Abstract
Microscopic observation of incised mesoappendiceal venules and muscular branches of mesenteric arteries and veins was performed in rats under nembutal. Both the cut normal or sympathecto-mized mesenteric vessels and the uninjured mesenteric vessel lying adjacent to the nicked vessel contract locally. The formation of a plug of agglutinated platelets is followed by cessation of bleeding. Bleeding frequently recurs for brief intervals after its initial cessation, perhaps due to the exptl. conditions which prevent the local formation of a fibrin clot. Non-muscular venules do not contract. When cut with a dull blade, hemorrhage is usually prevented, probably by adherance of the endothelium or by pressure of connective tissue fibers drawn over the cut vessel. Stasis frequently occurs. Transection with a sharp blade is followed by bleeding which is arrested by the formation of a platelet plug. Bleeding frequently recurs for brief periods. In some animals given large doses of heparin, no platelet plug forms at the incision, and bleeding is incessant. In other heparinized animals, and in rats in which the prothrombin level is markedly lowered by the administration of dicumarol, plugs are produced which are ineffective in arresting bleeding. The incised vessel in these animals contracts normally, but the uninjured vessel contracts only in the presence of a platelet plug. Heparin and dicumarol admn. impair hemostasis by diminishing the ability of the platelets to agglutinate. Rats with thrombocytopenic purpura induced by antiplatelet serum fail to form platelet plugs since the circulating platelets are unable to agglutinate. Bleeding is not arrested. Although contraction of the injured vessel occurs, the adjacent uninjured vessel fails to contract. It is concluded that contraction of the injured vessel is the result of mechanical stimulation, whereas constriction of the adjacent uninjured blood vessel is produced by the vasoconstrictor substances liberated from the platelets. The platelet plug is the most important factor in the production of hemostasis.