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'''Ichikawa, S, Wakao, Y, Muto, M and Takahashi, M''' (1990) Experimental studies of the load reducing effects of nitroglycerin in heart failure.''Nippon Juigaku Zasshi'' '''52''':361-9 | '''Ichikawa, S, Wakao, Y, Muto, M and Takahashi, M''' (1990) Experimental studies of the load reducing effects of nitroglycerin in heart failure. ''Nippon Juigaku Zasshi'' '''52''':361-9 | ||
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Animals; Blood Pressure; Chordae Tendineae; Dogs; Female; Heart Failure; Male; Mitral Valve Insufficiency; Myocardial Contraction; Nitroglycerin; Oxygen Consumption; Stroke Volume | Animals; Blood Pressure/drug effects; Chordae Tendineae/surgery; Dogs; Female; Heart Failure/etiology; Heart Failure/physiopathology; Male; Mitral Valve Insufficiency/etiology; Mitral Valve Insufficiency/physiopathology; Myocardial Contraction/drug effects; Nitroglycerin/pharmacology; Oxygen Consumption/drug effects; Stroke Volume/drug effects | ||
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Latest revision as of 04:37, 15 September 2013
| Citation |
Ichikawa, S, Wakao, Y, Muto, M and Takahashi, M (1990) Experimental studies of the load reducing effects of nitroglycerin in heart failure. Nippon Juigaku Zasshi 52:361-9 |
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| Abstract |
The load-reducing effect of nitroglycerin (NTG), a vasodilator, was studied in dogs with heart failure. The chordae tendineae of the mitral valve were transected to induce acute mitral regurgitation (MR) for hemodynamic evaluation. By such surgical treatment, preload indices such as left ventricular end-diastolic pressure (LVEDP) and left atrial pressure (LAP) increased significantly, and subsequent cardiac dysfunction and heart failure were indicated by another decrease in stroke volume, myocardial contractility, forward flow, and myocardial oxygen consumption. To dogs with artificially established acute MR, 3 micrograms/kg/min of NTG was administered intra-arterially by means of a continuous infusion, that resulted in decrease of LVEDP, LAP and central venous pressure (CVP). Thus, a reduction of preload was determined. Simultaneously, afterload indices such as aortic systolic pressure (Aos), aortic mean pressure (Aom) and total peripheral resistance (TPR) decreased remarkably. Afterload reduction depended on the amount of venous return; therefore, an extra-corporeal circulation system was applied in order to supply a constant venous return before NTG administration. This caused a significant decrease in aortic diastolic pressure (Aod), Aos, Aom, left ventricular systolic pressure (LVSP) and TPR, and an increase in myocardial contractility and cardiac output. This suggested that afterload reduction might be realized by the vasodilatory effect of NTG on the resistance vessels. |
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| Keywords |
Animals; Blood Pressure/drug effects; Chordae Tendineae/surgery; Dogs; Female; Heart Failure/etiology; Heart Failure/physiopathology; Male; Mitral Valve Insufficiency/etiology; Mitral Valve Insufficiency/physiopathology; Myocardial Contraction/drug effects; Nitroglycerin/pharmacology; Oxygen Consumption/drug effects; Stroke Volume/drug effects |
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