a thermistor probe; and NADH redox level, by surface fluorometry. For each inotropic agent, isometric tension increased by about 40%. However, the mean increase in coronary flow was 80 +/- 9.7% for adrenaline, 67 +/- 18% for tachycardia, and 1 +/- 10.8% for ouabain. The mean changes in intracellular NADH redox level were -17 +/- 4.4%, 49 +/- 8.4%, and -6 +/- 6.4% for noradrenaline, tachycardia, and ouabain, respectively. The time course of changes in the various parameters was different following the onset of each inotropic stimulus. Furthermore, inducing tachycardia while the heart was under the influence of the various inotropic agents caused a reduction in contractility at different rates. These results indicate a large variation in the oxygen cost of contraction produced by these inotropic interventions, and also demonstrate notable variations in the intracellular oxygen balance. The possible relation between the intracellular NADH level and the "mechanical reserve" of cardiac muscle is discussed.

Animals↗

PubMedDate not supplied

Microvascular, flow and O2 consumption responses of ischemic myocardium to prazosin.

The effects of selective alpha 1-adrenoceptor blockade with prazosin were investigated in ischemic rabbit heart. Using labeled microspheres, regional coronary blood flow was measured before and 1 hr after occlusion of the circumflex coronary artery in controls and animals given 1 mg/kg of prazosin 10 min after ligation. Small artery and vein O2 saturations were obtained microspectrophotometrically from hearts of anesthetized rabbits. Fluorescein isothiocyanate-dextran (150 mg/kg) was administered to mark the perfused microvessels and alkaline phosphatase stain was used to locate the total microvasculature. Prazosin depressed the arterial blood pressure. Coronary flow and O2 consumption (10.9 +/- 4.5 and 6.1 +/- 1.8 ml O2/min/100 g, nonoccluded and occluded) were significantly lower in the occluded region in the control group, while O2 extraction (4.9 +/- 1.4 and 6.8 +/- 2.6 ml O2/100 ml) was locally elevated. The results of occlusion in the prazosin-treated group were similar for flow, O2 consumption (9.9 +/- 4.5 and 6.7 +/- 5.3 ml O2/min/100 g, nonoccluded and occluded) and O2 extraction (6.6 +/- 2.3 and 8.2 +/- 2.3 ml O2/100 ml). The per cent of perfused microvessels was not significantly altered by occlusion in the control group. In the prazosin group, the percentage of occluded region subendocardial capillaries and arterioles perfused was significantly greater than in the control group, e.g., 65 +/- 9% perfused capillaries/mm2 in control occluded subendocardium vs 78 +/- 9% perfused capillaries/mm2 in prazosin-treated occluded subendocardium. Thus, the slight increase in microvessel utilization with prazosin was not sufficient to improve the flow or the O2 consumption in the ischemic myocardium.

Alkaline Phosphatase↗