Relative effects of nitroglycerin and nitroprusside during experimental acute myocardial ischemia

Abstract

When given during acute myocardial infarction (AMI), vasodilators such as nitroglycerin (TNG) and nitroprusside (NP) improve some of the hemodynamic determinants of myocardial oxygen demand. TNG has been shown to reduce ischemic injury during AMI, but variable results have been noted with NP therapy. To compare the effects of these two agents, 8 closed chest sedated dogs with pre-existing multi-vessel coronary constrictions underwent repeated, random-order, acute 15-min balloon occlusions of the left anterior descending coronary artery during the following conditions: (1) saline infusion (control), (2) TNG infusion, and (3) NP infusion. The severity of myocardial ischemia was estimated by summating the ST-segment elevations (xi ST) measured from 7 intramyocardial electrodes; mean left atrial pressure (LAP), heart rate (HR), and mean systemic arterial pressure (SAP) were also measured. No dog had left ventricular failure either before or after occlusion. Since HR and SAP responses to TNG and NP are different, the dogs were randomized into two subgroups: TNG and NP were infused in 4 dogs to produce similar increases in HR (10--20% greater than control), and in the other 4 to produce similar decreases in SAP (15--20% less than control). In each subgroup, xi ST was significantly lower following TNG than following NP. Moreover, in the total group of 8 dogs, xi ST after 10 min of occlusion averaged 38 +/- 10 mV during TNG treatment compared to 46 +/- 10 mV during control occlusion (P less than 0.05). In contrast, xi ST after 10 min of occlusion averaged 57 +/- 11 mV during NP treatment (P less than 0.01 compared to control occlusion). Thus, (1) when given to achieve similar hemodynamic changes following acute coronary occlusion, TNG reduced while NP increased myocardial ischemia, (2) although both 'vasodilators', TNG and NP appear to have different actions on various vascular beds, and (3) the hemodynamic changes induced by vasodilators do not in themselves provide an accurate index of directional alterations in myocardial ischemia.