title: Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels.
abstract: BACKGROUND
  We studied the effect of intracoronary administration of arginine-8-vasopressin on blood flow in nondiseased coronary arteries and determined whether this vasoconstriction was severe enough to produce ischemia in 30 dogs.
  
  
  RESULTS
  In group 1 (n = 6), after vasopressin administration coronary blood flow was decreased by 41% (p less than 0.002) without changes in heart rate or aortic pressure, and left ventricular ejection fraction measured by radionuclide angiocardiography was decreased by 18% (p less than 0.0005). In group 2 (n = 6), ischemia was confirmed by measurement of transmural pH changes. Administration of vasopressin decreased subendocardial pH of the infused zone from 7.40 +/- 0.03 to 7.31 +/- 0.07 (p less than 0.01). The subendocardial pH of the zone not infused with vasopressin did not change. To overcome the intrinsic regulation of blood flow, operating primarily in small coronary arteries, we hypothesized that vasopressin must increase resistance primarily in large rather than small coronary arteries. After intracoronary infusion in group 3 (n = 6), however, most (94%) of the increase in resistance during vasopressin administration was explained by an increase of resistance in small coronary arteries. In group 4 (n = 9), vasopressin decreased coronary blood flow by 50% and decreased local shortening by 90% at a time when systemic hemodynamics were unchanged. Coronary constriction induced by vasopressin, or the recovery from it, also was not altered by cyclooxygenase blockade.
  
  
  CONCLUSIONS
  Thus, vasopressin produces myocardial ischemia by constricting small, nondiseased coronary arteries severely enough to overcome the competition from normal coronary regulation, and this ischemic event is not mediated by prostaglandin products.
authors.affiliation: Experimental Physiology and Pharmacology Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
authors.forename: M F
authors.initials: MF
authors.lastname: Maturi
authors.forename: S E
authors.initials: SE
authors.lastname: Martin
authors.forename: D
authors.initials: D
authors.lastname: Markle
authors.forename: M
authors.initials: M
authors.lastname: Maxwell
authors.forename: C R
authors.initials: CR
authors.lastname: Burruss
authors.forename: E
authors.initials: E
authors.lastname: Speir
authors.forename: R
authors.initials: R
authors.lastname: Greene
authors.forename: Y M
authors.initials: YM
authors.lastname: Ro
authors.forename: D
authors.initials: D
authors.lastname: Vitale
authors.forename: M V
authors.initials: MV
authors.lastname: Green
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000139:chemically induced* / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D008297:Male; D009206:Myocardium / Q000378:metabolism; D014661:Vasoconstriction; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D016861:Cyclooxygenase Inhibitors; D001127:Arginine Vasopressin