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Biomedical subjects

H E Morgan

Publications and source records attributed to H E Morgan.

118 records · Page 7Linked to original sources
PubMedDate not supplied

Role of bradykinin in the antihypertrophic effects of enalapril in the newborn pig heart.

Rapid growth of the left ventricle of the newborn pig heart can be restrained by treating piglets with the angiotensin converting enzyme inhibitor, enalapril maleate. This reduced rate of growth is reflected in vitro by reduced rates of ribosome formation and protein synthesis, and may be due to decreased availability of angiotensin II (AII), a potentially hypertrophic agent; decreased numbers of AII receptors; increased availability of bradykinin, a potentially antihypertrophic agent; or reduced hemodynamic load on the left ventricle. Because enalapril decreases degradation of bradykinin, the role of bradykinin as an inhibitor of cardiac growth in the newborn heart was investigated. Addition of 1 x 10(-5) M bradykinin and 1 x 10(-6) M enalapril to the perfusate of isolated hearts from 2 day old piglets did not significantly alter heart rate, contents of ATP or creatine phosphate or rates of ribosome formation or protein synthesis during 1 h of perfusion. Similarly, exposure of myocytes isolated from the left ventricular free wall of piglets to 5 x 10(-6) M bradykinin for 72 h did not alter the rate of [3H]-phenylalanine incorporation into total protein. The reduced rate of left ventricular growth in vivo caused by enalapril administration was not reversed by simultaneous treatment with the specific bradykinin receptor antagonist, HOE 140. HOE 140 alone did not alter ventricular growth as compared to hearts from untreated piglets. In summary, these results demonstrate that the reduced rate of left ventricular growth in vivo and the reduced rate of ribosome formation and protein synthesis in the left ventricle in vitro after enalapril treatment of piglets is not the result of an inhibitory effect of bradykinin on cardiac growth.

Adenosine Triphosphate↗
PubMedDate not supplied

Factors determining the utilization of glucose in isolated rat hearts.

Glucose utilization by the isolated rat heart is restricted by flux through the membrane transport, phosphofructokinase and glyceraldehyde-3-P dehydrogenase reactions. These reactions can be accelerated by hormones, such as insulin, by mechanical factors, such as the "garden-hose effect", heart rate, and perhaps ventricular pressure development, and by oxygen deprivation. Glucose utilization is restricted by provision of exogenous non-carbohydrate substrates and by utilization of endogenous substrate stores. Isolated hearts perfused as Langendorff preparations with or without a ventricular drain, working hearts, and ischemic preparations are useful in defining rate-limiting steps and mechanisms of regulation. However, when glucose is supplied as the sole exogenous substrate, its rates of utilization do not reflect the more complex in vivo situation where competing substrates such as fatty acids are preferentially utilized.

Adenosine Triphosphate↗
PubMedDate not supplied

Factors accounting for growth and atrophy of the heart.

Growth of the rat heart was induced by intrathoracic aortic banding, while atrophy followed hypophysectomy. During the early phase of hypertrophy, RNA concentration increased markedly. During the period of atrophy, RNA concentration was reduced. These changes in RNA concentration seemed to account for either the increased or the decreased rates of protein synthesis that was observed during hypertrophy or atrophy, respectively. Rates of protein degradation were unaffected during changes in heart size. These findings suggest that alterations in synthesis, processing, or degradation of RNA play a key role in modification of heart size.

Aging↗