H1-ANTAGONISM IMPROVES INTESTINAL MUCOSAL pH AND HEART FUNCTION IN PORCINE HYPODYNAMIC ENDOTOXIC SHOCK

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Abstract
Porcine hypodynamic shock was induced by continuous infusion of 5 μg lipopolysaccharide/kg per hour. This resulted in a decrease of cardiac output from baseline values of 3.5 ± .9 L/min to 1.5 ± .8 L/min and a reduced left ventricular stroke work index in the endotoxin-group (n = 6 animals). Pretreatment with the H1-antagonist dimethindene (2 mg/kg) in a second group (n = 6) significantly prevented these effects. Furthermore animals pretreated with the H1-antagonist showed a stable mean arterial blood pressure, whereas the control endotoxin-treated group revealed a drastic reduction in mean arterial blood pressure (99 ± 4.7 mmHg versus 65.8 ± 10 mmHg after 240 min, respectively). Pulmonary function and systemic vascular resistance were not ameliorated by the H1-antagonist in hypodynamic shock. Gastrointestinal mucosal pH (pHi), which indicates oxygenation of the mucosa, was decreased by endotoxin-infusion (7.45 ± .32 baseline value to 6.92 ± .24 after 120 min). This parameter as well as base excess values and lactate levels were significantly improved by dimethindene-pretreatment (p < .05). These results may indicate a beneficial effect of H1-antagonist-pretreatment on endotoxin-induced deterioration of the microcirculation. Furthermore our results clearly demonstrated that only pretreatment before endotoxemia with H1-antagonism is effective, since infusion of H1-antagonist in hypodynamic shock 45 min after addition of endotoxin (n = 6 animals) did not improve the cardiovascular system or the microcirculation.

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