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D C Homans

Publications and source records attributed to D C Homans.

45 records · Page 3Linked to original sources
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↗
PubMed1986

Persistence of regional left ventricular dysfunction after exercise-induced myocardial ischemia.

To determine whether regional myocardial dysfunction occurring after exercise-induced ischemic might be caused by continued abnormalities of myocardial blood flow in the post-exercise period, nine dogs were instrumented with ultrasonic microcrystals for determination of circumferential segment shortening, circumflex artery electromagnetic flow probes, and hydraulic coronary artery occluders. Dogs performed treadmill exercise during partial inflation of the coronary artery occluder. When the stenosis was maintained after exercise (persistent stenosis), subendocardial flow = 0.79 +/- 0.42 ml/min per g vs. 1.39 +/- 0.43 ml/min per g control), and this was associated with continued dysfunction in the ischemic zone (segment shortening 45.4 +/- 36.9% of resting control). When the stenosis was released immediately after exercise (temporary stenosis), however, flow was markedly increased 1 min post-exercise (mean transmural flow 4.24 +/- 1.22 ml/min per g; subendocardial flow 4.18 +/- 1.52 ml/min per g), and this was associated with a transient increase in segment shortening to 104.5 +/- 9.3% of resting control. 5 min after exercise, however, moderate reductions in ischemic segment shortening were noted after both temporary stenosis and persistent stenosis runs, and these persisted for 30 min post-exercise. It is concluded that regional left ventricular dysfunction may persist for a significant period of time after exercise-induced ischemia. Furthermore, early after exercise, dysfunction is related to persistent abnormalities of myocardial blood flow, whereas late after exercise it is independent of primary reductions in myocardial blood flow.

Animals↗
PubMed1985

Reactive oxygen species may cause myocardial reperfusion injury.

The pathogenic mechanisms responsible for heart damage following temporary coronary artery occlusion are unknown. Some damage may be mediated by a normal cellular enzyme, xanthine dehydrogenase, which converts to xanthine oxidase during myocardial ischemia. Reperfusion, with restoration of oxygen supply, may then lead to formation of superoxide by xanthine oxidase, possibly initiating a cascade of oxidative events. In support of this, reperfusion of transiently ischemic canine myocardium leads to a rapid loss of cellular glutathione and a decrease in catalase activity, both indicative of enhanced generation of activated oxygen. Allopurinol--an inhibitor of xanthine oxidase--ameliorates both biochemical damage and functional deficits ordinarily triggered by ischemia and reperfusion, suggesting one possible mode of pharmacologic intervention following acute myocardial infarction.

Allopurinol↗
PubMed1985

Regional function and perfusion at the lateral border of ischemic myocardium.

To determine whether function is depressed in areas of myocardium adjacent to an area of myocardial ischemia, 16 open-chest dogs were studied with both two-dimensional echocardiography and ultrasonic microcrystals. Regional myocardial blood flow was measured with radioactive microspheres during control periods and after coronary arterial ligation. Segments of myocardium adjacent to the area of ischemia were found to have no significant change in transmural blood flow (1.02 +/- 0.38 ml/g/min control vs 0.95 +/- 0.3 ml/g/min after ligation) or subendocardial flow (1.18 +/- 0.41 ml/g/min control vs. 1.19 +/- 0.37 ml/g/min after ligation). Regional function assessed echocardiographically as percent change in segment area was significantly depressed in these normally perfused adjacent areas (69.5 +/- 18.8% control vs 52.5 +/- 19.8% after ligation; p less than .01). There was a significant relationship between proximity to border of infarction and degree of adjacent dysfunction (r = .50, p less than .01 for echocardiography; r = .70, p less than .01 for ultrasonic microcrystals). It is concluded that systolic performance is depressed in nonischemic myocardium directly adjacent to the lateral border of an area of acute myocardial ischemia.

Animals↗
PubMedDate not supplied

Effect of nifedipine on the myocardial and vascular response to myocardial ischemia.

Nifedipine reduces reactive hyperemia following brief coronary artery occlusions. To determine whether this is related to improvement in collateral blood flow to ischemic myocardium or alterations in myocardial oxygen consumption, ten chloralose anesthetized dogs were instrumented with coronary sinus catheters, circumflex artery flowmeters, and ultrasonic microcrystals for measurement of myocardial segment shortening. Myocardial oxygen consumption and circumflex coronary artery flow were determined at rest and during incremental infusions of isoproterenol. Myocardial blood flow measured with microspheres and segmental function were assessed during and following 30- and 60-second coronary artery occlusions. Thirty minutes after the intravenous administration of nifedipine, 10 micrograms/kg iv, all measurements were repeated. Nifedipine did not alter myocardial oxygen consumption or the relationship between oxygen consumption and circumflex coronary artery flow either at rest or during isoproterenol infusion. Following 60-second coronary occlusions, nifedipine reduced peak circumflex coronary artery flow (176 +/- 99 vs. 128 +/- 68 cc/min) and reactive hyperemia debt repayment (221 +/- 84 vs. 158 +/- 66%; p less than 0.01). Nifedipine did not alter flow to ischemic segments during coronary artery occlusions (0.16 +/- 0.10 vs. 0.19 +/- 0.13 ml/min/g mean transmural flow). Furthermore, nifedipine did not affect the severity of ischemic segment dysfunction, nor the rate of recovery of ischemic segment function following release of coronary artery occlusion. We conclude that the reduction in reactive hyperemia induced by nifedipine was not related to alterations in the severity of hypoperfusion in ischemic areas, or alterations in myocardial oxygen consumption. Reductions in reactive hyperemia produced by nifedipine did not impair recovery of mechanical function in postischemic myocardium.

Animals↗