Three cases of suspected sugammadex-induced hypersensitivity reactions.

Neuromuscular blocking agents have been implicated in 60-70% of anaphylactic events associated with anaesthesia. We report two cases of probable hypersensitivity reaction to sugammadex and an additional suspected but less supported case of possible immune-mediated reaction or other adverse reaction. The patients were given a bolus of sugammadex 100 mg immediately before extubation. In all three patients, a possible allergic reaction was suspected within 4 min of sugammadex administration, but with different degrees of severity. Skin testing was positive in two of these patients. Hypersensitivity to sugammadex unaccompanied by cardiovascular or respiratory symptoms might be missed during the course of anaesthesia. Careful monitoring for possible allergic responses is required in patients who have received sugammadex.

[A comparison of various ways of cardiac output measurement by thermodilution methods].

We compared cardiac output values obtained by the following 3 methods: 1. Iced bolus injectate method, using the injectate temperature actually measured for computation [bolus cardiac output with flow-through temperature probe: BCO (p)]. 2. Continuous cardiac output measurement, using Vigilance system (continuous cardiac output: CCO). 3. Iced bolus injectate method, assuming injectate temperature to be 0 degrees C (bolus cardiac output without flow-through temperature probe: BCO). Only the subject receiving cardiovascular surgeries using cardiopulmonary bypass (CPB), and requiring a thermodilution catheter for hemodynamic monitoring during anesthesia were selected for the study. The total cases consisted of 15 patients (10 males), in which 60 measurement were made. Following the anesthetic induction with fentanyl, midazolam, vecuronium bromide, and intubation, a Baxter Swan-Ganz CCO thermodilution catheter was inserted through the right internal jugular vein. Compared to BCO(p), CCO showed excellent precision and bias; (r2 = 0.935, P < 0.0001, bias = -0.19 l.min-1, SD = 0.36 l.min-1). Although BCO correlated well with BCO(p), the bias was much greater (r2 = 0.919, P < 0.0001, bias = -1.25 l.min-1, SD = 0.45 l.min-1) than BCO(p). In conclusion, the values obtained by BCO(p) and CCO methods were very accurate. On the other hand, a considerable overestimation was found with BCO since the compensation for actual injectate temperature was not performed

[Usefullness of transesophageal echocardiography in early detection of coronary spasm].

Intraoperative transesophageal echocardiography (TEE) was performed on a 62-year-old man who underwent abdominal aortic replacement for abdominal aortic aneurysm under general anesthesia combined with epidural anesthesia. Coronary artery spasm occurred after unexpected massive hemorrhage, and TEE showed hypokinesis in the posterior-inferior left ventricular wall. The changes in TEE preceded the ST elevation in the ECG. Bolus infusion of isosorbide dinitrate and continuous infusion of nitroglycerin alleviated these changes. TEE enabled us to detect and evaluate coronary spasm before the appearance of ST changes in ECG.

[Myocardial ischemia induced by air bubbles].

Intraoperative transesophagial echocardiography (TEE) was performed in a 27-year-old man who underwent direct suture for atrial septal defect (ASD) under general anesthesia. Myocardial ischemia occurred about five minutes after weaning from cardiopulmonary bypass, and at that time TEE showed that anteroseptal wall, lateral septal wall and lateral wall are severely hypokinetic and another wall is diffusely hypokinetic in the left ventricle after detecting air bubbles in the left ventricle by TEE. The changes in TEE preceded the ST elevation in the ECG. Bolus infusion of isosorbide dinitrate and continuous infusion of nitroglycerin showed no effects on these changes. Ten minutes after the onset of myocardial ischemia, these changes were alleviated. TEE enabled us to detect air bubbles and evaluates myocardial ischemia before the appearance of ST changes in ECG.

The effects of olprinone (a phosphodiesterase III inhibitor) on hepatic vascular bed in a porcine model of endotoxemia.

UNLABELLED: Decreased hepatic blood flow, and impaired hepatic oxygen delivery caused by endotoxin, result in hepatic metabolic deterioration followed by liver dysfunction and multiple organ failure. Among phosphodiesterase III inhibitors, only olprinone increases hepatosplanchnic blood flow. We evaluated the effects of olprinone on systemic hemodynamics, hepatic circulation, and hepatic oxygen delivery in a porcine model of endotoxemia. Fifteen pigs received a continuous infusion (1.7 microg. kg(-1). h(-1)) of endotoxin (lipopolysaccharide [LPS]) via the portal vein for 240 min. Seven of these pigs received olprinone infusion (0.3 microg. kg(-1). min(-1)) via a central vein from t = 150 min to t = 240 min, whereas the eight remaining pigs served as LPS controls. Continuous infusion of LPS caused significant reductions in hemodynamic variables and a significant increase in arterial lactate. After the administration of olprinone during the LPS infusion, portal venous flow and hepatic oxygen delivery were increased and were higher than in the LPS group. Furthermore, olprinone prevented any further increase in arterial lactate. We conclude that the administration of olprinone halted the disturbances in the hepatic circulation, especially in portal venous flow and hepatic oxygen delivery, in a porcine model of endotoxemia. IMPLICATIONS: Endotoxin is a causative factor in peripheral vascular failure, resulting in a hemodynamic depression that includes a reduction in liver blood flow. The administration of olprinone (phosphodiesterase III inhibitor) improves the liver blood flow circulation in a porcine model of endotoxemia.

Upregulation of toll-like receptor 2 gene expression in macrophage response to peptidoglycan and high concentration of lipopolysaccharide is involved in NF-kappa b activation.

Toll-like receptors 2 and 4 (TLR2 and TLR4) have been found to transduce signals of peptidoglycan (PGN) and lipopolysaccharide (LPS), respectively, for NF-kappa B activation. However, little is known about the expression and regulation of the TLR2 gene in monocytes/macrophages in response to the two typical bacterial products. We show in the present study that both PGN and a high concentration of LPS increase TLR2 gene expression in macrophage-like cells, 1 alpha,25-dihydroxyvitamin D(3)-differentiated human HL60 and mouse RAW264.7 cells, and human monocytes in a dose- and time-dependent manner. Actinomycin D and pyrrolidine dithiocarbamate inhibition of gene transcription and NF-kappa B activation, respectively, blocks LPS- and PGN-elevated TLR2 mRNA in monocytic cells. The LPS-induced increase in TLR2 mRNA in monocytic cells is abolished by polymyxin B pretreatment and is observed in peripheral blood mononuclear cells from pigs subjected to endotoxic shock. Further, high concentrations of LPS and synthetic lipid A increase TLR2 mRNA expression in peritoneal macrophages from both TLR4-deficient C3H/HeJ mice and normal C3H/HeN mice, a process that constitutes induction of TLR4-independent TLR2 expression. These findings demonstrate that TLR2 gene expression is upregulated in macrophage responses to PGN and to high concentrations of LPS in vitro and in vivo and correlates with NF-kappa B activation.