Vascular smooth muscle desensitization in rabbit epigastric and mesenteric arteries during hemorrhagic shock

Following initial homeostatic compensation, the “shock” phase of hemorrhage involves persistent vasoconstrictor-resistant vasodilation. This study suggests that such vascular hyporeactivity is explained by intrinsic vascular muscle desensitization caused by compensatory elevations in vasoconstrictors. Further investigations into molecular targets that block desensitization may reverse vasoconstrictor insensitivity allowing reanimation of shock victims.