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Biomedical subjects

S W Olde Damink

Publications and source records attributed to S W Olde Damink.

12 recordsLinked to original sources
PubMed2001

Restoration of cerebral blood flow autoregulation and reactivity to carbon dioxide in acute liver failure by moderate hypothermia.

In patients with acute liver failure (ALF) and uncontrolled intracranial hypertension, moderate hypothermia (32 degrees C) reduces intracranial pressure (ICP) and cerebral blood flow (CBF), and can be used as a bridge to liver transplantation. The purpose of this study was to test the hypothesis that moderate hypothermia reduced ICP by restoring CBF autoregulation. Nine patients with uncontrolled intracranial hypertension and ALF who fulfilled the criteria for poor prognosis were studied. CBF autoregulation and reactivity to carbon dioxide were evaluated before and 4 hours after cooling (32 degrees C). Significant reductions were observed in the ICP (median, 46 [range, 27-54] mm Hg to 19 [15-22] mm Hg; P <.01) and CBF (median, 111 [69-134] to 56 [38-67] mL/100 g/min; P <.05). The defective CBF autoregulation and the absence of reactivity to carbon dioxide that was observed in all patients was restored with cooling. The results of our study suggest that the improvement in ICP observed with hypothermia may be the result of its effects on CBF autoregulation and provides a tool to explore the mechanisms associated with the deranged CBF autoregulation in ALF.

Adult↗
PubMed2001

Acute changes in cerebral blood flow and metabolism during portasystemic shunting.

This report describes the instantaneous changes in cerebral blood flow (CBF), determined by intravascular ultrasound and Doppler, in a patient with cirrhosis undergoing placement of a transjugular intrahepatic stent-shunt for uncontrolled variceal bleeding. Acute changes in CBF were observed during and after portasystemic shunting, which culminated in cerebral edema and cerebral herniation.

Brain↗
PubMed2001

Hypothermia for the management of intracranial hypertension in acute liver failure.

Increased intracranial pressure in patients with acute liver failure remains a major cause of mortality. Treatment options are limited, and without urgent liver transplantation, mortality rates of up to 90% are common in those who fulfill criteria for poor prognosis. Several studies in animal models of acute liver failure set the stage for the clinical application of moderate hypothermia in humans. Few patients are treated with hypothermia for increased intracranial pressure. However, data indicate that moderate hypothermia is a safe and effective method of treatment for increased intracranial pressure that is unresponsive to other medical therapies, and that this treatment can be used as a successful bridge to liver transplantation. Recent data also suggest that increases in intracranial pressure can be prevented during the dissection and reperfusion phases of liver transplantation for acute liver failure if patients are kept hypothermic during the surgical procedure. This article focuses on the use of moderate hypothermia for the treatment of increased intracranial pressure in patients with acute liver failure.

Cerebrovascular Circulation↗
PubMed1999

Effects in vivo of decreased plasma and intracellular muscle glutamine concentration on whole-body and hindquarter protein kinetics in rats.

Glutamine is considered to be a 'conditionally' essential amino acid. During situations of severe stress like sepsis or after trauma there is a fall in plasma glutamine levels, enhanced glutamine turnover and intracellular muscle glutamine depletion. Under these conditions, decreased intramuscular glutamine concentration correlates with reduced rates of protein synthesis. It has therefore been hypothesized that intracellular muscle glutamine levels have a regulatory role in muscle protein turnover rates. Administration of the glutamine synthetase inhibitor methionine sulphoximine (MSO) was used to decrease glutamine levels in male Wistar rats. Immediately after the MSO treatment (t=0 h), and at t=6 h and t=12 h, rats received intraperitoneal injections (10 ml/100 g body weight) with glutamine (200 mM) to test whether this attenuated the fall in plasma and intracellular muscle glutamine. Control animals received alanine and saline after MSO treatment, while saline was also given to a group of normal rats. At t=18 h rats received a primed constant infusion of L-[2,6-3H]phenylalanine. A three-pool compartment tracer model was used to measure whole-body protein turnover and muscle protein kinetics. Administration of MSO resulted in a 40% decrease in plasma glutamine and a 60% decrease in intracellular muscle glutamine, both of which were successfully attenuated by glutamine infusions. The decreased intracellular muscle glutamine levels had no effect on whole-body protein turnover or muscle protein kinetics. Also, glutamine supplementation did not alter these parameters. Alanine supplementation increased both hindquarter protein synthesis and breakdown but the net balance of phenylalanine remained unchanged. In conclusion, our results show that decreased plasma and muscle glutamine levels have no effect on whole-body protein turnover or muscle protein kinetics. Therefore, it is unlikely that, in vivo, the intracellular muscle concentration of glutamine is a major regulating factor in muscle protein kinetics.

Amino Acids↗
PubMed1999

Upper gastrointestinal bleeding: an ammoniagenic and catabolic event due to the total absence of isoleucine in the haemoglobin molecule.

Upper gastrointestinal bleeding causes increased urea concentrations in patients with normal liver function and high ammonia concentrations in patients with impaired liver function. This ammoniagenesis may precipitate encephalopathy. The haemoglobin molecule is unique because it lacks the essential amino acid isoleucine and has high amounts of leucine and valine. Upper gastrointestinal bleeding therefore presents the gut with protein of very low biologic value, which may be the stimulus to induce a cascade of events culminating in net catabolism. This may influence the function of rapidly dividing cells and short half-life proteins. We hypothesize that, following a variceal bleed in a cirrhotic patient, the lack of isoleucine in blood protein is the cause of the exaggerated ammoniagenesis and catabolism. We propose that intravenous administration of isoleucine may serve as a simple therapeutic that transforms blood protein in a balanced protein, resulting in only a short-lived rise in ammonia and urea production, and preventing interference with protein synthesis.

Ammonia↗
PubMed1998

[Uremia after hemorrhages in the upper digestive tract].

Haemorrhages in the upper GI tract may lead to severe uraemia and, in patients with liver failure, to hyperammonaemia. The cause of this is not yet sufficiently clear. Recently we observed a decrease in arterial isoleucine levels after intragastric blood administration in pigs. This contrasted with elevated levels of most other amino acids, ammonia and urea. After an isonitrogenous control meal in these pigs all amino acids including isoleucine increased, and urea increased to a lesser extent, suggesting a relationship between the arterial isoleucine decrease and uraemia after gastrointestinal (GI) haemorrhage. Analysis of blood protein showed a complete absence of the essential amino acid isoleucine, making it a protein of low biological value. In additional porcine experiments, uraemia after intragastric blood administration could be prevented by simultaneous intravenous isoleucine administration. This led to the hypothesis that there was a causal relationship between the absence of isoleucine in blood protein and the uraemia and hyperammonaemia observed after GI bleeding. Similar results were seen in patients with intact and with impaired liver functions. These results support the hypothesis that the absence of isoleucine in blood protein causes decreased plasma and tissue isoleucine levels after GI haemorrhage. This might inhibit protein synthesis, and may contribute to uraemia and hyperammonaemia in patients with normal and impaired liver function, respectively. Intravenous isoleucine administration after GI haemorrhage could be beneficial.

Ammonia↗
PubMed1997

Decreased plasma and tissue isoleucine levels after simulated gastrointestinal bleeding by blood gavages in chronic portacaval shunted rats.

BACKGROUND: Previously, arterial concentrations of the essential branched chain amino acid isoleucine (Ile) were found to have decreased by more than 50% after gastrointestinal haemorrhage in patients and after intragastric blood administration in healthy humans and pigs. Hypothetically, this induced hypoisoleucinaemia could deplete tissue Ile pools. AIMS: To study the effect of repeated blood gavages on arterial and tissue Ile levels during normal and impaired liver function. SUBJECTS: Male Wistar rats. METHODS: 14 days after portacaval shunting or sham surgery, rats received 3 ml bovine erythrocytes or saline at 0, 1, 2, and 3 hours via a gastrostomy catheter in the duodenum. At 0, 2, 4, 6 and 8 hours arterial blood and at 8 hours intestine, liver, muscle, and cerebral cortex were sampled for determination of ammonia and amino acid concentrations. RESULTS: In both groups repeated blood administration resulted in a marked decrease in plasma Ile (40-60%). This was accompanied by decreased tissue Ile concentrations in liver (50%), muscle (40-60%), and cerebral cortex (40-50%), but unaltered intestinal Ile levels. In contrast, the arterial and tissue concentrations of ammonia, urea, and of most amino acids increased, most strikingly of the other two branched chain amino acids, valine and leucine. CONCLUSIONS: Simulated gastrointestinal bleeding by blood gavages in rats with and without impaired liver function leads to hypoisoleucinaemia and decreased tissue Ile pools.

Ammonia↗
PubMed1997

Effects of simulated upper gastrointestinal hemorrhage on ammonia and related amino acids in blood and brain of chronic portacaval-shunted rats.

Gastrointestinal (GI) hemorrhage during compromised liver function is known to precipitate portal-systemic encephalopathy (PSE). Hypothetically, the induced hyperammonemia depletes cerebral glutamate pools. To investigate this hypothesis, rats were studied 14 days after portacaval shunt (PCS) or sham surgery (SHAM). Rats received 3 mL bovine erythrocytes or saline at t = 0, 1, 2, and 3h via a previously placed gastrostomy catheter. At t = 0, 2, 4, 6 and 8h arterial blood and at t = 8h cerebral cortex were sampled for determination of ammonia and amino acids. Control rats (NORM) were sampled without previous surgery. Repeated intragastric blood administration increased the already elevated arterial ammonia levels in PCS rats further. This resulted in higher cerebral cortex ammonia and glutamine levels after blood administration. Despite the accumulation of ammonia and glutamine, cerebral cortex glutamate concentrations remained unaltered. Yet, PCS rats became more encephalopathic after blood gavages, suggesting that there is not a clear-cut relation between cerebral cortex glutamate concentrations and degree of PSE. Interestingly, cerebral cortex concentrations of GABA, tyrosine and phenylalanine were markedly increased. Whether these observations are pathogenetically related to PSE remains to be established. The present model of simulated GI hemorrhage in PCS rats seems to be a suitable, clinically valid model for future research regarding hepatic encephalopathy.

Amino Acids↗