[ACTH inhibits the development of primary decompensation of the systemic and portal circulation in acute blood loss in rats].
Using the method of contact luminescent biomicroscopy of the liver and intestine coupled with the measurement of systemic blood pressure by micromanometer and ultrasonic registration of blood flow velocity in portal vein and hepatic artery it has been established that in rats with acute decompensatory hemorrhage fragments of ACTH (1-24) and (4-10) improve the state of portal macro- and microcirculation and increase the life span 2-3-fold. ACTH does not influence the dynamics of acute compensatory hemorrhage and the development of the posthemorrhagic microcirculatory disturbances (local microstases, microthromboses, erythrocyte aggregation).
Kovalenko
N Ia
NIa
Matsievskiĭ
D D
DD
D000208:Acute Disease; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D001775:Blood Circulation / Q000187:drug effects* / Q000502:physiology; D006470:Hemorrhage / Q000503:physiopathology*; D007422:Intestines / Q000098:blood supply / Q000187:drug effects; D008099:Liver / Q000098:blood supply / Q000187:drug effects; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000503:physiopathology; D010446:Peptide Fragments / Q000494:pharmacology*; D011168:Portal System / Q000187:drug effects* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar
D010446:Peptide Fragments; C038513:ACTH (1-14); D000324:Adrenocorticotropic Hormone; C011394:ACTH (4-10)
AKTG tormozit razvitie pervichnoĭ dekompensatsii sistemnogo i portal'nogo krovoobrashcheniia pri ostroĭ krovopotere u krys.