Influence of prestorage leucocyte depletion and storage time on rheologic properties of erythrocyte concentrates.

BACKGROUND AND OBJECTIVES: Rheological blood properties were studied during storage. MATERIALS AND METHODS: Blood viscosity, erythrocyte morphology and ATP levels were determined in filtered samples (Leukotrap WB filter system) and their unfiltered counterparts during storage with saline-adenine-glucose-mannitol (SAG-M) for 42 days. RESULTS: Prestorage leucocyte depletion decreased blood viscosity at a high shear rate and reduced the degree of anisocytosis of erythrocytes. During storage, erythrocytes underwent a time-dependent echinocytic shape transformation, which increased the suspension viscosity at high and low shear rates. On day 42, high shear viscosity in filtered units remained lower than in unfiltered counterparts, the mean cellular volume and red blood cell distribution width (RDW) were lower and erythrocytic ATP levels were higher. CONCLUSIONS: Prestorage leucocyte depletion by Leukotrap WB filters improves biophysical properties of erythrocyte concentrates throughout storage, which is, however, outweighed by a time-dependent echinocytic shape transformation and deterioration of these properties.

Effects of high-altitude exposure on vascular endothelial growth factor levels in man.

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and permeability factor that is inducible by hypoxia. Its contribution to high-altitude illness in man is unknown. We measured VEGF levels in 14 mountaineers at low altitude (490 m) and 24 h after their arrival at high altitude (4,559 m). At high altitude, VEGF increased from [mean (SEM)] 32.5 (9.2) to 60.9 (18.5) pg.ml(-1) (P < 0.004) in the arterial blood, and from 15.9 (2.9) to 49.3 (15.9) pg.ml(-1) (P= 0.0001) in the mixed venous blood. Whereas at low altitude venous and arterial VEGF levels were not statistically different from each other (P= 0.065), the VEGF concentration was significantly lower in venous than in arterial blood samples at high altitude (P=0.004). The pulmonary capillary VEGF concentration remained unchanged at high altitude [14.8 (2.5) vs 17.1 (5.4) pg.ml(-1), P=0.85]. VEGF levels in the nine mountaineers who developed symptoms of acute mountain sickness (AMS), and in the six subjects who had radiographic evidence of high-altitude pulmonary edema were similar to those in subjects without symptoms. VEGF was not correlated with either AMS scores, mean pulmonary arterial pressures, arterial partial pressure of O2, or alveolar-arterial O2 gradients. We conclude that VEGF release is stimulated at high altitude, but that VEGF is probably not related to high-altitude illness.

No influence of C-peptide, insulin, and glucagon on blood viscosity in vitro in healthy humans and patients with diabetes mellitus.

The influence of the hormones most involved in glucose homeostasis, C-peptide, insulin and glucagon on blood viscosity was tested in vitro. Whole blood (adjusted to haematocrit 45%) from healthy volunteers (n=24) and patients with diabetes mellitus (n=17) was incubated with 10(-7)-10(-10) M C-peptide, insulin or glucagon. None of these peptide hormones, neither at physiological nor at supraphysiological levels, had an influence on high (94.5 s(-1)) or low (0.1 s(-1)) shear rate viscosity. The small group of diabetic patients had a higher plasma viscosity and increased blood viscosity at 94.5 s(-1), which is in agreement with earlier studies, but decreased viscosity at low shear rate. We conclude that C-peptide, insulin and glucagon have no direct effect on blood viscosity in vitro. It is, therefore, unlikely that microvascular disturbances seen with either deficiency or excess of these hormones is due to haemorheological factors.

Creatine kinase MB during myocardial infarction: relationship to preexisting coronary heart disease and medication.

Creatine kinase (CK) and its isoenzyme CK-MB are important tools for the diagnosis of acute myocardial infarction. The content of CK-MB relative to total CK in myocardial cells is variable; it is low in normal myocardium and increased several-fold in hypoxic myocardium. We tested the hypothesis that CK-MB mass (CK-MBm) could be related to cardiovascular history, preinfarctional medication and clinical course during myocardial infarction. In a prospective study CK and CK-MBm were measured 0, 6, 12, 18, 24, 36, 48 and 72 h after the admission to the coronary care unit. Peak values and areas under the curve (AUC) were determined and normalized for total CK activity (CK-MBm/CK). Of 185 patients with acute chest pain, 70 patients had 71 acute myocardial infarctions and were enrolled in the study. A history of chronic angina pectoris or hypertension had no influence on CK-MBm/CK levels. In contrast, treatment with beta-blockers before infarction resulted in a lower relative CK-MBm peak value (CK-MBm/CK 6.0 (median value), range 3.1-15.3, versus 7.0, range 0.5-17.3: p < 0.05). Other drugs had no influence. Patients with persistent pain on admission tended to have higher relative CK-MBm values (peak CK-MBm/CK: 6.8, range 0.5-17.3, versus 5.3, range 1.4-7.9, p = 0.08; AUC CK-MBm/CK: 0.05, range 0.01-0.10, versus 0.03, range 0.01-0.06, p < 0.05). Three vessel disease on coronary angiography was associated with higher peak CK-MBm/CK values during the acute phase of myocardial infarction than those with 1-2 vessel disease (Peak CK-MBm/CK: 7.9, range 5.5-17.3, versus 6.4, range 3.1-10.2, p < 0.05; AUC CK-MBm/CK: 0.06, range 0.02-0.11, versus 0.04, range 0.02-0.07, p < 0.05). We conclude that relative CK-MBm/CK levels reflect to a certain degree the extent of the coronary disease and that preinfarctional beta-blockade may result in lower CK-MBm levels.

Cisapride increases peak plasma and saliva ethanol levels under fasting conditions.

OBJECTIVES: Alcohol absorption is influenced by gastric first-pass metabolism through an alcohol dehydrogenase and the gastric emptying time. Whilst an influence of antisecretory drugs and aspirin on gastric alcohol metabolism has been described, the role of prokinetic drugs has not been determined. DESIGN: A randomized, placebo-controlled double-blind cross-over study was performed. SETTING: Out-patient facilities of a referral hospital. SUBJECTS: Eight male volunteers (age range 25-46 years). INTERVENTION: Treatment with two doses of either placebo or cisapride 150 micrograms/kg 7 h and 20 min before drinking 0.5 g/kg alcohol either in a fasting state or during a standardized meal (12 kcal/kg). MAIN OUTCOME MEASURES: Plasma and saliva ethanol concentrations were measured during 4 h. RESULTS: Cisapride increased peak plasma ethanol levels in fasting subjects from 15.6 (SD 1.4, 95%-KI 14.7;16.6) to 17.8 (SD 2.7, 95%-KI 15.9;19.7) mmol/L and saliva ethanol 30 min after alcohol ingestion from 11.4 (SD 2.2. 95%-KI 9.9;12.9) to 15.9 (SD 4.3, 95%-KI 12.9;18.8) mmol/L. A significant interaction between fasting state and drug intake was found for the 30 min saliva ethanol values (P < 0.05, ANOVA for repeated measurements). CONCLUSIONS: Cisapride may increase ethanol levels under fasting conditions. Patients treated with prokinetic drugs should be informed about this possibility.