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Hemodynamic alterations in splanchnic arterial occlusion shock and the effects of dexamethasone sodium phosphate



Hemodynamic alterations in splanchnic arterial occlusion shock and the effects of dexamethasone sodium phosphate



Circulatory Shock 2(4): 287-299



The ability of dexamethasone sodium phosphate (DSP) to modify cardiac performance and the biochemical alterations associated with splanchnic artery occlusion (SAO) shock was investigated. Dexamethasone (5 mg/kg i.v.) or placebo was infused 30 min before subjecting dogs to lethal SAO shock and again before (10-15 min) release of the occlusion. Left ventricular function curves were performed before SAO, before release of the occlusion, and 30 min postrelease. There was no evidence of a direct positive inotropic effect of DSP in sham shocked dogs. A marked depression in peak cardiac work was noted in placebo-treated shocked dogs (35% decrease, postrelease) and a significant decrease in dP/dt [change in pressure/change in time] and index of cardiac contractility. In shocked dogs treated with steroid there was no significant depression in cardiac work or dP/dt. After release of the occlusion, the aortic flow of DSP- and placebo-treated shocked dogs exhibited qualitatively similar decreases; the response was significantly less sustained in DSP-treated dogs. Splanchnic tissues of DSP-treated shocked dogs showed a significantly higher degree of lysosomal stability compared with tissues from placebo-treated shocked dogs. Plasma levels of myocardial depressant factor (MDF), a cardiotoxic peptide, were also lower in DSP-treated shocked dogs than in placebo-treated shocked animals. The maintenance of cardiac performance in DSP-treated shocked animals correlated with the failure of these animals to exhibit significant increases in plasma MDF and free splanchnic lysosomal enzyme activities. DSP may exert its protective action on cardiac function in SAO shock indirectly by preventing the disruption of lysosomal membranes, the release of lysosomal acid proteases and the subsequent formation of the cardiodepressant peptide, MDF.

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Accession: 005556378

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