Biomedical subjects
Publications and source records attributed to B Benjamin.
A technique of anaesthesia for microlaryngeal surgery is described utilizing a new catheter and the venturi jet injector. Access and exposure for the surgeon are excellent and the laser can be used without special precautions. The central position and lack of movement of the distal end of the tube in the trachea prevent the potential complication of rupture of the trachea or of a bronchus.
Among normal peripheral blood leukocytes, lymphocytes were found to contain most of the de novo purine synthesizing capacity. The rate of purine synthesis de novo was accelerated in leukocytes from patients with acute and chronic myelocytic leukemias, chronic monocytic leukemia, myelofibrosis and plasma cell leukemia, but was normal in most patients with chronic lymphocytic leukemia. The rate of de novo purine synthesis exhibited positive correlation with the percentage of immature cells in the leukocyte population. The metabolic availability of phosphoribosylpyrophosphate (PRPP) exhibited positive correlation with the state of de novo purine synthesis. These finding suggest that the accelerated rate of de novo purine synthesis and the increased metabolic availability of PRPP are characteristic properties of the immature leukemic granulocyte.
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In previous studies on the modification of polar head groups of membrane phospholipids with the unnatural base analog, N-isopropylethanolamine, we reported an unidentified phospholipid in addition to phosphatidyl-N-isopropylethanolamine in the various membrane fractions of rat liver. The structure of this phospholipid has now been identified as phosphatidyl-N-methyl-N-isopropylethanolamine by nuclear magnetic resonance spectroscopy, and by chromatographic and enzymic analysis. In addition, we found that when rats were injected intraperitoneally with the N-methyl-N-isopropylethanolamine, 19% of the liver microsomal phospholipid was phosphatidyl-N-methyl-N-isopropylethanolamine.
This study was designed to examine the response of the baboon during a 24-hour period following Escherichia coli endotoxin infusion. Experiments were conducted on young adult baboons, unrestrained and maintained at a light plane of anesthesia induced with pentobarbital sodium. Light and electron microscopic studies on lung, heart, liver, and kidney were conducted; hematologic changes and physiologic responses were measured. The efficacy of heparin to prevent the coagulopathy and increase survivability was assayed. Hepatic sinusoidal fibrin thrombi with underlying hepatocyte cellular damage was seen in the endotoxin-treated group. In contrast, the experimental group receiving heparin showed no sinusoidal fibrin thrombi but demonstrated hepatocellular damage. Liver dysfunction was indicated by elevation of blood levels of enzymes. Glomerular fibrin thrombi were not present. Although heparin prevented the formation of hepatic thrombi in endotoxin-treated baboons, it did not increase survival. Platelet and complement levels decreased in both experimental groups, while wide variations in white blood cell and fibrinogen levels were observed. Polymorphonuclear leukocyte-platelet aggregations previously reported in the pulmonary vasculature during acute shock were not observed in the present study, and their absence may have been related to the longer time of survival.
Samplings of canine capsular and hilar lymph, and intrarenal venous blood were investigated as in vivo techniques for detecting renal cortical function in control and NH4Cl pretreated anesthetized animals. The glucose concentration of capsular, but not hilar, lymph was indicative of cortical drainage in both groups. When lymph flow was increased by elevating renal venous pressure, capsular lymph glucose concentration reflected cortical function only in the NH4Cl animals. The glucose concentration of intrarenal venous blood indicated cortical drainage in both the control and NH4Cl animals but the cortical function of a high para-aminohippuric acid extraction was only detectable in the NH4Cl group. Conclusions are that sampling of capsular lymph and intrarenal venous blood may prove to be useful techniques for studying certain in vivo cortical functions but the intrarenal venous technique is less sensitive than capsular lymph collection.
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The roles of renal gluconeogenesis and glucose utilization in control, hemorrhaged, and endotoxin-injected animals were investigated using anesthetized, eviscerated, nonnephrectomized and nephrectomized dogs. Results demonstrate an increased glucose utilization in both hemorrhagic and endotoxic shock which was marked after endotoxin. Since blood glucose values dropped more in nephrectomized, hemorrhaged animals, in contrast to the nonnephrectomized, hemorrhaged dogs, the kidneys were assumed to perform a significant gluconeogenic role. The kidneys did not appear to perform gluconeogenesis in endotoxin shock since blood glucose levels were comparable in eviscerated, endotoxin-treated animals whether nephrectomized or not. To ascertain the tissue responsible for the increased glucose utilization in endotoxin shock, a study was performed with endotoxin added to blood in vitro (estimated LD100 concentration). The endotoxin-treated blood (n = 7) demonstrated an increased glucose utilization compared with saline controls (n = 7) (P less than or equal 0.02). Acclerated glucose utilization rates were comparable between the eviscerated, nephrectomized animals and in vitro experiments. These data suggest that excessive glucose demand by certain blood components may partially explain the lethal hypoglycemia of endotoxin shock.
Past studies reported by this laboratory have documented myocardial dysfunction and progressively developing hypoglycemia in canine endotoxin shock. The purpose of the present study was to determine the effects of glucose concentrations and insulin infusions on myocardial performance following endotoxin administration. Experiments were carried out on isolated, working canine left ventricular heart preparations exchanging blood with intact dogs. Myocardial function was evaluated following endotoxin and correlated with concentrations of glucose and effects of insulin infusion. Cardiac dysfunction occurred within 2-4 hr postendotoxin and the degree of malfunction was not related to arterial blood glucose concentrations. Maintaining blood glucose at control, preshock, levels by infusion of 50% glucose did not prevent myocardial dysfunction as evidenced by elevations of left ventricular end diastolic pressure, and depressed power. Infusions of insulin reversed cardiac failure and maintained normal performance in spite of wide ranges in glucose concentration (5-120 mg%). Findings suggest that myocardial dysfunction is not precipitated or enhanced by the hypoglycemia of endotoxin shock. The beneficial actions of infused insulin on cardiac performance appear to be elicited on the basis of mechanisms other than myocardial glucose transport.
Tracheomalacia is an important cause of morbidity and death following correction of congenital tracheoesophageal fistula and is a well defined syndrome which requires recognition and appropriate treatment. The symptoms and signs allow division into mild, moderate, and severe groups. When the clinical features suggest the presence of tracheomalacia, endoscopy should be carried out in order to confirm the diagnosis and document the severity. Mild and moderate cases can be managed conservatively; efficient and regular physiotherapy is the mainstay of treatment. Severe cases warrant consideration for the operation of tracheopexy which may be lifesaving and will certainly reduce the period of hospitalization and will simplify management.
The present study was designed to develop an animal model applicable to the clinical patient in the investigation of the pathogenesis of septic shock. The model currently described is a lightly anesthetized, unrestrained monkey, carefully monitored during a 24 hour observation period. Varying doses of live Excherichia coli organisms were infused intravenously during a 30 minute period, and a variety of hemodynamic, respiratory and metabolic parameters were monitored. Doses of organisms varied between 7.6X10(9) and 3.0X10(11) organisms per kilogram of body weight, and there was no obvious correlation between size of dose and survival time. Two of nine experimental monkeys survived the Excherichia coli, while times of death of the remaining monkeys varied between three and 27 hours. Two control monkeys, not administered organisms, survived the 24 hour period with minimal changes in all measured parameters. Results reveal two patterns in response to organism administration. These were early acute death, after three to four hours, and prolonged life, death after 20 to 27 hours. The acute response was characterized by marked systemic hypotension, hypoglycemia, hypoinsulinemia, increased lactate level, decreased pH or respiratory depression. The other type of response involved profound sustained hypotension with hypoglycemia and hypoinsulinemia in most monkeys and elevations in lactate, blood urea nitrogen potassium creatinine, serum glutamicoxalacetic, lactic dehydrogenase and fractionatedlactic dehydrogenase levels. Depressions in respiration were not evident in the group which survived a longer period of time. Renal fibrin thrombi, prominent in baboons administered Escherichia coli, were absent in the rhesus monkey regardless of the size of the dose of organisms. The results of this study suggest the operation of a multifactiorial mechanism in septic shock with interactions between hemodynamic and metabolic factors varying within the species.