Search PubMed⌕ Search

Biomedical subjects

G Kleinberger

Publications and source records attributed to G Kleinberger.

At least 37 records · Page 2Linked to original sources

Hemodynamic, pulmonary, and renal reactions to inadvertent transfusion of outdated blood.

A patient who received an erroneous transfusion of outdated and partly homogenized blood is reported. Although marked hemoglobinemia was present, only transient hemodynamic, pulmonary, and renal alterations were observed. Massive embolism of microaggregates and norepinephrine release might explain our findings. Dopamine (3 micrograms/kg . min) might have beneficial effects on renal function in this pseudohemolytic transfusion reaction.

Blood Preservation↗

Elimination of amino acids in acute renal failure.

Plasma amino acid concentrations and the elimination of parenterally administered amino acids were investigated in 12 patients with nonhypercatabolic acute renal failure. A distinctive plasma amino acid pattern could be observed: plasma concentrations of phenylalanine and methionine were increased, those of valine and leucine decreased. Of the nonessential amino acids, cystine, taurine und tyrosine had elevated but none of them reduced plasma concentrations. The elimination of amino acids was evaluated in a monocompartment model after bolus injection of an amino acid solution containing essential and nonessential amino acids. Pharmacokinetic parameters of 17 amino acids were calculated. The mean elimination half-time was raised by 25%. The elimination half-time of phenylalanine, methionine, glutamic acid, proline and ornithine was increased. Histidine was the only amino acid with--however insignificantly--accelerated elimination from the intravascular compartment. The total clearance rate and total transfer rate was not altered (107 and 97% of normal, respectively). The clearance of threonine, lysine, serine, glycine and histidine was increased, of valine, phenylalanine, glutamic acid and to a minor degree of methionine was decreased. The transfer rate of methionine, lysine, glycine was elevated, of valine, aspartic acid, glutamic acid and ornithine reduced. The demonstration of these pronounced alterations of amino acid elimination in acute renal failure may have major consequences in parenteral amino acid therapy.

Acute Kidney Injury↗

Elimination of amino acids in chronic renal failure.

Elimination of parenterally administered amino acids was investigated in patients with chronic renal failure (CRF) (10 on conservative treatment = CT, 13 on regular hemodialysis therapy = HD). In a bolus injection protocol 0.1 g amino acids as a 10% solution containing essential and nonessential amino acids were infused and pharmacokinetic parameters of 17 amino acids were calculated. The mean elimination half life was increased by 40% in CT and 87% in HD (p less than 0.001 CT and HD versus controls). Total clearance was reduced in CT (p less than 0.001 versus HD and controls). In CT clearance of phenylalanine, proline, alanine, histidine and arginine was reduced, of none of the amino acids elevated. In HD clearance of methionine, lysine, aspartic acid and serine was increased, of proline decreased. The total transfer rate was reduced in CT (p less than 0.025 versus controls) and transfer of threonine, aspartic acid, glutamic acid, alanine, histidine and arginine was reduced in these patients. Mainly due to elevated basal plasma concentration transfer of methionine was elevated in CT and HD. In dialysis patients transfer of isoleucine, tryptophan, glycine and serine was increased. Despite variations of absolute values of clearance between the two groups investigated relative clearance rates of amino acids were similar because of a uniform increase of clearance of about 37% in HD compared to CT (p less than 0.001). Results indicate that the elimination of parenterally administered amino acids is grossly altered in uremia and that in patients on CT and HD a uniform elimination pattern can be observed.

Amino Acids↗

[Circulatory behavior of patients with liver insufficiency].

Haemodynamic data were obtained in 26 patients with hepatic failure admitted to the intensive care unit of the First Department of Medicine, Vienna University. There was a significant increase in heart rate (101 vs 78 beats/min) and decreased diastolic pressure (56 vs 71 mm Hg) as compared with healthy persons. The cardiac index was elevated (5.1 vs 3.5 l/m2) and the total peripheral resistance was lowered (621 vs 1130 dyn/sec/cm-5). The systolic blood pressure was within the normal range except in 8 patients whose illness was complicated by sepsis. In those 8 patients the systolic blood pressure (86 vs 128 mm Hg), the diastolic blood pressure (42 vs 61 mm Hg) and the total peripheral resistance (434 vs 764 dyn. sec. cm-5) were all decreased as compared with patients with hepatocellular disease without sepsis. The decreased total peripheral resistance, however, was not associated with a further increase in the heart rate or stroke volume. On the contrary, in these 8 patients the left ventricular performance was lowered. The increase in cardiac output was not associated with an increase in oxygen consumption in patients without sepsis. Oxygen consumption was increased in patients with hepatocellular insufficiency and sepsis (157 ml/m2 vs 123 ml/m2) and this was accompanied by a diminished oxygen extraction rate (16% vs 26% in these 8 patients.

Adult↗

[Determination of extravascular lung water in critical patients: comparison with radiological, hemodynamic and functional lung findings].

Measurement of extravascular lung water (EVLW) was performed by the thermal-dye technique in 55 critically ill patients. The EVLW values were compared with the corresponding radiographic, hemodynamic and functional pulmonary data. EVLW values revealed a positive correlation with the chest X-ray score (CXR) (r = 0.836; p less than 0.001), mean pulmonary artery pressure (PP) (r = 0.414; p less than 0.01), pulmonary capillary wedge pressure (PCWP) (r = 0.353; p less than 0.01), venous admixture (Qs/Qt) (r = 0.288; p less than 0.05), and alveo-arterial oxygen difference/fraction of inspired oxygen (AaDO2/FiO2) (r = 0.441; p less than 0.001). No correlation was found between EVLW values and colloid-osmotic pressure minus PCWP (COP-PCWP) (r = 0.221). Though different positive correlations between EVLW values and these parameters were found, they cannot replace EVLW measurement. Rather, EVLW measurement provides additional information on the degree of pulmonary edema which is useful in differentiating between cardiac and non-cardiac pulmonary edema and in states of radiologic over- or underestimation of EVLW.

Adult↗

[Bedside chest x-rays and extravascular lung water determination in intensive care patients].

Radiological staging of pulmonary oedema was compared with the determination of extra-vascular lung water by means of a double indicator dilution technique. One hundred and forty-six ward chest radiographs were evaluated and compared with the results of simultaneous measurements of lung water. Seventy-seven cases could be evaluated statistically. Chest x-rays regarded as normal corresponded to extra-vascular lung water of 5 to 9 ml./kg. body weight. Interstitial oedema (radiological stage I and II) corresponded to extravascular lung water levels of 8 to 12 ml./kg. Differentiation of stages I and II was not possible. During stage III, extra-vascular lung water was 15 to 21 ml./kg. A comparative analyses of these findings revealed a discrepancy of 34%. The reasons for this are discussed.

Adult↗

Enhancement of renal function with ornipressin in a patient with decompensated cirrhosis.

An infusion with Ornipressin (8-ornithin vasopressin) in a patient with decompensated alcoholic liver cirrhosis increased urinary volume from 30 ml/h to 500 ml/h, creatinine clearance from 24 to 65 ml/min, and fractional sodium excretion from 0.86% to 11.1%. Free water clearance decreased from -10.2 ml/h to -26.2 ml/h and noradrenaline plasma concentrations dropped from 2.04 to 1.37 ng/ml. After stopping Ornipressin infusion all values returned to initial concentrations. Possible effects are an increase of renal blood flow secondary to an increase in arterial blood pressure, possibly potentiated by the vasodilatory effect of the fall in noradrenaline and/or angiotensin concentration.

Adult↗

[Changes in and modulation of receptor activity in hepatic encephalopathy].

In hepatic encephalopathy (HE) brain uptake of large neutral amino acids is impaired with tryptophan crossing the blood brain barrier (BBB) to a much larger extent than all other competing amino acids (AA). The disturbance in the steady-state of transmitter is paralleled to the change of their kinetic data. This is reflected by an increase in serotonin (5-HT) synthesis and turnover, while the number of post-synaptic 5-HT1-binding sites is decreased, 5-HT2-receptor activity is dropping to a much smaller extent. On the other hand, presynaptic dopaminergic activity remains unchanged with no change in D2-receptor activity. Valine (VAL) improves the postsynaptic 5-HT function via modulating activity due to a regulatory mechanism at the membranal level in vitro and ex vivo. Furthermore, VAL leads to a significant reduction of serum ammonia (NH4+) and brain NH4+ concentration. VAL is able to antagonize the binding density diminishing effects of NH4+ on 5-HT binding sites. This effect could be characterized by the measurement of VAL binding sites being 5 to 10 fold higher than the number of leucin (LEU)-sites. Considering the chemical bonds involved in the attachment of biogenic amines and aminoacids (Schiff-bases equilibria) the modulating action of NH4+ on neural transmission may be clarified. Tryptamine can displace the postsynaptic binding of 5-HT in brain tissue and is a possible antagonist to physiological and pharmacological effects of 5-HT. The dynamic changes of the kinetic behaviour of tryptamine-binding might demonstrate a compensating effect as shown in an increase of tryptaminergic receptor activity. As a working hypothesis, the different relative strengths of electron-pair donor and -acceptor sites of both compounds are suggested to their complementary physiological interaction. GABA, an inhibitory transmitter of the CNS is diminished in its maximal binding capacity in severe HE and is independent of NH4+ influence. Furthermore, glutamate and aspartate-receptors decrease in experimentally induced hepatic coma. L-LEU shows modulating effects of glutamine binding. Glycin-activity is increased, while naloxone- and D-ala2-methionine-encephalinamid binding are not different from controls. These data demonstrate a different influence of various brain receptors and binding sites by HE and indicate a differentiated disturbance of (neuronal) membrane activity. Therefore disturbed interneuronal dynamics might be important pathophysiological mechanisms underlying hepatic coma.

Ammonia↗

[Liver function disorders and damage in critically ill intensive care patients].

The course of the disease of critically ill patients is complicated and prognosis worsened by failure of one or more organs. During intensive care monitoring and treatment of vital functions most attention usually is paid to the cardio-pulmonary and renal system; liver function is neglected rather often. In a retrospective study 100 critically ill patients were evaluated, who had serum bilirubin levels above 3,0 mg/dl, but no primary liver disease. Excluded were patients who had liver destruction caused for instance by liver abscess or metastases, and patients with acute hemolysis and extrahepatic cholestasis. Severe infection was the primary cause of disease in 64% of these critically ill patients without primary liver dysfunction; 52% patients had septicemia, 37% patients were in a post-operative or post-traumatic status, 28% patients had severe gastrointestinal complications, 23% had myocardial pump failure, 32% had protracted shock, 29% had hematological disease, 59% had lung failure, and 58% renal failure. It was tried to find a correlation between the different liver function parameters in this group of patients. In spite of rather pronounced pathological findings a statistically significant correlation could only be found between SGPT and SLDH. This study demonstrates the importance of liver involvement in critically ill patients on the one side and the necessity of comprehensive and repeatedly performed investigations of liver function in such patients on the other side.

Adolescent↗

Post-heparin lipolytic activity in acute renal failure.

Total post-heparin lipolytic activity (PHLA), hepatic triglyceride lipase (HTGL) and protamine inactivated lipoprotein lipase (LPL) and plasma lipoprotein pattern were investigated in 8 patients with acute renal failure (ARF). PHLA was determined at 5, 10, 15, 30, 45 and 60 minutes after heparin administration (100 U/kg b.w.). Maximal PHLA in ARF was 6.12 +/- 1.56 mumol FFA/ml/h at 10 minutes versus 14.62 +/- 4.29 at 45 min in controls (= 42%, p less than 0.001). PHLA was reduced in ARF throughout the study period (p less than 0.001). Maximal HTGL activity (3.06 +/- 0.84 mumol FFA/ml/h) was obtained at 10 min in ARF versus 8.97 +/- 3.11 after 15 min in controls (= 34%, p less than 0.001). HTGL in ARF differed from controls at all points of determination (p less than 0.001). LPL maximum was 3.12 +/- 1.93 mumol FFA/ml/h at 15 min in ARF and 7.65 +/- 3.44 at 45 min in controls (= 40%, p less than 0.001). LPL activity was different from controls at 30, 45 and 60 min (p less than 0.001) but not at 5, 10 and 15 min after heparin injection. Due to a rapid decrease of LPL activity (half maximal activity after 34 min in ARF versus 94 min in controls, p less than 0.05) activity half life of PHLA was diminished in ARF (49 min in ARF versus 112 min in controls, p less than 0.01). Thus both the activity of HTGL and LPL is impaired in ARF. Because of the different activation kinetics of the two PHLA fractions no conclusions concerning maximal enzyme activities can be drawn from single determinations as suggested in previous studies on chronic renal failure.

Acute Kidney Injury↗

[Circulatory behavior in critically ill patients during hemodialysis].

Haemodynamic data were obtained during haemodialysis on 21 occasions in 7 patients with septicaemia and pancreatitis, and in 5 patients with primary renal failure without septicaemia or pancreatitis. In the former group of patients there was a lowering of the blood pressure 30, 60, 90 and 120 minutes after haemodialysis had been initiated, which was significantly greater than in the later group. The drop in the blood pressure was caused by a decreased cardiac output. The pulmonary wedge pressure dropped in all patients. Peripheral resistance and heart rate did not change during the whole procedure.

Adult↗

[Pathophysiology and therapy of diabetic ketoacidosis and of non-ketoacidotic hyperosmolar diabetic coma].

Metabolic derangements in diabetic coma are the sequelae of insulin deficiency. These defects are aggravated by the actions of insulin counteracting ("diabetogenic") hormones and hypertonic dehydration, which both impair insulin action. Conversely, it has been shown that hypo-osmolar rehydration of a hyperosmolar, severely hyperglycaemic diabetic patient reduces insulin resistance and restores biological responsiveness of previously dehydrated insulin-dependent tissues towards insulin. Thus treatment of diabetic coma requires appropriate fluid and electrolyte replacement as a life-saving emergency action alongside insulin replacement. The use of proper rehydration during the past decade might also explain the reported fall in the insulin requirement for the treatment of diabetic coma from approximately 1,000 units per coma to low-dose insulin therapy. In order to guarantee proper treatment of severe hyperglycaemia and normalization of the hyperosmolar state, we feel that hypo-osmolar rehydration has to be initiated in parallel with low-dose insulin therapy (5 to 6 U/h) to restore the physiological response of the respective target tissues to insulin action and to ameliorate glucose utilization. This approach probably avoids a too rapid fall in plasma osmolarity, minimizes the risk of cerebral oedema and hypokalaemia, and improves survival. The development of severe diabetic ketoacidosis or of hyperosmolar non-ketotic diabetic coma should be prevented by advice to patients on the importance of metabolic monitoring, which can be done by proper self-monitoring of blood glucose. In addition, information should be provided on the detrimental metabolic effects of both dehydration and stress.

Amino Acids↗