Biomedical subjects

J Bleier

Publications and source records attributed to J Bleier.

6 recordsLinked to original sources

PubMed1998

Different intracellular compartmentations of cardiac troponins and myosin heavy chains: a causal connection to their different early release after myocardial damage.

We investigated the net myocardial release of creatine kinase isoenzyme MB (CKMB), myoglobin, cardiac troponin T (cTnT), cardiac troponin I (cTnI), and cardiac beta-type myosin heavy chain (beta-MHC) into the coronary circulation after cardioplegic cardiac arrest in humans. Cardiac markers were measured in paired arterial, central venous, and coronary sinus blood in 19 patients undergoing elective coronary artery bypass grafting (CABG) before aortic cross-clamping and 1, 5, 10, and 20 min after aortic declamping. cTnT and cTnI were released into the coronary sinus in parallel to each other and almost simultaneously to myoglobin and CKMB within 20 min of reperfusion. In contrast, no beta-MHC was released in the same patients during the study period. The average soluble cTnT and cTnI pools in right atrial appendages of 11 patients with right atrial and right ventricular pressures within reference values were comparable and were approximately 8% of total myocardial troponin content. The soluble beta-MHC pool was <0.1% in all patients. Our results demonstrate the impact of the different intracellular compartmention of regulatory and contractile proteins on their early release from damaged myocardium.

Adult↗

PubMed1997

Augmented release of brain natriuretic peptide during reperfusion of the human heart after cardioplegic cardiac arrest.

The aim of the study was to investigate the release of natriuretic peptides during myocardial ischaemia and reperfusion associated with cardioplegic cardiac arrest. Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in paired arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 min after aortic declamping. Peak myocardial BNP release after aortic declamping was significantly higher than baseline values before aortic crossclamping. Both peak and cumulative BNP release during reperfusion correlated significantly with the severity of ischaemia, as assessed by myocardial lactate production. In 3 patients with perioperative myocardial ischaemia, cumulative and peak myocardial BNP release after aortic unclamping was markedly higher than in the remaining 16 uneventful patients. Myocardial ANP release during reperfusion was not significantly different from baseline values before aortic crossclamping. In conclusion, our data demonstrate a significantly enhanced myocardial BNP release early during reperfusion of the human heart after global ischaemia associated with cardioplegic cardiac arrest.

Adult↗

PubMed1995

Reperfusion after cardioplegic cardiac arrest--effects on intracoronary leucocyte elastase release and oxygen free radical mediated lipid peroxidation.

In experimental animal models reperfusion of ischaemic myocardium causes sequestration of leucocytes within the coronary circulation. Leucocytes contribute to postischaemic myocardial injury by releasing proteolytic enzymes and by generating oxygen free radicals. The aim of this study was to investigate whether leucocytes also contribute to myocardial injury following ischaemia and reperfusion associated with cardioplegic cardiac arrest. Therefore, we studied the release of the proteolytic enzyme elastase and oxygen free radical initiated myocardial lipid peroxidation in coronary sinus blood during reperfusion after cardioplegic cardiac arrest. The elastase-alpha-1-proteinase inhibitor complex and malondialdehyde (a byproduct of myocardial lipid peroxidation) were measured in arterial, central venous and coronary sinus blood samples in 19 patients undergoing elective coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 m in after aortic declamping. Malondialdehyde concentrations did not increase significantly during the study period, whereas elastase concentrations showed a significant increase during cardiopulmonary bypass in arterial, central venous as well as coronary sinus blood. Neither elastase nor malondialdehyde concentrations in coronary sinus blood differed significantly from arterial or central venous blood at any time point measured. Our data demonstrated increased elastase concentrations during cardiopulmonary bypass, but we did not find enhance intracoronary elastase release or myocardial during cardiopulmonary bypass, but we did not find enhanced intracoronary elastase release or myocardial lipid peroxidation. Our data suggest that patients are sufficiently protected from leucocyte mediated ischaemia reperfusion injury during uncomplicated coronary artery bypass grafting with cardioplegic arrest.

Adult↗

PubMed1995

Coronary sinus endothelin-1 concentrations after cardioplegic cardiac arrest.

BACKGROUND: Data from animal experiments demonstrate that endothelin-1 is released into the coronary circulation during myocardial ischaemia and reperfusion, indicating that endothelin-1 may contribute to the pathophysiology of ischaemia and reperfusion. The aim of this study was to investigate the release of endothelin-1 into the coronary circulation during reperfusion of the human heart after hypothermic cardioplegic cardiac arrest. METHODS: Endothelin-1 was measured in arterial, central venous and coronary sinus blood in 19 patients undergoing elective uncomplicated coronary artery bypass grafting before aortic crossclamping and 1, 5, 10 and 20 min after aortic declamping. RESULTS: Endothelin-1 concentrations showed a slight non-significant increase over baseline values 1, 5, 10 and 20 min after aortic declamping. Endothelin-1 concentrations were not significantly higher in coronary sinus blood than in arterial blood at any time point measured, indicating no net release of endothelin-1 by the heart. CONCLUSIONS: Our results did not demonstrate endothelin-1 release into the coronary circulation after myocardial ischemia and reperfusion associated with hypothermic cardioplegic cardiac arrest.

Adult↗

PubMed1984

Nutrient bioavailability from nasojejunally administered enteral formulas: comparison to solid food.

The net absorption and retention of energy, fat, nitrogen, and six elements (potassium, phosphorus, calcium, magnesium, sodium, and chloride) from two intrajejunally infused enteral formulas were compared to solid food. Undernourished patients (group 1) underwent two consecutive 7-day balance studies on a predigested protein-low fat (elemental) formula and an intact protein-standard fat (polymeric) formula, the initial diet selected randomly. Periods were isocaloric and isonitrogenous, but differed in the amounts of remaining elements. The undernourished patients in group 2 ate a solid food standard hospital diet for the 7-day balance study in an amount equal in energy and protein to group 1. There were no major differences in the nutrient absorption between the three diets. Nitrogen balance was similar for the two formulas (mean +/- SD) (elemental 6.1 +/- 3.5 g/day; polymeric 4.8 +/- 3.2 g/day) and solid food (5.2 +/- 3.5 g/day), and the balance for the six remaining elements was approximately proportional to the amount supplied. Subjective tolerance of both formulas was good, with a tendency for superior tolerance of the polymeric formula. We conclude that for the nutrients investigated, 1) intrajejunally administered enteral formulas are capable of renourishing hospitalized patients with an efficacy similar to that of solid food, and 2) predigestion of the formula does not improve absorption.

Biological Availability↗

PubMed1982

Hypocitraturia in calcium nephrolithiasis.

Several investigators have reported that hypocitraturia is frequent in patients with idiopathic kidney stones. In these studies, however, glomerular filtration rate, urinary tract infection, sex, diet, time of day, and medications, all potentially influential variables, were uncontrolled. Fifteen men, aged 30-52 yr, with recurrent idiopathic calcium oxalate stones and 15 normal age-matched men were studied. Patients with hyperparathyroidism, renal tubular acidosis, reduced creatinine clearance (less than 80 ml . min/1.73 M2), or urinary infection were excluded. Medications were stopped 2 weeks before the study began. A standard constant diet, furnishing 800 mg calcium and free of citrate, was fed for 20 days. During the last 10 days, 4.5 g sodium citrate were given orally. Eight-hour collections of urine were analyzed for calcium and citrate. Filtered load and net tubular reabsorption of citrate were also calculated. The 24-h urinary excretion of calcium was elevated in eight stone formers, and citrate excretion was depressed in seven. Five patients were both hypercalciuric anc hypocitraturic. The hypocitraturia resulted from excessive net tubular reabsorption of a normal filtered load of citrate. Urinary citrate was highest between 0800-1600 h, whereas calcium was highest between 1600-2400 h; both components were lowest between 2400-0800 h. The diurnal profiles of urinary calcium and citrate were similar in the stone formers and in the normal men. Oral sodium citrate did not influence urinary citrate in either group. These data suggest that in adult men, hypocitraturia may be a common predisposing factor for calcific nephrolithiasis.

Adult↗