Open AccessEARLY ENDOTOXIC SHOCK RESULTS IN ENHANCED VASODILATOR RESPONSES TO NITROGLYCERIN BUT UNALTERED RESPONSES TO NEUROPEPTIDES CALCITONIN GENE-RELATED PEPTIDE AND SUBSTANCE P
Author(s) -
W. A. Arden,
Ronald R. Fiscus,
Xian Wang,
Richard H. Maley,
Sherrie Lanzo,
David R. Gross
Publication year - 1994
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/00024382-199406000-00006
Subject(s) - substance p , calcitonin gene related peptide , vasoactive intestinal peptide , medicine , endocrinology , vasodilation , norepinephrine , septic shock , nitric oxide , neuropeptide , neurokinin a , shock (circulatory) , chemistry , sepsis , receptor , dopamine
To determine the role that vasoactive neuropeptides, calcitonin gene-related peptide, and substance P play in tissue-blood flow regulation during early septic shock, we examined the responsiveness of arteries removed from pigs 3 h after administration of Escherichia coli lipopolysaccharide or saline vehicle. The carotid, cranial mesenteric, and left anterior descending coronary arteries were excised, and rings were cut from each vessel. Constrictor responses were obtained to cumulative doses of norepinephrine or potassium chloride. Rings were reconstricted and challenged with acetylcholine, substance P, calcitonin gene-related peptide, and nitroglycerin. Lipopolysaccharide significantly increased the cranial mesenteric artery's response to high concentrations of norepinephrine and the response to nitroglycerin in all vessels. This enhancement of responses to nitroglycerin suggests augmented smooth-muscle responsiveness to an exogenous source of nitric oxide, possibly associated with early depression of basal endothelial function. Depression of agonist-induced nitric oxide release may mask such enhancement with endothelial-dependent dilators and may enhance the response to adrenergic constrictors in some vascular beds.