Preoperative prediction of prolonged stay in the intensive care unit for coronary bypass surgery.

OBJECTIVES: To construct a predictive model for a prolonged stay in the intensive care unit (ICU) for coronary artery bypass graft surgery (CABG). METHODS: Eight hundred and eighty-eight patients undergoing CABG were studied by univariate and multivariate analysis. Prolonged stay in the ICU was defined as >/=3 days stay. Stepwise selective procedure (P/=0.40 was used as cut-off point for the prognostic test. The specificity of this test for prolonged stay in the ICU was 99%; sensitivity 9%; positive predictive value 60%; and negative predictive value 89%. CONCLUSIONS: The results show that individual patients presented for CABG, can be stratified according to their risk for prolonged stay >/=3 days in the ICU.

Predictors of nephrological morbidity after coronary artery bypass surgery.

AIM: The aim of this study was to analyse the nephrological morbidity after myocardial revascularization. METHODS AND RESULTS: We analysed the pre- per and postoperative data of 3815 patients who underwent a primary isolated coronary bypass grafting between January 1987 and December 1995. Nephrological complications were divided into renal dysfunction and requiring dialysis. The increase in nephrological complications (1.2-4%) is the result of an increase of patients with renal dysfunction. Unifactorial risk analysis identified age, diabetes, hypertension, nephrological pathology, perfusion time, aortic cross-clamp time, emergency operation and perioperative myocardial infarction as risk factors. Multifactorial risk analysis identified age, diabetes, hypertension, nephrological pathology, perfusion time, perioperative myocardial infarction and the cohorts operated upon in 1990-92, 1993-95 as independent risk factors for renal dysfunction, and age, nephrological pathology and perioperative myocardial infarction for those needing dialysis. CONCLUSION: Several variables have been identified as risk factors for nephrological complications; especially important are pre-existing nephrological pathology and perioperative myocardial infarction.

Isolation, visualization, characterization, and osmotic reactivity of crayfish BLMV.

Procedures were developed to isolate basolateral membrane vesicles (BLMV) from gill, hepatopancreas, and antennal gland of intermolt freshwater crayfish, Procambarus clarkii. Individual procedures involved a discontinuous sucrose gradient (gill), a 65% sucrose cushion (hepatopancreas), or differential centrifugation (antennal gland). BLMV were visualized, characterized (37 degrees C), and tested for osmotic reactivity with a view to using them for Ca2+ uptake studies. Mean diameters of BLMV were 159 nm (gill), 363 nm (hepatopancreas), and 226 nm (antennal gland). Enrichments of basolateral membranes and mitochondria in BLMV were, respectively, 18- and 1.7-fold for gill, 9- and 0.4-fold for hepatopancreas, and 10- and 1-fold for antennal gland. Apical contamination was negligible in BLMV. Percentages of resealing of vesicles as inside out, right side out, or leaky/sheets were 17:27:56% (gill), 14:26:60% (hepatopancreas), and 21:39:40% (antennal gland). Vesicles exhibited osmotic reactivity, as indicated by a linear relationship between vesicular 45Ca2+ uptake and osmolality. Nonspecific 45Ca2+ binding was 20% in gill, 39% in hepatopancreas, and 31% in antennal gland. Data were compared with published values for marine crustaceans.

Shrinkage-induced activation of Na+/H+ exchange: role of cell density and myosin light chain phosphorylation.

Previously, we suggested that myosin light chain kinase (MLCK) is involved in shrinkage-induced activation of the Na+/H+ exchanger in rat astrocytes. Here we have studied the effects of hyperosmotic exposure in C6 glioma cells, a common model for astrocytes. Shrinkage-induced activation of the Na+/H+ exchanger in C6 cells is directly proportional to the degree of shrinkage, results in an alkaline shift in the pK' of the exchanger, is dependent on ATP, and is inhibited by ML-7 (an MLCK inhibitor) and by various calmodulin inhibitors. Cell shrinkage also results in increased phosphorylation of myosin light chain (MLC). Interestingly, shrinkage-induced activation of the exchanger does not occur in subconfluent C6 cells. However, phosphorylation of MLC still occurs in subconfluent cultures of C6 cells on shrinkage, suggesting that the lack of activation in these cells occurs at a point between MLC phosphorylation and Na+/H+ exchange activation. The lack of activation of Na+/H+ exchange in subconfluent C6 cells can be utilized to further elucidate the shrinkage-induced activation pathway.

Membrane domain localization of pH-regulating transporters in frog skeletal muscle membrane vesicles.

The distribution of pH-regulating transporters in surface and transverse (T) tubular membrane (TTM) domains of frog skeletal muscle was studied. 2',7'-Bis(carboxyethyl)-5(6)- carboxyfluorescein-loaded giant sarcolemmal vesicles, containing surface membrane, exhibited reversible Na+/H+ exchange. A microsomal vesicle fraction was shown to be enriched in TTM on the basis of high Na(+)-K(+)-ATPase and Mg(2+)-ATPase activity, high ouabain and nitrendipine binding, and low Ca(2+)-ATPase activity. TTM vesicles were well sealed and oriented inside out. Vesicles were loaded with the pH-sensitive dye pyranine. In response to an inwardly directed Na+ gradient, vesicles displayed virtually no alkalinization unless monensin was present. No pH response to an imposed Na+ gradient was seen regardless of the direction of the pH gradient across the vesicles, after phosphorylation of the vesicles with protein kinase C, or when exposed to guanosine 5'-O-(3-thiotriphosphate). In the presence of CO2, addition of Na+ or Cl- had no effect on vesicle pH. These data indicate that the TTM lacks functional pH-regulating transporters [Na+/H+ and (Na+ + HCO3-)/Cl- exchangers], suggesting that pH-regulating transporters are localized only to the surface membrane domain in frog muscle.

Effect of changes of pHi on intracellular calcium in a smooth muscle-like cell line.

The effect of changes of pHi on Cai were studied using fluorescent dyes in cells of the cultured smooth muscle-like line, BC3H-1. Resting Cai in these cells was 182 +/- 12 nM (n = 74) at pHo of 7.4. Upon exposure to NH4Cl, which rapidly alkalinized cells, a transient increase of Cai to 394 +/- 55 nM (n = 29) was observed. The peak of the transient occurred within 30 s of exposure to NH4Cl and returned to baseline within 1 minute. Two other procedures which resulted in rapid cellular alkalinization also caused a transient rise in Cai: exposure to and then removal of CO2 (Cai increased from 182 +/- 22 to 248 +/- 28 nM; n = 8); and exposure to and then removal of Na propionate (Cai increased from 242 +/- 32 to 456 +/- 71 nM; n = 9). The NH4Cl-induced Cai transient was eliminated by exposure to 0.2 mM TMB8 and to Ca-free solutions, but not by exposure to 0.5 mM LaCl3. Sustained changes of pHi can be induced by varying pHo. When pHo was lowered to 6.9, Cai fell by 49 +/- 11 nM but increased by 203 +/- 51 nM (n = 6) when pHo was raised to 7.9. These data indicate that rapid alkalinization of BC3H-1 cells results in a rapid transient rise of Cai. This transient is most likely due to the release of Ca from intracellular stores but may also involve an increase of Ca influx. Steady state values of Cai are positively correlated with steady state pHi. These data may have implications for the contractile state of smooth muscle during periods of acid/base disturbances and relate to the role of elevated pHi in cells from hypertensive animals.