ABSTRACT
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.
Subject(s)
Animals , Rats , Anesthetics , Arterial Pressure , Cardiac Output , Central Venous Pressure , Diltiazem , Equidae , Heart , Heart Atria , Heart Rate , Hemodynamics , Injections, Intravenous , Ketamine , NitroglycerinABSTRACT
The ratio of acetoacetate to 8-hydroxybutyrate (ketone body ratio) in the blood may reflects the mitochondrial free NAD+/NADH ratio in the liver. Also arterial ketone body ratio will reflects the energy status of the hepatocytes, because mitochondrial free NAD+/NADH ratio is closely related to oxidative phosphorylation. Arterial ketone body ratio and osmolal gap, the difference between measured osmolality and calculated osmolality, were measured 30 min after the induction of hemorrhagic shock with mean arterial blood pressure at 40 mmHg in ten rabbits. Arterial ketone body ratios decreased significantly (p<0.05) from 0.74+/-0.17 to 0.38+/-0.09 and osmolal gap increased significantly (p<0.05) from 17.7+/-5.9 mOsm/Kg to 32.8+/-12.3 mOsm/Kg at 30 min after the induction of hemorrhagic shock. These results suggest that in hemorrhagic shock, decreased arterial ketone body ratio which reflects the inhibition of the TCA cycle is associated with increase of osmolal gap.
Subject(s)
Rabbits , Arterial Pressure , Hepatocytes , Liver , Osmolar Concentration , Oxidative Phosphorylation , Shock, HemorrhagicABSTRACT
The hemodynamic changes of naloxone and nalbuphine following intravenous administra tion of high-dose fentanyl were studied using dogs anesthetized with halothane and ventilated artificially. After 50ug/kg of fentanyl was given to all experimental animals, they were randomly divided into two groups, such as group 1 and group 2. Group 1 and 2 were given 20ug/kg of naloxone and 0.3mg/kg of nalbuphine known as antagonists of fentanyl-induced respiratory depression respectively. Hemodynamic parameters were recorded before, 5 and 30 minutes after fentanyl and 1,10 and 20 minutes after naloxone or nalbuphine. During halothane anesthesia, fentanyl significantly decreased mean arterial pressure, heart rate, cardiac index, rate pressure product, left ventricular stroke work index and right ventricular stroke work index in all dogs(p<0.05). After fentanyl reversal by antagonists, dogs in group 1 promptly developed significant increases above baseline values in mean arterial pressure, heart rate, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, rate pressure product and left ventricular stroke work index(p<0.05), whereas dogs in group 2 did not show significant hemodynamic changes. These results suggest that the abrupt, untoward and significant hyperdynamic events which accompany narcotic reversal with naloxone can be avoided if nalbuphine instead of naloxone is administered.