ABSTRACT
BACKGROUND: Recent studies demonstrated that volatile anesthetics suppress the NO-cGMP system in the vascular system. It has been known that the hemodynamic changes produced by volatile anesthetics in septic patients are mediated by upregulation of iNOS leading to excessive release of NO. The mechanisms underlying suppression of the NO-cGMP system by anesthetics are still controversial. It has been elucidated that nitric oxide synthase (NOS) plays a major role in the regulatory function in the L-arginine-NO system. So we examined the effects of NOS inhibitor (L-NAME, aminoguanidine) and NO scavenger (hydroxocobalamin) on vascular smooth muscle contractile function in lipopolysaccharide (LPS)-treated rat aorta during halothane administration. METHODS: Aortic ring preparations were obtained from LPS-treated (1.5 mg/kg, ip, for 18 h) rats. We evaluated the effects of hydroxocobalamin, L-NAME and aminoguanidine on contractile responses to phenylephrine during halothane (1 & 2 MAC) administration respectively. Statistical significances (P<0.05) were analyzed according to data characterictics by repeated measures ANOVA test and student's t-test. RESULTS: The contractile responses to phenylephrine in LPS-treated rats aorta were significantly (P<0.05) increased in the presence of hydroxocobalamin and L-NAME. During the halothane (1 and 2 MAC) administration, the contractile responses to phenylephrine in LPS-treated rats aorta were increased significantly (P<0.05) in the presence of hydroxocobalamin and L-NAME. CONCLUSIONS: From these results, it is suggested that hydroxocobalamin and L-NAME may be useful in the therapy of septic shock.
Subject(s)
Animals , Humans , Rats , Anesthetics , Aorta , Halothane , Hemodynamics , Hydroxocobalamin , Muscle, Smooth, Vascular , NG-Nitroarginine Methyl Ester , Nitric Oxide Synthase , Phenylephrine , Shock, Septic , Up-RegulationABSTRACT
We have experienced one case of anesthesia for living related liver transplantation with propofol. The recipient was 18-month-old girl and 10.5 kg. She was suffered from congenital liver disease (biliary atresia). We decided propofol as an anesthetic agent of the recipient with permission of the recipient's parents. Total anesthetic time was about 13 hours and anhepatic phase was 110 min. Careful attention was paid to prevent infection, hypothermia, hepatic artery thrombosis and to keep proper lung function. Hemodynamic changes were relatively stable throughout the operation and postoperative mechanical ventilatory support was required for about 2 days.
Subject(s)
Female , Humans , Infant , Anesthesia , Hemodynamics , Hepatic Artery , Hypothermia , Liver Diseases , Liver Transplantation , Liver , Lung , Parents , Propofol , ThrombosisABSTRACT
We have experienced one case of anesthesia for living related liver transplantation with propofol. The recipient was 18-month-old girl and 10.5 kg. She was suffered from congenital liver disease (biliary atresia). We decided propofol as an anesthetic agent of the recipient with permission of the recipient's parents. Total anesthetic time was about 13 hours and anhepatic phase was 110 min. Careful attention was paid to prevent infection, hypothermia, hepatic artery thrombosis and to keep proper lung function. Hemodynamic changes were relatively stable throughout the operation and postoperative mechanical ventilatory support was required for about 2 days.
Subject(s)
Female , Humans , Infant , Anesthesia , Hemodynamics , Hepatic Artery , Hypothermia , Liver Diseases , Liver Transplantation , Liver , Lung , Parents , Propofol , ThrombosisABSTRACT
BACKGROUND: This study was aimed to elucidate the effect of propofol anesthesia on circulatory response to hemorrhage in rats by power spectral analysis of heart rate and blood pressure variability. METHODS: Nineteen male Sprague-Dawley rats weighing 350-580 g were divided into propofol (2 mg/kg, iv)-anesthetized (P, n=10) and saline control (C, n=9) groups. Blood pressure signal was digitized at 500 Hz for 5 min at basal, during hemorrhage and after hemorrhage. The signal was analyzed with fast Fourier transform algorithm to yield power spectra of systolic (SPV) and diastolic (DPV) blood pressure and cycle length variability (HRV). Very low frequency (VLF, 0.02-0.26 Hz), low frequency (LF, 0.26-0.75 Hz), high frequency (HF, 0.75-5.00 Hz) powers, LF/HF ratio and total power were obtained. Powers of each band were expressed as percent of total power. RESULTS: Blood pressure was decreased during hemorrhage in C and with a greater magnitude in P. Heart rate tended to increase during hemorrhage in C, but was not changed in P. LF powers of SPV in P was decreased after propofol injection. Hemorrhage decreased LF and increased HF. LF powers of DPV in P was decreased after propofol injection. Hemorrhage caused a further decrease in LF. LF powers of HRV in P was decreased after propofol injection. Hemorrhage caused a further decrease in LF. Powers of SPV, DPV and HRV in C were not changed by hemorrhage. LF/HF of SPV, DPV and HRV were decreased during hemorrhage in P, but not in C. CONCLUSIONS: These results suggest that propofol depressed sympathetic activity to diminish peripheral vascular tone and hemorrhage under propofol anesthesia resulted in a greater blood pressure fall due to impaired sympathetic compensation including attenuated baroreflex mechanism.