The present study was conducted to examine the effect of dopamine on arterial blood pressure, liver blood flow, cathepsin D activity, and free amino nitrogen concentration in hemorrhagic shock. Dopamine at a dose of 4 μg/kg/min increased both mean arterial blood pressure and liver blood flow in postoligemic shock, but failed to prevent the marked increases in circulating cathepsin D and free amino nitrogen. In fact, dopamine infusion resulted in an increased plasma cathepsin D activity in shock. This increased accumulation of a lysosomal marker enzyme probably results from increased washout of the enzyme from the splanchnic or hepatic vascular bed in response to increased blood flow in these areas rather than from a direct effect of dopamine on lysosomal integrity. The increase in hepatic artery and portal vein flows appeared to result from stimulation of dopaminergic receptors since the dopamine dose was in the dopaminergic range and because haloperidol, a dopamine blocker, abolished the improved hemodynamic effects of dopamine. This study suggests that dopamine benefits the animal in hemorrhagic shock hemodynamically, but does not reverse the metabolic and cellular problems in shock. Perhaps, in combination with a drug opposing the biochemical basis of shock, dopamine may provide a greater anti-shock action.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Dec 1 1977|