Comparison of Effects of Nitroglycerin and Diltiazem on Venous Capacitance in Rats / 대한마취과학회지

The change of venous capacitance has an influence on venous return to the heart and cardiac output, and causes the alteration of preload, cardiac filling pressure and myocardial wall tension. Venous capacitance is assesed by measuring the mean circulatory filling pressure (MCFP), and MCFP is measured during brief periods of circulatory arrest produced by inflating an indwelling balloon in the right atrium It is important to know the effects of vasodilator and anesthetic drugs on venous capacitance. Therefore, this study was performed to know the effects of nitroglycerin and diltiazem on venous capacitance in rats. Rats were anesthetized with ketamine 125 mg/kg given intraperitoneally and added 10 mg/kg every 30 minutes. Their mean arterial pressure (MAP) was lowered to 60 mmHg by intravenous injection of 0.82+/-0.36 mg/kg nitroglycerin and/or 6.7+/-1.5 mg/kg diltiazem. Hemodynamic parameters such as MAP, heart rate, central venous pressure and MCFP were measured before and after drug-injection. Hemodynamic values measured before drug-injection in two groups were little differences statistically. However, the MCFP of nitroglycerin was significantly decreased (p<0.01) from 7.3+/-0.61 mmHg to 5.4+/-0.58 mmHg after drug-injection, and that of diltiazem was not significantly changed from 7.1+/-0.54 mmHg to 6.9+/-0.63 mmHg. The results suggested that nitroglycerin was predominantly a venous dilator in terms of MCFP but diltiazem had little effect of venodilation.

Changes in Arterial and Mixed Venous Carbon Dioxide Tension and Hemodynamic States after Sodium Bicarbonate during Hemorrhagic Shock / 대한마취과학회지

Recently, several investigators have begun to question the routine use of sodium bicsrbonate in metabolic acidosis, based on a failure to clearly demonstrate the efficacy of alkali therapy, which includes the production of carbon dioxide and variability of the effect on hemodynamic state. We studied the use of sodium bicarbonate in a canine model of hemorrhagic shock to determine its effect on arterial, mixed venous blood gases and hemodynamic states. Nine adult mongrel dogs were anesthetized with pentothal sodium and mechanical ventilation was adjusted to maintained the PaCO2 at 30 to 35mmHg. Ar Swan-Ganz catheter was inserted via a right femoral vein and the right femoral artery was cannulated for continuous pressure monitoring and intermittent blood sampling. 30 minutes after hemorrhagic shock, sodium bicarbonate (1mEq/kg) was administered and 1, 5, 15, 30 and 60 minutes after administration of sodium biearbonate we analyzed the arterial, mixed venous blood gases and measured hemodynamic states. The results were as follows, 1) The arterial carbon dioxide tensions(PaCO2) of 1,5,15,30 and 60 minutes after administration of sodium bicarbonate were 44,42,41,42 and 46mmHg which increased significantly compared to control value, 33mmHg. 2) The mixed venous carbon dioxide tensions(PvCO2) ofr 1, 5, 15, 30 and 60 minutes after administration of sodium bicarbonste were 57, 55, 56, 55 and 55mmHg which also increased significantly compared to control value, 46mmHg. 3) The mean arterial pressures of 1, 5, 15, 30 and 60 minutes after administration of sodium bicarbonate were 61, 60, 64, 68 and 70mmHg which increased significantly compared to control value, 50mmHg, but there were no increasements of cardiac output. It is undesirable to use sodium bicarbonate routinely during hemorrhagic shock because the use of sodium bicarbonate in metabolic acidosis increased arterial and mixed venous carbon dioxide tension and did not show the improvement of hemodynsmic derangement.