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Mesenteric Vasoconstriction After Endotoxin Administration in Cats Pretreated with Aspirin

Overview
Journal Br J Pharmacol
Publisher Wiley
Specialty Pharmacology
Date 1971 Oct 1
PMID 4333802
Citations 11
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Abstract

1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.

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References
1.
Hinshaw L, Kuida H, Gilbert R, VISSCHER M . Influence of perfusate characteristics on pulmonary vascular response to endotoxin. Am J Physiol. 1957; 191(2):293-5. DOI: 10.1152/ajplegacy.1957.191.2.293. View

2.
Stark R, McNeill J, GREENWAY C . Sympathetic and hypophyseal roles in the splenic response to hemorrhage. Am J Physiol. 1971; 220(3):837-40. DOI: 10.1152/ajplegacy.1971.220.3.837. View

3.
Vick J . TRIGGER MECHANISM OF ENDOTOXIN SHOCK. Am J Physiol. 1964; 206:944-6. DOI: 10.1152/ajplegacy.1964.206.5.944. View

4.
KOBOLD E, THAL A . QUANTITATION AND IDENTIFICATION OF VASOACTIVE SUBSTANCES LIBERATED DURING VARIOUS TYPES OF EXPERIMENTAL AND CLINICAL INTESTINAL ISCHEMIA. Surg Gynecol Obstet. 1963; 117:315-22. View

5.
HAINING C . Inhibition of histamine release by sodium salicylate and other compounds. Br J Pharmacol Chemother. 1956; 11(4):357-63. PMC: 1510554. DOI: 10.1111/j.1476-5381.1956.tb00002.x. View