Gastroenterology

Gastroenterology

Volume 74, Issue 1, January 1978, Pages 38-43
Gastroenterology

Effect of acid and pepsin on blood coagulation and platelet aggregation: A possible contributor to prolonged gastroduodenal mucosal hemorrhage

https://doi.org/10.1016/0016-5085(78)90352-9Get rights and content

Abstract

In a series of in vitro studies, both the soluble (plasmatic) coagulation system and the cellular (platelet-mediated) aspect of blood coagulation were shown to be extremely sensitive to relatively minor increases in hydrogen ion concentration. All studies became abnormal at pH 6.8. At pH 6.4, assays of the intrinsic and extrinsic coagulation systems, the polymerization of fibrinogen, and assay of the availability of platelet phospholipid (platelet factor 3) were twice prolonged over control values. Platelet aggregation was reduced by more than 50%. At pH 5.4 in vitro, platelet aggregation and plasma coagulation were both virtually abolished. Furthermore, previously formed platelet aggregates disaggregated at a slightly acid pH. Pepsin further enhanced platelet disaggregation. Because gastric acidity is normally two to four orders of magnitude greater than that which abolishes platelet aggregation and plasma clotting in vitro, and pepsin is present in abundance, we call attention to the probable antihemostatic effect of hydrocloric acid and pepsin in the upper gastrointestinal tract. This in vitro study may provide a rationale for meticulous regulation of intragastric pH in an effort to control upper gastrointestinal hemorrhage.

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    This study was supported in part by Training Grant AM-5424 and by Research Grant AM-10571 from the National Institutes of Health.

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