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Biomedical subjects

J A Spath

Publications and source records attributed to J A Spath.

28 records · Page 2Linked to original sources
PubMed1976

Lack of a significant protective effect of augmented circulating glucose on the ischemic myocardium.BJ.

Infusion of glucose alone or glucose with insulin in cats subjected to acute myocardial ischemia did not alter the hemodynamic response of the cats to coronary artery ligation. Furthermore, determination of myocardial creatine phosphokinase (CPK) (ATP:creatine N-phosphotransferase, EC 2.7.3.2) activities failed to reveal a protective effect of glucose and insulin upon the status of the developing infarct in the ischemic myocardium. However, glucose and insulin apparently promote clearance of CPK from the plasma and inhibit proteolysis during the early phase of myocardial ischemia. These actions may be of value in generalized adaptive response of the animal to the stress of ischemia, but does not per se appear to diminish the spread of the ischemic damage within the heart not to limit the extension of the evolving infarct.

Animals↗
PubMed1975

Effects of dexamethasone on myocardial cells in the early phase of acute myocardial infarction.

Dexamethasone exerted no significant hemodynamic effect in sham-operated cats or in cats subjected to acute myocardial ischemia. However, the glucoccortcoid did normalize elevated S-T segments toward pre-ischemic values, and prevented much of the increase in plasma CPK activity following coronary artery ligation. Moreover, dexamethasone prevented loss of CPK activity and restricted the loss of lysosomal hydrolase within ischemic myocardial tissue. These data indicate that lysosomal disruption is an early consequence of myocardial ischemia and that treatment with dexamethasone prevents the loss of myocardial lysosomal and cellular enzymes as reflected in normalization of the ECG and plasma CPK activity of ischemic cats. In this way, dexamethasone may act to retard the spread of the developing infarct within the ischemic myocardium.

Animals↗
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↗
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↗