title: In vitro femoral arterial responses to vasoconstrictor and vasodilator agents in endotoxin shock.
abstract: The hypothesis for this study is that the decreased arterial response to catecholamines may be due to the effect of endotoxemia on vessel tone. One control ring was taken from one femoral artery of a Wistar rat and after endotoxin (ENDT) infusion (i.v. 6 mg/kg-1 hr.), one ring was removed from the contralateral artery. The post-ENDT rings were tested in four groups which were determined by the mean arterial pressure (MAP) levels at the time of dissection: 100 mmHg (120 min), 80 mmHg (270 min), 60 mmHg (300 min) or 40 mmHg (330 min). KCl, phenylephrine (PHE) and arginine-vasopressin (AVP) dose-response curves (DR) were obtained at a preload of 500 mg which allowed the maximum response in control rings. When compared at 500 mg preload the maximal active response to all agonists post-ENDT was decreased by about 50%. By increasing the preload on the ENDT rings to 800 mg, the active tension became 2.49 times the active tension of the control rings. Length-tension experiments also showed a greater response for post-ENDT rings and a greater preload at maximum response but the ring circumference was the same. In contrast the in vivo femoral artery diameters at 90 min post-ENDT (100 mmHg) were 82.6% of control. Endothelium-dependent relaxation by acetylcholine (ACh) was abolished by ENDT but endothelium-independent relaxation to nitroprusside (NP) was not affected. It is concluded that the resting tone and active tension of femoral artery smooth muscle is increased by ENDT and the decreased in vivo responsiveness to vasoconstrictor agonists may be the result of vessel constriction due to loss of endothelium. The results also suggest that in vitro comparison of vessels in studies of endotoxin shock be done at the same muscle length rather than at the same preload.
authors.affiliation: Department of Physiology and Biophysics, College of Medicine, Tampa 33612.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhou
authors.forename: J M
authors.initials: JM
authors.lastname: Price
authors.forename: E T
authors.initials: ET
authors.lastname: Sutton
authors.forename: C H
authors.initials: CH
authors.lastname: Baker
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001127:Arginine Vasopressin / Q000494:pharmacology; D001920:Bradykinin / Q000494:pharmacology; D005263:Femoral Artery / Q000187:drug effects* / Q000503:physiopathology; D066298:In Vitro Techniques; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000503:physiopathology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012772:Shock, Septic / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*; D019323:omega-N-Methylarginine
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D001127:Arginine Vasopressin; D010656:Phenylephrine; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D011189:Potassium Chloride; D001120:Arginine; D000109:Acetylcholine; D001920:Bradykinin