Effect of hypoxia on mechanical properties of isolated rat heart. Comparison of the effects of hypoxic and histotoxic hypoxia.
Direct myocardial effects of hypoxic (N2) and histotoxic (CO) hypoxia were studied in isolated rat hearts perfused by the modified Langendorff technique. During 30 min of hypoxic perfusion coronary resistance and left ventricular diastolic pressure increased significantly in CO but not in N2 hypoxia. The more deleterious myocardial effects of CO hypoxia were attributed to the direct inhibition of cellular oxygen utilization by CO. During early hypoxia pressure development declined rapidly, while the rate of pressure development (dp/dtmax) was maintained. It is suggested that these transient changes during early hypoxia be due to differences in the induced changes of the intensity and duration of the active state. After a period of rapid decline, left ventricular pressure work was stabilized at approximately 25% of the prehypoxic value if glucose was present in the perfusate. In the absence of glucose pressure development fell rapidly to zero reflecting the importance of anaerobic glycolysis in the maintainance of hypoxic cardiac function. The ability of the hypoxic myocardium to respond to inotropic procedures (electrical pacing and elevation of Ca2+ concentration in the perfusate) implies that depletion of high-energy phosphate supply cannot be the sole limitation of muscle function during hypoxia, while it appears to be related to a large extent to alterations in the excitation-contraction coupling system.
D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D051381:Rats; D013268:Stimulation, Chemical; D013997:Time Factors
D002118:Calcium