Effect of endotoxin and trypsin on the blood pressor response to catecholamines in normo- and hypothermic rabbits.

The action of endotoxin, trypsin or hypothermia on the vascular reactivity to catecholamines was investigated in rabbits, and with trypsin in normothermic dogs as well. In rabbits, LD10 of Escherichia coli 0111 endotoxin increased the blood pressor effect of i.v. adrenaline or noradrenaline with maxima at 60-90 min. LD50 endotoxin elicited a vascular hyporeactivity to catecholamines within an hour. 22 hours later, however, a hyperreactivity to catecholamines developed. At this time, repeated administration of LD50 endotoxin did not reduce the increased catecholamine responsiveness. Trypsin (i.v. 1.5 mg/kg) also potentiated the pressor effect of catecholamines in rabbits and dogs with maxima at 5-10 min. Higher trypsin doses induced a hyporeactivity. LD50 endotoxin in a single or a repeated dose after 22 hours did not decrease the blood pressure of cooled rabbits and failed to alter the vascular reactivity to adrenaline or noradrenaline. The blood pressure effect of trypsin differed in character in normo- and hypothermic rabbits, depending on the depth of cooling. Low body temperature eliminated the potentiating effect of trypsin to the blood pressor action of catecholamines. In normothermic rabbits pretreated with amino-pyrine and phenylbutazone, the blood pressure and the catecholamine potentiation effects of endotoxin or trypsin were inhibited or considerably reduced. The results support the significance of altered vascular reactivity to catecholamines under different pathologic conditions where endotoxin and/or proteases may occur.