Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion.
The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D004285:Dogs; D004562:Electrocardiography; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D007263:Infusions, Parenteral; D007773:Lactates / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D005996:Nitroglycerin / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D011188:Potassium / Q000378:metabolism; D014059:Tongue
D007773:Lactates; D005996:Nitroglycerin; D011188:Potassium