English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

During the clotting of whole human blood or plasma, we have observed the generation of vasospasmodic activity with isolated smooth muscle preparations. Since kallikreins reportedly have musculotropic effects, such effects of related serine proteases were examined on isolated guinea pig ileum and rat uterus smooth muscle preparations. Like glandular kallikrein, human α-thrombin caused pronounced muscular contractions of these preparations and did so more effectively than trypsin and much more so than plasmin, activated coagulation factor X or XII, or noncoagulant β- and γ-thrombins. Levels as low as 0.1 to 1 clotting (NIH) units/ml final bath concentration of α-thrombin caused such contractions(5 units/ml grossly contracted muscle preparations) and the contractile activity was inhibited by either hirudin or antithrombin III plus heparin, indicating the requirement for the catalytically active enzyme. These contractions were not blocked by antihistamic (tripell ana- mine), antimuscarinic (atropine), or antiganglionic (mecamylamine) agents, further suggesting that the contractions were not mediated by an autonomic mechanism but rather were attributable to a direct function of the enzyme. Because physiologic concentrations of less than 5 units/ml were effective, our data imply that vasospasmodic responses may not only result from thromboxanes and platelet release products (e.g. serotonin and ADP) but also to direct α-thrombin induced contractile effects on smooth muscles exposed at sites of vascular injury. Such smooth muscle contractions may facilitate in the prevention of blood loss or may contribute to pathologic states (e.g. ischemia, stroke) impeding blood circulation.

Thrombin Induced Contraction Of Isolated Smooth Muscles