Post-induction hypotension and early intraoperative hypotension associated with general anaesthesia.

BACKGROUND: We hypothesized that different phases of intraoperative hypotension should be differentiated because of different underlying causative mechanisms. We defined post-induction hypotension (PIH; i.e. arterial hypotension occurring during the first 20 min after anaesthesia induction) and early intraoperative hypotension (eIOH; i.e. arterial hypotension during the first 30 min of surgery). METHODS: In this retrospective study, we included 2037 adult patients who underwent general anaesthesia. Arterial hypotension was defined as a systolic arterial blood pressure (SAP) <90 mm Hg or a need for norepinephrine infusion at > 6 µg min -1 at least once during the phases of PIH and eIOH. Multivariate logistic regression analysis was used to test for association of clinical factors with PIH and eIOH. RESULTS: Independent variables significantly related to PIH were pre-induction SAP [odds ratio (OR) 0.97 (95% confidence interval 0.97-0.98)], age [OR 1.03 (1.02-1.04)], and emergency surgery [OR 1.75 (1.20-2.56); P <0.01 each]. Pre-induction SAP [OR 0.99 (0.98-0.99), P <0.01], age [OR 1.02 (1.02-1.03), P <0.01], emergency surgery [OR 1.83 (1.28-2.62), P <0.01], supplementary administration of spinal or epidural anaesthetic techniques [OR 3.57 (2.41-5.29), P <0.01], male sex [OR 1.41 (1.12-1.79), P <0.01], and ASA physical status IV [OR 2.18 (1.19-3.99), P =0.01] were significantly related to eIOH. CONCLUSIONS: We identified clinical factors associated with PIH and eIOH. The use of these factors to estimate the risk of PIH and eIOH might allow the avoidance or timely treatment of hypotensive episodes during general anaesthesia.

Cholesterol crystal binding of biliary immunoglobulin A: visualization by fluorescence light microscopy.

AIM: To assess potential contributions of biliary IgA for crystal agglomeration into gallstones, we visualized cholesterol crystal binding of biliary IgA. METHODS: Crystal binding biliary proteins were extracted from human gallbladder bile using lectin affinity chromatography.Biliary IgA was isolated from the bound protein fraction by immunoaffinity chromatography. Pure cholesterol monohydrate crystals were incubated with biliary IgA and fluoresceine isothiocyanate (FITC)conjugated anti IgA at 37 degree. Samples were examined under polarizing and fluorescence light microscopy with digital image processing. RESULTS: Binding of biliary IgA to cholesterol monohydrate crystals could be visualized with FITC conjugated anti IgA antibodies. Peak fluorescence occurred at crystal edges and dislocations. Controls without biliary IgA or with biliary IgG showed no significant fluorescence. CONCLUSION: Fluorescence light microscopy provided evidence for cholesterol crystal binding of biliary IgA. Cholesterol crystal binding proteins like IgA might be important mediators of crystal agglomeration and growth of cholesterol gallstones by modifying the evolving crystal structures in vivo.