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Biomedical subjects

N T Ryan

Publications and source records attributed to N T Ryan.

18 recordsLinked to original sources
PubMed1978

Persisting structural abnormalities in liver, kidney, and muscle tissues following hemorrhagic shock.

Hemorrhagic shock-induced abnormalities of liver, kidney, and muscle morphology were studied sequentially for eight days following shock and resuscitation in rabbits. The findings revealed marked structural changes, some of which became more pronounced between one and three days after shock and all of which persisted for at least three days. All of the tissue changes reverted to near normal by eight days. The specific findings included hepatic sinusoidal compression with cellular swelling and vacuolization one day after shock; renal vacuolization and swelling of proximal tubular convolutions, culminating in widespread cellular damage three days after shock; and separation of myofibrils and disruption of the band pattern in muscle tissue. These findings demonstrated the prolongation of the morphological abnormalities induced by shock, previously observed only in the acute phase, and the capacity for structural repair by the tissues after reversible hemorrhagic shock.

Abdominal Muscles↗
PubMed1977

Endocrine activation and altered muscle metabolism after hemorrhagic shock.

Studies were conducted to examine glucose and amino acid metabolism by skeletal muscle isolated from rhesus monkeys before and sequentially after an episode of resuscitated hemorrhagic shock. After shock and reinfusion, the tissue exhibited decreased effect of insulin on glucose utilization increased leucine oxidation, and a reduced rate of leucine incorporation into protein. These changes were observed 15 min after reinfusion and persisted in part for at least 3 days. All of the observed abnormalities were more pronounced 24 h after shock and reinfusion than 15 min after and returned to normal by 2-4 wk. The shock-induced metabolic abnormalities in skeletal muscle occurred in spite of prevention of shock-induced adrenal steroid and catecholamine secretion and of changes in blood insulin concentration using adrenalectomized-streptozotocin diabetic monkeys receiving replacement cortisol and insulin infusions. This study thus demonstrated that hemorrhagic shock in rhesus monkeys was followed by insulin resistance plus abnormalities of glucose and amino acid metabolism by skeletal muscle that were not dependent on the concurrent changes in plasma levels of adrenal steroids or catecholamines or on altered circulating insulin levels associated with shock.

Amino Acids↗
PubMed1977

A metabolic approach to the evaluation of peripheral vascular disease.

Thirty-five patients with occlusive disease of the arteries underwent metabolic studies. The arteriovenous differences of lactate, glucose and oxygen varied with the severity of the ischemic process, as assessed clinically. Lactate release and glucose extraction were significantly different from control values of patients with rest pain or with ischemic gangrene, while values in patients with claudication were comparable with those in the control group. Percutaneous muscle surface pH measurements, which reflect lactate release, decreased directly with diminished perfusion. Metabolic assessment of arterial occlusive disease may prove to be a useful clinical approach.

Aged↗
PubMed1976

Proteolysis associated with a deficit of peripheral energy fuel substrates in septic man.

Sixteen seriously septic patients were studied to determine whether proteolysis occurred to satisfy a deficit of peripheral fuel, as suggested by out previous experimental observations. Concentrations of glucose, lactate, free fatty acids,and alanine were measured in blood samples from the femoral artery and vein to determine extraction (+) and release (-) by the leg. Simultaneously, cardiac index (CI) was determined by thermal dilution, so that an estimate of uptake or production of fuel substrates could be made from the proportional relationship of cardiac index to peripheral blood flow. Due to the antilipolytic effect of elevated levels of insulin (42 +/- 4 muM per milliliter) in those patients with elevated cardiac indices (4.38 +/- 0.33 L. per square meter per minute), free fatty acid uptake (-0.59 +/- 0.021 mM.) was reduced. In low-flow septic shock (CI, 1.66 +/- .41 L. per square meter per minute), the majority of glucose taken up by the limb was converted to lactate (arterial lactate, 3.14 +/- 0.7 mM.; deltaA-V 0.68 +/- 0.17). Free fatty acid uptake also was impaired in low-flow sepsis. As opposed to fasting, arterial levels and uptake of ketone bodies were insignificant in sepsis. These findings suggest that there is a deficit of peripheral fuel with respect to glucose and fat. That protein is oxidized to fill this deficit is substantiated by the increased alanine release (-0.13 +/- 0.01, -0.33 +/- 0.12 mM.) in the high-flow and low-flow septic groups, respectively, whereas alanine production was three- and fourfold greater than that observed in fasting patients. Enhanced release of alanine reflects the magnitude of oxidation of branched-chain amino acids and accounts for the high rates of gluconeogenesis and proteolysis observed in sepsis.

Adult↗
PubMed1975

Liver metabolism and glucogenesis in trauma and sepsis.

The relationship of glucogenesis and other energy-requiring functions of the liver to the proteolysis which is characteristic of trauma and sepsis was studied in conscious pigs following laporotomy and after the induction of intraperitoneal sepsis. By means of appropriately placed thermal dilution catheters, portal and hepatic arterial blood flows, hepatic oxygen consumption, glucogenesis, and uptake of the fuel, substrates were measured. No animal was in shock. Despite significant increases of lactate and aminoacids delivered to the liver, the blood concentrations were maintained in the normal range. The rate of glucogenesis was proportional (r equals 0.71) to the sum of the glucogenic precursors (lactate, pyruvate, glycerol, and alanine) taken up by the liver. Higher rates of glucose production were accompanied by elevated blood insulin values. Hepatic oxygen consumption and the uptake of free fatty acids also were related directly to the glucogenic rate, the correlation coefficients being 0.69 and 0.74, respectively. In the absence of shock, the liver function and hepatic energy production remained normal in post-traumatic and septic states. Under the conditions insulin-resistant muscle in the presence of reduced free fatty acid availability mobilize protein to satisfy local energy requirements. Skeletal muscle can oxidize only branch chain aminoacids; other aminoacids, including alanine, are transported to the liver for glucogenesis or other purposed. This concept accounted for failure of glucose infusion to eliminate post-traumatic and septic proteolysis, since alanine is cleared only from blood by conversion in the liver to glucose. Thus it is concluded that in sepsis the release of glucogenic substrates because of altered metabolism in peripheral tissues determines the rate of hepatic glucogenesis. This relationship constitutes an important metabolic homeostatic mechanism.

Alanine↗
PubMed1974

Chronic tissue insulin resistance following hemorrhagic shock.

Metabolism of fat and muscle tissue was measured for 30 days following shock and reinfusion in rabbits. Tissue insulin resistance in the post-shock period was demonstrated by decreased oxidation of glucose and decreased incorporation of glucose into neutral lipid or glycogen during incubation with insulin. In addition, the insulin stimulated incorporation of amino acids into muscle protein was markedly reduced after shock. Conversely, the capacity of muscle to oxidize leucine was enhanced by shock, even in the presence of insulin. Tissue insulin resistance and increased leucine catabolism are likely to contribute to the general metabolic response to shock and trauma.

Adipose Tissue↗