title: Diltiazem and regional left ventricular function during graded coronary constriction and propofol anesthesia in the dog.
abstract: Although calcium channel blockers may preserve function in ischemic myocardium, they may also produce myocardial depression and dysfunction in the presence of decreased coronary flow. This study was designed to examine the issue of possible protection afforded by diltiazem against ischemia-induced myocardial dysfunction during propofol anesthesia. In eight anesthetized and ventilated dogs, regional myocardial (ultrasonic crystals in both left anterior descending [LAD] and left circumflex [LC] perfusion areas) and global ventricular function were evaluated during progressively severe degrees of myocardial ischemia (LAD constriction) before and after intravenous diltiazem (150 micrograms/kg). As coronary flow decreased, heart rate increased, and arterial and coronary perfusion pressures, left ventricular dP/dt, and cardiac output decreased. Systemic vascular resistance was unaffected. Diltiazem without coronary constriction increased heart rate, and decreased diastolic arterial pressures, left ventricular (LV) end-diastolic, coronary perfusion pressures, LV dP/dt max, LAD coronary blood flow, stroke volume, and cardiac output. At all levels of coronary constriction following diltiazem, there were decreases in systolic and diastolic arterial pressures, stroke volume, cardiac output, LV dP/dt, and coronary perfusion pressure. Heart rate increased at critical coronary constriction, and then remained constant relative to the prediltiazem state. The regional muscle effects of the reductions in coronary flow in the LAD perfusion territory included decreased systolic shortening and increased postsystolic shortening before and after diltiazem. Diltiazem did not alter the magnitude of the alterations in systolic or postsystolic shortening brought about by coronary constriction. No changes occurred in the LC area.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Medical College of Wisconsin 53226.
authors.forename: A H
authors.initials: AH
authors.lastname: Goldberg
authors.forename: J
authors.initials: J
authors.lastname: Diedericks
authors.forename: J W
authors.initials: JW
authors.lastname: Sear
authors.forename: M B
authors.initials: MB
authors.lastname: Hopwood
authors.forename: P
authors.initials: P
authors.lastname: Foëx
mesh_terms: D000771:Anesthesia, Intravenous; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D004110:Diltiazem / Q000494:pharmacology*; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015742:Propofol; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
chemical_list: D004110:Diltiazem; D015742:Propofol