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Biomedical subjects

M L Hess

Publications and source records attributed to M L Hess.

At least 145 records · Page 8Linked to original sources
PubMed1980

Differential subendocardial perfusion and injury during the course of gram-negative endotoxemia.

This laboratory has been investigating the concept that a progressive state of global myocardial ischemia is a major precipitating factor in the etiology of the myocardial failure in endotoxin shock. To further test this hypothesis, endotoxin shock (E coli, B5, 4 mg/kg) was induced in the canine model, and coronary and systemic hemodynamics were monitored for five hours. Coronary flow decreased from 90.05 +/- 28 ml/min/100 gm left ventricle (n = 7) to 45 +/- 10 at five hours (n = 6), with two experimental deaths between four and five hours. Coronary vascular resistance increased from 61.82 +/- 2.5 X 10(3) dynes . sec . cm-5 to 128.6 X 10(3) +/- 18 X 10(3) dynes . sec . cm-5. Sham controls (n = 7) demonstrated no significant difference in either flow or resistance between zero to five hours. Gross examination of the shocked hearts demonstrated patchy to diffuse subendocardial hemorrhage not present in the sham preparations. Thioflavin S injection (4%, 1 ml/kg) demonstrated uniform perfusion under UV light (360 nm) in the sham preparations and marked nonuniform perfusion in the subendocardial surface of the shocked hearts. Histologic examination demonstrated diffuse intramyocardial hemorrhage, more marked in the subendocardium than the midmyocardium. Electron micrographs demonstrated swelling and distortion of the subendocardial sarcoplasmic reticulum and T-tubules and dehiscence of the myofibrils. It is concluded that the decrease in flow and concomitant increase in intramyocardial resistance progresses to a state of global ischemia and ischemic necrosis at the more vulnerable subendocardial surface.

Animals↗
PubMed1979

Diphenhydramine protection of the failing myocardium during gram-negative endotoxemia.

Gram-negative endotoxin (Escherichia coli, 4 mg/kg) was found to produce a sustained fall in systemic arterial pressure, left ventricular pressure, and cardiac output that could be blocked by the histamine antagonist diphenhydramine. Histamine infusion was found to produce a parallel depression of systemic arterial pressure. Further, endotoxemia was found to produce a significant depression of myocardial contractility (dP/dt max) that could also be blocked by diphenhydramine. Cardiac myofibrillar adenosine triphosphatase (ATPase) activity from endotoxin-shocked hearts was found to be depressed, ATPase activity from subendocardial myofibrils being more depressed than that from subepicardial myofibrils. Myofibrillar ATPase activity was significantly protected by pretreating the animals with diphenhydramine. It is concluded that the initial hemodynamic phase of endotoxin shock is histamine-mediated and that this hemodynamic depression can be blocked with diphenhydramine. Further, it appears that endotoxin is capable of depressing myocardial contractility by depressing contractile protein function (myofibrillar ATPase activity)--the subendocardial surface more so than the subepicardial surface--and this depression of myocardial contractility can be blocked with diphenhydramine.

Adenosine Triphosphatases↗
PubMed1979

Augmented venous return: protection of the ischemic myocardium during endotoxemia.

The effects of gram-negative endotoxin (Escherichia coli 4 mg/kg) induced myocardial failure in the pentobarbital-anesthesized dog were examined by monitoring its influence on coronary and systemic hemodynamics and correlating these results with myofibrillar ATPase activity. An identical series of studies was performed incorporating a femoral-femoral arterial-venous shunt to augment venous return. Over a five-hour period, gram-negative endotoxemia was associated with a progressive fall in arterial pressure, stroke volume, cardiac output, coronary flow, and a rise in total peripheral resistance and diastolic coronary vascular resistance. Augmenting venous return by 313 +/- 71 ml/min significantly increased cardiac output, stroke volume, and coronary flow and substantially reduced total peripheral resistance and coronary vascular resistance. Myofibrillar ATPase activity from both endocardium and epicardium was significantly depressed in the endotoxin-shocked preparations. However, with the augmentation of venous return with the A-V shunt in the endotoxin-treated animal, myofibrillar ATPase activity is normal. It appears that endotoxin causes a decrease both in venous return and in cardiac contractility by increasing total peripheral resistance, coronary vascular resistance, and impedance to left ventricular ejection. Augmenting venous return by optimizing preload and reducing afterload prevents any significant increase in total peripheral resistance, coronary vascular resistance, or impedance to left ventricular ejection. This is manifested by a rise in cardiac output, stroke volume, and coronary flow and the preservation of myocardial function. This is the first successful application of left ventricular afterload reduction in noncardiogenic shock.

Adenosine Triphosphatases↗
PubMed1978

Endotoxin and myocardial failure: role of the myofibril and venous return.

The effects of gramnegative endotoxin-induced myocardial failure in the pentobarbital-anesthetized dog were examined by monitoring its influence on cardiac myofibrillar ATPase activity. Myofibrils were isolated from endo- and epicardial portions of the left ventricular wall. ATPase activities were determined in animals treated with 4 mg/kg endotoxin and monitored 5 h, in animals monitored for 5 h without endotoxin (controls), and in animals implanted with a unilateral femoral shunt and given endotoxin. No differences were seen in the activities between the endo- and epicardial portions of any preparation. Activity was significantly depressed in endotoxemic animals. Increasing venous return by 313 +/- 71 ml/min significantly increased coronary flow by reducing coronary vascular resistance and prevented any observed depression of myofibrillar ATPase activity. In in vitro studies, adding endotoxin directly to a myofibril preparation did not modify normal activity. It appears that the mechanical and myofibrillar dysfunctions are due to the action of endotoxin at sites not associated with the actomyosin ATPase, but may be due to the production of an intermediary agent in concert with a decreased venous return.

Adenosine Triphosphatases↗
PubMed1978

Influence of endotoxin on myocardial calcium transport and the effect of augmented venous return.

The influence of endotoxin shock and of experimentally increased venous return during endotoxin shock on myocardial vesicular calcium uptake and calcium stimulated ATPase activity was investigated. Vesicular calcium uptake was depressed (p less than 0.01) from 0.9 mumoles/mg protein/min to 0.3 mumoles/mg/min after 5 hr of endotoxin shock. Control ATPase did not differ between endocardial surface and epicardial surface. This was accompanied by a depressed (p less than 0.01) ATPase activity from 1.2 mumoles Pi/mg/min at the endocardial surface, and to 0.9 mumoles Pi/mg/min at the epicardial surface. A femoral arteriovenous shunt was used to increase venous return by 313 +/- 71 ml/min (approximately 17 ml/kg) during the shock period. Vesicles from AV shunted animals after endotoxin were capable of normal calcium uptake and normal ATPase activity. Results suggest that myocardial depression during endotoxin shock is more severe on the endocardial surface and is caused by depressed vesicular calcium uptake secondary to depressed ATPase activity. Furthermore, this depression may be avoided by maintenance of an adequate venous return.

Adenosine Triphosphatases↗
PubMed1977

The influence of venous return on cardiac mechanical and sarcoplasmic reticulum function during endotoxemia.

E. coli endotoxin (0.03 mg/ml) added to blood perfusing a heart-lung preparation with a venous return of 600 ml/min produced a significant depression in ventricular function within 4 hours. Fragmented sarcoplasmic reticulum isolated from the myocardium of the endotoxin-perfused heart-lung preparations showed depressed calcium uptake rates and ATPase activity. When venous return was increased to 1,200 ml/min, gram-negative endotoxin had no effect on ventricular function, isolated fragmented sarcoplasmic reticulum calcium uptake, or ATPase activity. These observations suggest that gram-negative endotoxin or a product thereof acts in synergism with low venous return in order to depress myocardial function.

Adenosine Triphosphatases↗
PubMed1975

Calcium-accumulating properties of subcellular fractions of bovine vascular smooth muscle.

This study examined the calcium transport properties of two subcellular fractions of bovine aorta obtained by differential centrifugation. The vesicular fraction had a high-affinity (Km = 1.05 X 10(-6)M) calcium transport mechanism which could be potentiated by using the calcium-precipitating anion, oxalate. The mitochondria-enriched fraction's calcium transport system had a lower affinity for calcium than did that of the vesicular fraction. The calcium capacity of the vesicular fraction was determined by comparing the steady-state calcium uptake in the presence of oxalate in the whole homogenate with the same uptake by the vesicular fraction alone. A calcium capacity of about 100 mumoles Ca2+/kg aorta was obtained. It is concluded that the vesicular fraction has all of the properties of a major site of subcellular calcium regulation in vascular smooth muscle.

Adenosine Triphosphatases↗