Protection of functional and structural integrity of the rat myocardium by dexamethasone in hemorrhagic shock.
Rat hearts were isolated from control animals (C), following 2.5 hours of hemorrhagic hypotension (Sh) and from rats pretreated with 10 mg/kg dexamethasone (Sh + D), and they were perfused by the modified Langendorff technique. Dexamethasone pretreatment prevented the development of depression of left ventricular mechanical performance and increase of coronary resistance, but the reduction of O2 consumption observed in Sh hearts was not influenced by the synthetic glucocorticoid. Sh animals exhibited elevation of blood inorganic phosphate level, which was significantly diminished in Sh + D rats. Zonal lesions of myofilaments and mitochondria were not seen in electron micrographs of Sh + D hearts, but there was an increase in the number of cellular glycogen particles following dexamethasone pretreatment. The protection of contractile function and coronary circulation during shock cannot be the result of direct inotropic or coronary dilating action, since addition of dexamethasone (10 mg/liter) to the perfusate of C hearts did not alter contractility and coronary resistance. It is assumed that systemic hemodynamic and local cellular effects lead to the protection of myocardial integrity, which may contribute to the general beneficial action of dexamethasone in hemorrhagic shock.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D006321:Heart / Q000187:drug effects*; D007022:Hypotension / Q000517:prevention & control; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000648:ultrastructure*; D010477:Perfusion; D011292:Premedication; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000473:pathology / Q000503:physiopathology*
D003907:Dexamethasone