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Biomedical subjects

A M Lefer

Publications and source records attributed to A M Lefer.

At least 433 records · Page 24Linked to original sources
PubMed1975

Influence of increased circulating levels of splanchnic lysosomal enzymes on the response to myocardial ischemia.

The ability of increased circulating activities of lysosomal hydrolases to disrupt myocardial cellular membranes was studied in anesthetized cats. Increased activities of lysosomal hydrolases were achieved by splanchnic artery occlusion (SAO) shock or by infusion of liver extract (LE). Myocardial ischemia (MI) was produced by ligation of the left coronary artery. Coronary artery ligation resulted in sustained S-T segment elevation associated with significant increases in plasma creatine phosphokinase (CPK) activity within 5 hours. Combinations of SAO or LE infusion did not modify the increase in either the plasma CPK activity or the S-T segment following MI. However, SAO shock or infusion of LE increased CPK loss from normal and ischemic myocardium, the loss being greater when MI was combined with infusion of LE or SAO shock. Similarly, MI plus SAO shock increased the loss of the lysosomal protease cathepsin D from normal and ischemic myocardial tissue. Moreover, cats subjected to MI and given LE inhibited increased mortality and decreased clearance of infused lysosomal hydrolases. These results indicate that conditions affecting increased plasma levels of hydrolases promote increased disruption of normal and ischemic myocardial tissue. These findings are consistent with the concept that hydrolases originating in the splanchnic viscera during shock play a role in enhancing damage to normal and ischemic myocardial tissue following coronary artery occlusion.

Abdomen↗
PubMed1975

Myocardial substrate utilization in perfused hearts isolated from adrenalectomizedcats.

Isolated hearts form chronically adrenalectomized cats were perfused with Krebs-Henseleit buffer plus either glucose (10mM) or palmitate (0.4 mM) under various conditions of constant pressure and constant flow. Glucose uptake in adrenalectomizedhearts was not diminished from control values under conditions of constant pressure, constant flow, anoxia, or insulin stimulation. Palmatic acid uptake and oxygen consumption were significantly reduced (P less than 0.02) in adrenalectomized hearts. This diminished fatty acid utilization was also reflected in a significantly lower CO'2 production and incorporation of the palmitate into myocardial triglycerides. The decreased fatty acid uptake by adrenalectomized cat hearts may represent aserious defect in myocardial metabolism since lipids are the major energy substrate forthe heart. Whether the defect occurs in fatty acid transport or activation cannot beelucidated by this study. However, it is unlikely that this defect has a major contributory effect on the dysfunction of adrenalectomized hearts since the myocardium iscabable of using other energy substrates readily.

Adrenal Insufficiency↗
PubMed1975

Actions of a leukocytic inflammatory substance on isolated tissue responses.

LIS had no action on the mechanical activity of isolated cat vascular, intestinal smooth, or cardiac muscle. No effect on platelet aggregation was observed, and PGF2alpha activity was absent in LIS preparations. Isolated lysosomal enzyme release was increased significantly when LIS was added to the incubation medium. This action may help to explain the inflammatory action of this naturally occurring material found in the inflamed synovial fluid of the canine knee joint.

Animals↗
PubMed1974

Pancreatic hypoperfusion and the production of a myocardial depressant factor in hemorrhagic shock.

Hemorrhagic shock was produced in dogs by bleeding to a systemic blood pressure of 45 mm Hg for 3 hours, followed by reinfusion of the shed blood. A rapid decrease in pancreatic blood flow occurred and pancreatic perfusion remained at 15-25% of control over the entire 3-hour oligemic period. As a consequence of this marked degree of pancreatic hypoperfusion, autolytic changes occurred in pancreatic acinar cell ultrastructure, particularly in the enlarging of lysosomes which developed many vacuoles. Plasma proteolytic indices (e.g., cathepsin D activity and amino nitrogen concentration) markedly increased during shock as well as the activity of a myocardial depressant factor (MDF). MDF was also produced in incubated pancreatic homogenates obtained from nonshocked dogs and in non-incubated homogenates from shocked dogs. MDF activity in the homogenates was closely correlated with amino nitrogen concentration. These data suggest that pancreatic hypoperfusion plays a key role in MDF formation and ultimately in the pathogenesis of circulatory shock. Moreover, MDF activity was found not to be associated either with pentobarbital concentration or the salt content of active fractions of plasma and pancreatic tissue. Ashing of active fractions was very effective in destroying MDF activity. These data are consistent with the earlier findings that indicate MDF to be a peptide having a molecular weight of 500-1,000.

Acid Phosphatase↗