Acute gastrointestinal bleeding during experimental hypercarbia

• Published in: Chest Vol. 71; no. 4; p. 514
• Main Authors: Abdel-Rassoul, M, DeBellis, J, Stein, M
• Format: Journal Article
• Language: English
• Published: United States 01.04.1977
• Subjects: Animals; Chromium Radioisotopes; Disease Models, Animal; Dogs; Erythrocytes; Gastrointestinal Hemorrhage - etiology; Gastrointestinal Hemorrhage - pathology; Humans; Hypercapnia - complications; Hypercapnia - pathology; Intestine, Large - pathology; Intestine, Small - pathology; Mesenteric Arteries - diagnostic imaging; Radiography
• ISSN: 0012-3692
• DOI: 10.1378/chest.71.4.514

Experimental acute hypercarbia in dogs produced significant blood loss from the upper gastrointestinal tract, as well as from the small and large intestines. At necropsy, gross and microscopic examinations demonstrated necrotizing lesions resembled the postmortem ulcerations found in some patients with severe hypercarbia. Superior mesenteric arteriograms performed in four animals shortly after onset of hypercarbia showed abnormalities consistent with vasoconstriction. Vagal inhibition by atropine and correction of respiratior acidosis by TRIS buffer failed either to reduce the blood loss or to alter the pathologic lesions. Multiple studies of blood coagulation in the hypercarbic animals revealed no consistent changes when compared with eucarbic animals. In four animals treated with phenoxybenzamine during hypercarbia, blood loss and hemorrhagic gastrointestinal lesions were diminished, suggesting possible pathogenetic role of alpha-adrenergic stimulation. Although the mechanism is not proved, vasoconstriction secondary to adrenergic stimulation may play an important bleeding occurring with hypercarbia.