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Biomedical subjects

R J Bache

Publications and source records attributed to R J Bache.

At least 127 records · Page 7Linked to original sources
PubMed1988

Postsynaptic alpha 1- and alpha 2-adrenergic mechanisms in coronary vasoconstriction.

This study examined the relative importance of postsynaptic alpha 1- and alpha 2-adrenoceptors in mediating coronary vasoconstriction in open chest dogs in which the left circumflex coronary artery was cannulated and perfused at a constant rate. The cervical vagus nerves and central connections of the stellate ganglia were transected, and beta-adrenergic blockade was produced with propranolol. Coronary vasoconstriction occurred in response to intraarterial administration of both the alpha 1-agonist phenylephrine and the alpha 2-agonist BHT 933. The response to phenylephrine was partially blocked with prazosin and nearly completely eliminated by yohimbine. The response to BHT 933 was resistant to prazosin, but almost completely blocked by yohimbine. Coronary vasoconstriction produced by norepinephrine was resistant to prazosin, but was blunted by alpha 2-adrenergic blockade with yohimbine or idazoxan. Prazosin produced some blunting of coronary vasoconstriction in response to small doses of epinephrine, while yohimbine markedly attenuated epinephrine-induced vasoconstriction at all doses used. Measurements of regional myocardial blood flow with radioactive microspheres demonstrated no transmural redistribution of perfusion during vasoconstriction produced by either alpha 1- or alpha 2 stimulation. Thus, although stimulation of both alpha 1- and alpha 2-adrenoceptors is capable of causing coronary vasoconstriction, vasoconstriction in response to norepinephrine and epinephrine is mediated principally by postsynaptic alpha 2-adrenoceptors.

Animals↗
PubMed1988

Effect of ouabain on large coronary artery diameter.

Cardiac glycosides have previously been shown to constrict small coronary resistance vessels. This study evaluated the effect of a bolus intravenous dose of ouabain (20 micrograms/kg) on large left circumflex coronary arterial diameter measured by sonomicrometry in nine awake chronically instrumented dogs. Between 5 and 10 min after ouabain administration external circumflex coronary diameter decreased (3.87 +/- 0.21 to 3.83 +/- 0.21 mm, p less than 0.05). Twenty minutes after ouabain administration, coronary diameter had returned to control. At the time of the peak decrease in coronary diameter, heart rate had decreased (104 +/- 7 to 82 +/- 7 beats/min, p less than 0.05), circumflex coronary blood flow had decreased (45 +/- 7 to 38 +/- 6 ml/min, p less than 0.05), total circumflex coronary resistance had increased (2.7 +/- 0.4 to 3.5 +/- 0.6 U, p less than 0.05) and aortic pressure was unchanged (108 +/- 4 to 113 +/- 4 mm Hg). Alpha-adrenergic blockade with phentolamine did not prevent the decrease in circumflex coronary arterial diameter in each of five dogs (3.67 +/- 0.28 to 3.60 +/- 0.28 mm, p less than 0.05). Therefore, intravenous ouabain caused vasoconstriction of large coronary arteries. These vasocontrictor effects were not mediated by alpha-adrenergic mechanisms. This constriction could have important consequences in the presence of coronary stenoses.

Adrenergic alpha-Antagonists↗
PubMed1988

Postsynaptic adrenoceptor-mediated vasoconstriction in coronary and femoral vascular beds.

This study examined the response to intra-arterial norepinephrine and sympathetic nerve stimulation on perfusion pressure of cannulated dog femoral and left circumflex coronary arteries perfused at constant flow rates. Sympathetic nerve stimulation was delivered through the decentralized inferior cardiac nerve and the lumbar sympathetic chain; beta-adrenergic blockade was maintained with propranolol. In the coronary artery, the vasoconstrictor response to norepinephrine was blunted by alpha 1-adrenergic blockade with prazosin but was abolished by alpha 2-adrenergic blockade with rauwolscine, indicating postsynaptic alpha 2-adrenoceptor-mediated vasoconstriction. In the femoral artery, prazosin decreased norepinephrine-induced vasoconstriction by 20-40%; the subsequent addition of rauwolscine completely abolished vasoconstriction, indicating that both alpha 1- and alpha 2-adrenoceptors contributed to vasoconstriction. Sympathetic nerve stimulation produced frequency-dependent increases of perfusion pressure in both coronary and femoral vascular beds. Prazosin caused approximately 50% reduction in the vasoconstrictor response of the coronary vascular bed and approximately 30% reduction in the femoral bed. The addition of rauwolscine completely blocked the response to sympathetic nerve stimulation in coronary and femoral vascular beds. These studies demonstrate that postsynaptic alpha 2-adrenoceptor-mediated mechanisms participate in vasoconstriction in response to both exogenous norepinephrine and sympathetic nerve stimulation in the canine coronary and femoral vascular beds.

Adrenergic beta-Antagonists↗
PubMed1988

Subendocardial and subepicardial wall thickening during ischemia in exercising dogs.

To determine whether ischemia in the exercising dog is associated with preservation of subepicardial thickening relative to subendocardial thickening, 10 dogs were chronically instrumented with circumflex artery flow probes, hydraulic occluders, and pairs of ultrasonic microcrystals for determination of wall thickness in the circumflex artery distribution. One pair of crystals spanned the entire ventricular wall (transmural), and the other spanned the outer half of the ventricular wall. Inner wall thickness was computed as the difference between transmural wall thickness and outer wall thickness. Dogs performed control treadmill exercise and exercise with a coronary stenosis that reduced circumflex artery flow to resting control levels. Percent systolic thickening at rest for the transmural, inner, and outer regions was 21.3 +/- 11.8%, 35.5 +/- 20.3%, and 10.3 +/- 5.0% (mean +/- SD), respectively. During exercise without stenosis, systolic thickening increased to 143 +/- 37% of control for outer wall crystals and 137 +/- 26% of control for the inner portion of the wall. During exercise, the addition of a coronary stenosis caused a reduction in thickening to 17.7 +/- 28.5% of control for the outer wall and 40.1 +/- 32.3% of control for the inner portion of the wall; these were not significantly different. In contrast, normalized inner wall blood flow during exercise with circumflex artery stenosis (25.0 +/- 16.0%) was significantly less than for the outer portion of the wall (48.5 +/- 20.9%). Further, there was a close relation between changes in inner wall thickening and inner wall blood flow (r = 0.84), whereas there was only a very weak relation between changes in outer wall blood flow and function (r = 0.62; p = 0.04). During ischemia in the exercising dog, outer wall thickening is depressed out of proportion to reductions in outer wall blood flow and is not preserved relative to inner wall thickening.

Animals↗
PubMed1988

Effects of atrial natriuretic peptide in the canine coronary circulation.

Atriopeptin II has been reported to cause profound coronary vasoconstriction in the isolated perfused guinea pig heart and in the blood perfused canine heart. Consequently, this study was carried out to examine possible mechanisms by which vasomotor effects of human atrial natriuretic peptide (ANP) occur in the canine coronary circulation. Bolus dosages of ANP were administered into the left circumflex coronary artery of in situ dog hearts perfused at constant flow rate. ANP produced dose-related coronary vasodilation with a threshold dosage of 2 ng/kg; a dosage of 2 micrograms/kg caused a 27 +/- 4% decrease in coronary vascular resistance. Coronary vasodilation produced by ANP was not altered by beta-adrenergic blockade with propranolol (1 mg/kg i.v.). In addition, neither adenosine receptor blockade with 8-phenyltheophylline (5 mg/kg i.v.) nor cyclooxygenase inhibition with indomethacin (5 mg/kg i.v.) significantly altered the response to intra-arterial ANP. These data demonstrate that in the in vitro blood perfused canine heart, ANP administered intra-arterially results in coronary vasodilation that does not utilize adenosine-dependent or prostaglandin-dependent mechanisms.

Animals↗
PubMed1988

Role of adenosine in coronary vasodilation during exercise.

This study examined the hypothesis that increases in myocardial blood flow during exercise are mediated by adenosine-induced coronary vasodilation. Active hyperemia associated with graded treadmill exercise and coronary reactive hyperemia were examined in chronically instrumented awake dogs during control conditions, after intracoronary infusion of adenosine deaminase (5 units/kg/min for 10 minutes), and after adenosine receptor blockade with 8-phenyltheophylline. Both adenosine deaminase and 8-phenyltheophylline caused a rightward shift of the dose-response curve to intracoronary adenosine; 8-phenyltheophylline was significantly more potent than adenosine deaminase. Adenosine deaminase caused a 33 +/- 7 to 39 +/- 3% decrease in reactive hyperemia blood flow following coronary occlusions of 5-20 seconds duration, respectively, while 8-phenyltheophylline produced a 40 +/- 6 to 62 +/- 8% decrease in reactive hyperemia. Increasing myocardial oxygen consumption during treadmill exercise was associated with progressive increase of coronary blood flow. Neither adenosine deaminase nor 8-phenyltheophylline attenuated the increase in coronary blood flow or the decrease of coronary vascular resistance during exercise. Neither agent altered the relation between myocardial oxygen consumption and coronary blood flow. Thus, although both adenosine deaminase and 8-phenyltheophylline antagonized coronary vasodilation in response to exogenous adenosine and blunted coronary reactive hyperemia, neither agent impaired coronary vasodilation associated with increased myocardial oxygen requirements produced by exercise. These findings fail to support a substantial role for adenosine in mediating coronary vasodilation during exercise.

Adenosine↗
PubMed1988

Differences in the effects of alpha-1 adrenergic blockade with prazosin and indoramin on coronary blood flow during exercise.

This study compared the effects of two selective alpha-1 adrenergic blockers, prazosin and indoramin, on the response of coronary blood flow and myocardial oxygen consumption during treadmill exercise in chronically instrumented dogs. Left circumflex coronary artery blood flow was measured with an electromagnetic flowmeter, whereas myocardial arteriovenous oxygen difference was determined with indwelling aortic and coronary sinus catheters. During control conditions, coronary blood flow, arteriovenous oxygen extraction and myocardial oxygen consumption increased regularly with exercise. Both prazosin and indoramin decreased arterial pressure at rest and during exercise, but during heavier levels of exercise blood pressure was lower and heart rates were higher after prazosin. Prazosin did not alter myocardial oxygen consumption, whereas indoramin tended to decrease oxygen consumption; myocardial oxygen consumption was significantly less after indoramin than after prazosin during the heaviest levels of exercise. Prazosin, but not indoramin, significantly decreased coronary vascular resistance both at rest and during exercise, and blunted the decrease in coronary sinus oxygen tension which occurred during exercise. In comparison with prazosin, during heavy exercise coronary blood flow was significantly decreased, myocardial oxygen extraction significantly increased and myocardial oxygen consumption significantly decreased after indoramin.

Adrenergic alpha-Antagonists↗
PubMed1987

Effects of nifedipine on coronary reactive and exercise induced hyperaemia.

The effects of nifedipine on coronary vasodilation were studied during reactive hyperaemia after a transient coronary occlusion and during active hyperaemia associated with graded treadmill exercise. Studies were performed in 10 chronically instrumented dogs in which left circumflex coronary artery flow was measured with an electromagnetic flowmeter and myocardial oxygen extraction was determined from indwelling aortic and coronary sinus catheters. Thirty minutes after administration of nifedipine (10 micrograms.kg-1 iv), when coronary blood flow, arterial pressure, and heart rate had returned to control values, the vasodilatation following a 10 s coronary occlusion was significantly blunted, so that reactive hyperaemia blood flow debt repayment (mean(SEM)) was reduced from 387(39)% during control conditions to 270(33)% after nifedipine (p less than 0.05). In contrast, nifedipine did not alter the coronary vasodilatation that occurred in response to graded treadmill exercise so that the increase in coronary blood flow during exercise was not different from the control response. Thus, although nifedipine blunted ischaemic coronary vasodilatation during reactive hyperaemia, it did not alter coronary vasodilatation during active hyperaemia resulting from physiological increases of myocardial oxygen consumption.

Animals↗
PubMed1987

Vasomotor properties of immature canine coronary collateral circulation.

This study examined the ability of the immature coronary collateral circulation to undergo vasodilation in response to nitroglycerin and vasoconstriction in response to alpha-adrenoceptor stimulation. Studies were performed in 12 anesthetized dogs. Collateral flow was estimated from measurements of retrograde flow from the acutely ligated and cannulated anterior descending branch of the left coronary artery. Antegrade flow into the collateral-dependent myocardium was minimized by embolizing the anterior descending artery with 25-microns microspheres. Drugs to be tested were introduced into the left main coronary artery to reach collateral vessels arising from the left circumflex and septal arteries. Intracoronary administration of nitroglycerin (6 micrograms X kg-1 X min-1) resulted in a 33 +/- 7.7% increase in retrograde blood flow (P less than 0.01) and a 23 +/- 3.8% decrease in calculated collateral resistance (P less than 0.01). No significant change occurred in retrograde blood flow or calculated collateral resistance during cardiac sympathetic nerve stimulation after beta-adrenergic blockade with propranolol, selective alpha-adrenergic stimulation with phenylephrine (1 microgram X kg-1 X min-1), or selective alpha 2-stimulation with BHT 933 (2 micrograms X kg-1 X min-1). Thus, the immature coronary collateral circulation was capable of active vasomotion, as demonstrated by vasodilation in response to nitroglycerin, but did not undergo vasoconstriction in response to alpha-adrenoceptor stimulation.

Animals↗
PubMed1987

Myocardial blood flow during exercise in dogs with left ventricular hypertrophy produced by aortic banding and perinephritic hypertension.

This study tested the hypothesis that for similar degrees of left ventricular hypertrophy, subendocardial blood flow would be facilitated by the increased diastolic coronary perfusion pressure associated with arterial hypertension, as compared with hypertrophy produced by banding the ascending aorta. Left ventricular hypertrophy was produced with perinephritic hypertension in seven adult dogs and by banding the ascending aorta in nine adult dogs. Left ventricular/body weight ratios were 6.15 +/- 0.59 g/kg in the hypertensive animals and 6.87 +/- 0.47 g/kg in dogs with aortic banding, as compared with 4.23 +/- 0.23 g/kg in seven normal dogs (p less than .01). Studies were performed at rest and during two stages of treadmill exercise to achieve heart rates of 195 and 260 beats/min. Diastolic aortic pressure was increased in animals with hypertension but not in dogs with aortic banding. Systolic ejection period was prolonged in dogs with aortic banding but not in hypertensive dogs. Mean blood flow per gram of myocardium measured with microspheres was similar at rest and during light exercise in all three groups of animals, whereas during heavy exercise blood flow was significantly greater than normal in both groups with hypertrophy. In normal dogs subendocardial/subepicardial (endo/epi) flow ratios did not change significantly during exercise. In both groups with hypertrophy, endo/epi ratios were normal at rest but decreased significantly during exercise. During heavy exercise the endo/epi ratio decreased to 0.73 +/- 0.08 in dogs with aortic banding as compared with 1.07 +/- 0.12 in hypertensive dogs (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effect of anesthesia on reactivity of large coronary arteries in the dog.

Epicardial coronary arteries dilate after release of a transient coronary occlusion in awake chronically instrumented dogs but not in anesthetized dogs studied acutely after surgery. To determine whether anesthesia or surgical trauma is responsible for this lack of reactive dilation, we evaluated the effect of anesthesia on reactive coronary dilation in six chronically instrumented dogs. Circumflex coronary diameter was measured with sonomicrometry. Response to release of a 20- or 30-s coronary occlusion was studied before and after sodium pentobarbital (20 +/- 2 mg/kg) and before and after alpha-chloralose (100 mg/kg) plus either morphine or fentanyl and droperidol. Pentobarbital blunted the peak flow response to release of a transient coronary occlusion (114 +/- 15 vs. 128 +/- 16 ml/min, p less than 0.05) but did not affect the increase in large coronary diameter (before pentobarbital: 3.68 +/- 0.30-3.74 +/- 0.30 mm; after pentobarbital: 3.66 +/- 0.31-3.71 +/- 0.31 mm). alpha-Chloralose blunted the peak flow response to release of a transient coronary occlusion (96 +/- 12 vs. 141 +/- 25 ml/min, p less than 0.05) but did not affect the increase in large coronary diameter (before chloralose: 4.00 +/- 0.28-4.06 +/- 0.28 mm; after chloralose: 3.91 +/- 0.31-3.98 +/- 0.31 mm). Therefore, each drug blunted the peak flow response to release of a transient coronary occlusion, but dilation of large coronary arteries was not impaired. The lack of reactivity of large coronary arteries in acutely studied dogs is probably due to the trauma of recent surgery and not the anesthesia.

Anesthesia↗
PubMed1987

Effects of nonselective and selective alpha 1-adrenergic blockade on coronary blood flow during exercise.

This study was made to evaluate the relative importance of alpha 1- and alpha 2-adrenergic vasoconstrictor influences in opposing the increase in coronary blood flow that occurs during exercise. The effects of selective alpha 1-adrenergic blockade with prazosin were compared with nonselective alpha-adrenergic blockade with phentolamine on coronary hemodynamics during exercise in chronically instrumented dogs. During control conditions, graded treadmill exercise resulted in progressive increases of myocardial oxygen consumption; this was associated with increased coronary blood flow as well as with increased myocardial oxygen extraction. Although prazosin and phentolamine caused similar reductions of arterial pressure, phentolamine increased heart rate, myocardial oxygen consumption, and coronary blood flow at equivalent exercise levels, and prazosin did not significantly alter these variables. These effects of phentolamine appeared to result from blockade of presynaptic alpha 2-adrenergic receptors, which normally modulate norepinephrine release, that resulted in increased sympathetic effects on the heart. However, at comparable levels of myocardial oxygen consumption, prazosin and phentolamine resulted in similar significant increases of coronary venous PO2 and decreases of coronary vascular resistance. These data support a modest role for alpha 1-adrenergic coronary vasoconstriction during exercise but fail to document an additional role for postsynaptic alpha 2-adrenergic coronary vasoconstriction during exercise.

Animals↗
PubMed1987

Hemodynamic and regional blood flow response to piroximone (MDL 19,205) in dogs with congestive heart failure: a comparison with dobutamine.

This study compares the effects of piroximone (MDL 19,205), a new inotropic agent, with dobutamine in dogs with congestive heart failure. With dobutamine, (15 micrograms/kg/min) left ventricular (LV) dp/dt increased from 2220 +/- 215 (mean +/- S.E.M.) to 2815 +/- 280 mm Hg/sec and cardiac index increased from 2.9 +/- 0.2 to 3.7 +/- 0.4 liters/min/m2, whereas LV filling pressure was essentially unchanged (18.7 +/- 2.6-16.3 +/- 2.4 mm Hg). The hemodynamic effects of piroximone (50 micrograms/kg/min) were more pronounced. LV dp/dt increased from 2615 +/- 260 to 3760 +/- 410 mm Hg/sec and cardiac index from 3.0 +/- 0.1 to 4.4 +/- 0.6 liters/min/m2, whereas LV filling pressure decreased from 15.6 +/- 2.4 to 6.4 +/- 1.8 mm Hg (all P less than .05). Systemic vascular resistance index decreased from 2730 +/- 225 to 1905 +/- 256 dynes sec cm-5 m-2. Regional blood flow to the myocardium increased 48% with dobutamine and 24% with piroximone, whereas skeletal muscle flow increased 59% with dobutamine and 36% with piroximone. Renal blood flow remained unchanged with either drug. We conclude that piroximone is an inotropic agent with vasodilator properties that has an interesting hemodynamic profile somewhat similar to that of dobutamine but with the advantage of being orally active; therefore piroximone could be useful in the treatment of heart failure.

Animals↗
PubMed1987

Pharmacologic vasodilators in the coronary circulation.

Pharmacologic vasodilators are used to treat hypertension, myocardial ischemia, and congestive heart failure. These drugs may indirectly affect coronary blood flow by their effects on the peripheral circulation, effects that modify myocardial oxygen demand. They also have direct effects on the coronary circulation, with some drugs affecting mainly the large epicardial coronary arteries and others affecting mainly the small resistance vessels. Some coronary stenoses are compliant and are capable of changes in caliber. Drugs that dilate large coronary arteries, such as nitroglycerin and the calcium channel-blocking agents, can dilate these stenotic segments. This dilation may contribute to the relief of myocardial ischemia by increasing coronary blood flow. Alternatively, drugs that dilate resistance vessels without an effect on large coronary arteries may cause passive narrowing or collapse of coronary stenoses and could potentially worsen myocardial ischemia. Therefore, in the presence of coronary stenoses, a vasodilator may be beneficial or harmful depending, at least in part, on the site of action of the drug in the coronary circulation.

Animals↗
PubMed1986

Reactive hyperemia following one-beat coronary occlusions in the awake dog.

This study was performed to examine the effect of alterations of cardiac activity during brief coronary artery occlusions on the subsequent reactive hyperemic response. Reactive hyperemia following coronary occlusions equal in duration to one cardiac cycle were examined in 12 chronically instrumented awake dogs while heart rate was maintained constant by cardiac pacing. During continuous pacing, one-beat coronary occlusions resulted in reactive hyperemia with excess flow equal to 220 +/- 23% blood flow debt repayment. When coronary occlusions of identical duration were performed while a single cycle of pacing was omitted during the interval of occlusion, the subsequent reactive hyperemia was decreased. Conversely, when coronary occlusion was produced during the first potentiated beat following a single cycle of paired ventricular stimulation, the reactive hyperemia was increased. Since, in the absence of coronary occlusion, omitting a single paced beat caused a transient decrease in coronary flow, while a single cycle of paired ventricular stimulation caused a brief increase in coronary flow, the reactive hyperemic responses were corrected for these perturbations in flow. Despite these corrections, the influence of alterations of myocardial activity during the interval of occlusion persisted, with the decreased reactive hyperemia when occlusion occurred during an omitted beat and increased hyperemia when occlusion was performed during a potentiated beat. These data indicate substantial coupling between myocardial activity during coronary occlusions as brief as one cardiac cycle in duration and the subsequent reactive hyperemic response.

Animals↗
PubMed1986

Myocardial blood flow in left ventricular hypertrophy developing in young and adult dogs.

This study was performed to test the hypothesis that growth of coronary vasculature would be facilitated if myocardial hypertrophy occurred during the period of normal body growth rather than in mature adult animals. Left ventricular hypertrophy was produced by banding the ascending aorta in eight young dogs 7 wk of age and in nine adult dogs. Adult dogs were studied 2 mo after aortic banding, whereas young dogs were allowed to grow to adulthood before study. Left ventricular weight-to-body weight ratios were increased to 6.88 +/- 0.36 g/kg in the young dogs and 6.64 +/- 0.47 in adult dogs; both were significantly greater than seven normal control animals (4.32 +/- 0.05; each P less than 0.01). Myocardial blood flow per gram measured with microspheres during quiet resting conditions was significantly higher in young dogs with left ventricular hypertrophy than in normal dogs. Myocardial blood flow rates during maximum coronary vasodilation with adenosine (4 mumol X kg-1 X min-1 iv) were similar in all three groups. However, since mean coronary perfusion pressure was higher in the dogs with aortic banding, minimum coronary vascular resistance per gram of myocardium was significantly higher in both young (21.1 +/- 3.1 mmHg X ml-1 X min X g) and adult dogs with left ventricular hypertrophy (21.8 +/- 2.2) than in the normal dogs (16.8 +/- 3.1; each P less than 0.01). Mean coronary vascular resistance for the total left ventricle was similar in all three groups of animals, suggesting that growth of coronary vasculature did not occur as the myocardium underwent hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1986

Mechanisms of remote myocardial dysfunction during coronary artery occlusion in the presence of multivessel disease.

Myocardial dysfunction may occur in areas remote from an acutely occluded coronary artery if those areas are served by a critically stenosed vessel. Although subendocardial hypoperfusion of such remote myocardium has been demonstrated in experimental preparations of this situation, this study was undertaken to determine whether actual reductions in subendocardial perfusion below control levels were necessary for such dysfunction to occur. A 20 mg dose of pentobarbital was injected into the left anterior descending artery (LAD) in 14 anesthetized dogs to create a large anterior regional wall motion abnormality without drawing significant collateral flow from the circumflex vascular bed. Circumflex subendocardial flow was found to rise during injections of pentobarbital and occlusion of the LAD (1.12 +/- 0.38 and 1.17 +/- 0.34 ml/min/g, respectively, vs control 0.91 +/- 0.23 ml/min/g; p less than .05) in the absence of circumflex stenosis. In the presence of circumflex stenosis, circumflex subendocardial flow fell during left anterior descending occlusion (0.59 +/- 0.21 vs 0.89 +/- 0.19 ml/min/g control; p less than .01) but did not change during pentobarbital injections in the LAD (0.77 +/- 0.36 ml/min/g). In the absence of circumflex stenosis, circumflex segment shortening increased during injection of pentobarbital or occlusion of the LAD (14.3 +/- 4.9% and 14.4 +/- 3.5%, respectively, vs 12.3 +/- 3.3% control). In the presence of circumflex stenosis, it did not change (12.5 +/- 4.0% pentobarbital, 11.8 +/- 3.6 LAD occlusion vs 13.1 +/- 4.0% control). We concluded that the presence of large regional wall motion abnormalities may increase the oxygen consumption of remaining myocardium and that dysfunction of that myocardium may result from relative hypoperfusion if blood flow cannot increase appropriately.

Animals↗