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Biomedical subjects

R R Wolfe

Publications and source records attributed to R R Wolfe.

At least 343 records · Page 19Linked to original sources
PubMed1978

The realiability of rates of glucose appearance in vivo calculated from constant tracer infusions.

The rate of appearance of unlabelled glucose was calculated from tracer data and compared with the actual rate of infusion of unlabelled glucose into a anaesthetized dog with all sources of endogenous glucose production surgically removed. The mean steady-state rate of appearance of unlabelled glucose calculated from the equilibrium specific radioactivity was insignificantly higher (0.3%) than the actual rate of infusion of unlabelled glucose (n = 6). During non-steady states, a time-variable volume of distribution of glucose (V) was necessary to predict the rate of appearance of unlabelled glucose correctly from the pool-dependent equation described by Steele [(1959) Ann. N.Y. Acad. Sci. 82, 420--430]. Rapid fluctuations in the rate of appearance of glucose could be predicted reasonably well by using a fixed value of V for 40ml/kg, but by using larger fixed values for V (100--160ml/kg) the rates were inaccurate. The pool-dependent two-radiactive-isotope technique described by Issekutz, Issekutz & Elahi [(1974) Can. J. Physiol. Pharmacol. 52, 215--224] predicted single-step increases in the rate of infusion of glucose reasonably accurately, but the Steele (1959) equation was better at predicting sequential changes in the rate of infusion of unlabelled glucose.

Animals↗
PubMed1978

Metabolic and hemodynamic aspects of the hypothermia of early burn shock.

Guinea pigs briefly anesthetized with Halothane were burned over 70% of their body surface area. Core temperature progressively decreased over an 8 hour period reaching its lowest level just before death. Heart rate, cardiac output, and oxygen consumption also diminished over this period. The fractional distribution of the cardiac output to the pancreas, adipose tissue, burned and unburned skin and muscles fell sharply. Actual volume flow to the heart and brain also decreased while plasma FFA concentration exhibited little change. However, hyperglycemia was noted due in part to peripheral insulin resistance. Although plasma catecholamines increased during this trauma, their effect was muted by a low plasma pH and a rising lactic acid concentration. It is postulated that the destroyed peripheral temperature receptors, hypoxic areas of the brain, decreased blood flow through high metabolic areas and low oxygen and substrate utilization in the periphery brought about the hypometabolism.

Animals↗
PubMed1978

Fallibility of the intravenous glucose tolerance test as a measure of endogenous glucose turnover.

We have used hepatectomized, nephrectomized dogs receiving a constant infusion of unlabeled glucose as well as conscious, unrestrained guinea pigs in order to investigate the calculation of basal glucose kinetics from intravenous glucose tolerance tests (IVGTT). In the dogs, we were not able to determine the known rate of appearance (Ra) or disappearance (Rd) of glucose within 50% of the actual value by means of IVGTT. In the guinea pigs, we found that Ra calculated from IVGTT was 250% higher than Ra determined by means of the validated technique of the primed-constant infusion of 6-3H-glucose in tracer quantities. When live Escherichia coli were infused into the guinea pigs, the isotope-tracer technique revealed a 100% increase in Ra yet Ra appeared to be decreased by 80% when calculated by means of IVGTT. We concluded that basal glucose kinetics cannot be determined reliably from IVGTT, and that in certain pathologic conditions the direction of change in Ra and Rd from the basal state may be incorrectly predicted.

Animals↗
PubMed1978

The silent ductus arteriosus.

Preterm infants at risk of developing a patent ductus arteriosus were followed sequentially by physical examination, echocardiographic determinations of the LA/AO ratio, and chest roentgenograms. The results show that a significant number of infants who have no clinical signs or symptoms of a PDA have large left-to-right shunts. The presence of this shunt was suggested by acute increase in left atrial size by ECHO determination and confirmed by retrograde single-film aortography. Clinical signs and symptoms often developed several days after documentation of the left-to-right shunt.

Aortography↗
PubMed1978

Effect of glucose infusion on glucose and lactate metabolism in normal and burned guinea pigs.

We have used the simultaneous primed-constant infusion of 6-3H-glucose and U-14C-lactate to investigate the effect of an exogenous glucose infusion (55 mumole/kg.min) on glucose and lactate metabolism in normal and burned guinea pigs. Before the unlabeled glucose infusion, glucose turnover was higher in the burned animals than in the controls, but lactate turnover was similar. During the unlabeled glucose infusion, lactate production increased in both control (73%) and burned animals (104%), yet arterial lactate concentration did not rise in either group. The ability of tissue uptake of lactate to keep pace with increased lactate production appeared to be related to an enhancement of lactate oxidation. When a two-pool model was used to calculate glucose-lactate interrelationships, it was concluded that during the glucose infusion Cori cycle flux (glucose to lactate to glucose) was higher in burned animals than in controls. Also, the primary route of oxidation of infused glucose in controls and particularly in burned animals appeared to be through conversion to lactate and subsequent oxidation of lactate.

Animals↗
PubMed1978

Tracer priming the bicarbonate pool.

We have described a technique whereby the time necessary to reach an equilibrium enrichment of expired CO2 during a primed-constant infusion of [U-13C]glucose was shortened from 7 to 8 h to 1 hour or less. We applied the theory of the primed-constant infusion technique to the bicarbonate pool, with the "constant infusion" of labeled carbon dioxide originating from oxidation of the infused [13C]glucose rather than from a labeled infusion of bicarbonate.

Bicarbonates↗
PubMed1978

Chylothorax and chylopericardial tamponade following Blalock-Taussig anastomosis.

A case of chylothorax following a right-sided Blalock-Taussig shunt is presented. Chylopericardial tamponade eventually developed, because the mediastinal leakage of chyle was sealed off from the pleural cavity and diverted into the pericardium. Chylopericardium is a rare cause of an enlarged cardiac silhouette on a postoperative chest roentgenogram, but the importance of differentiating it from congestive heart failure is illustrated. When chylopericardial tamponade occurs, treatment consists of (1) aspiration for immediate relief and, if there is recurrence, (2) surgical evacuation of the pericardium with tube drainage or pericardiectomy and (3) ligation of the source of chylous drainage.

Cardiac Tamponade↗
PubMed1978

Glucose kinetics and responsiveness to insulin in the rat injured by burn.

The are persistent alterations in glucose metabolism in the rat during the first week after a 20 per cent body surface area burn injury. The basal rate of endogenous glucose production is elevated, and it is not suppressed to a normal degree by an exogenous glucose infusion. The hormonre data suggest that increased glucagon levels are responsible for the elevated rate of gluconeogenesis both before and during an exogenous glucose infusion. Basal glucose uptake was also elevated after injury, and there was a normal increment in the glucose metabolic clearance rate during an exogenous glucose infusion. The increase in the glucose metabolic clearance rate relative to the increase in the insulin concentration was equivalent in the burn and control groups of rats. This indicated a normal responsiveness to insulin after injury. Because there was no impairment in the capacity to take up an exogenous glucose infusion, we would question the insulin resistance rationale for administering insulin to patients rendered hyperglycemic by glucose infusion.

Animals↗
PubMed1978

Gastric mucosal lesions after burn injury: relationship to H+ back-diffusion and the microcirculation.

Rats were subjected to a 30% body surface area full-thickness burn. Two hours after injury, 93% of animals had gastric mucosal erosions. At 5 hours this increased to 100%, but at 24 and 72 hours, lesions were fewer and less severe. Histologic study suggested that lesions noted at 24 and 72 hours represented erosions formed earlier. No mucosal abnormalities were noted in control rats. A causal relationship between mucosal ischemia and the development of erosions is suggested by the presence of A-V shunts at 2 and 5 hours only. Significant increases in H+ back-diffusion and protein leakage into the gastric lumen at 2 and 5 hours also implicated changed mucosal permeability in the etiology of erosions. The return of H+ back-diffusion to control values at 24 and 72 hours, when lesions were still present, appears to contradict the theory that permeability changes are secondary to erosion formation.

Animals↗
PubMed1977

Glucose kinetics in dogs following a lethal dose of endotoxin.

The effects of a lethal dose of Escherichia coli endotoxin on the glucose kinetics and cardiovascular responses of conscious dogs were studied. The plasma glucose level fell steadily after endotoxin administration to severely hypoglycemic levels preterminally. The fall in plasma glucose appeared to be due primarily to an increased tissue uptake in the early phase, whereas decreased hepatic glucose output also contributed in the later, preterminal phases.

Animals↗
PubMed1977

Glucose and lactate kinetics after endotoxin administration in dogs.

We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.

Animals↗
PubMed1977

Glucose and lactate kinetics in burn shock.

We studied the glucose and lactate kinetics during burn shock by means of the primed constant infusion of [6-3H]glucose and Na-L-(+)-[U-14C]lactate. We found an early postburn hyperglycemia that was due to an increased rate of appearance (Ra) of glucose. Later, the ability of the tissues to extract glucose became impaired, and the plasma glucose concentration increased even more in spite of the return of Ra of glucose to the control level. The Ra of lactate rose rapidly postburn, whereas the rate of disappearance (Rd) of lactate stayed at the control level for 30 min. Consequently, plasma lactate rose approximately 350%. After 30 min, Rd of lactate increased to the same level as Ra; and Ra, Rd, plasma lactate concentration, and the percent of glucose derived from lactate remained elevated for the duration of the experiment. These results indicate an important role of lactate in burn shock metabolism and substrate kinetics.

Animals↗
PubMed1977

Effect of burn trauma on glucose turnover, oxidation, and recycling in guinea pigs.

The simultaneous primed-constant infusion of [6-3H]- and [U-14C]glucose was used to determine the effect of burn injury on glucose turnover, oxidation, and recycling in guinea pigs. Eleven burned animals survived more than 72 h (survivors), whereas five died between 60 and 72 h postburn. All of the controls (n = 9) survived more than 72 h. At 48 h postburn, glucose turnover in the burned survivors was elevated 40% above that in control animals. A greater portion of the burned survivors' turnover was due to recycling and less was directed towards oxidation. The nonsurvivors had both a significantly depressed rate of appearance of glucose and an increased glucose clearance rate. Consequently, they were profoundly hypoglycemic and had a low rate of glucose oxidation. The alterations in glucose kinetics and oxidation apparent after burn did not reflect an inability of burned animals to oxidize exogenously infused glucose, however, because of 2-h infusion of 55 mumol/kg-min of unlabeled glucose doubled glucose oxidation in the burned survivors and tripled it in the nonsurvivors.

Animals↗