In 8 patients with coronary artery disease and symmetrical left ventricular contraction, an echocardiographic study of left ventricular function was performed before and 3 minutes after the administration of 0-6 mg nitroglycerin sublingually. The left ventricular end-diastolic diameter decreased from 5-2 +/- 0-2 to 4-9 +/- 0-2 cm (P less than 0-05) and the end-systolic diameter from 4-2 +/- 0-2 to 3-7 +/- 0-2 cm (P less than 0-001). The estimated stroke volume did not change significantly, while the cardiac output increased, 5-8 +/- 0-6 to 7-7 +/- 0-6 l min-1 (P less than 0-001) and the heart rate increased from 72 +/- 5 to 90 +/- 6 (P less than 0-001). The mean arterial blood pressure decreased from 105 +/- 4 to 88 +/- 3 mmHg (P less than 0-001). The ejection fraction increased from 53 +/- 3 per cent to 65 +/- 6 per cent (P less than 0-001) and the mean velocity of circumferential fibre shortening (VCF) from 0-81 +/- 0-05 to 1-15 +/- 0-10 circumferences per second (P less than 0-001). The estimated midsystolic midwall stress decreased from 155 +/- 14 g cm-2 to 102 +/- 12 g cm-2 after mitroglycerin (P less than 0-001). The administration of nitroglycerin was associated with a significant decrease in left ventricular preload and afterload. A vasodilating effect is suggested by the fall in peripheral resistance. The overall improvement in ejection fraction and VCF may not reflect a true increase contractility, because of the concomitant fall in wall stress.

This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the alpha and beta 2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG alpha and beta 2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.