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Biomedical subjects

A D Mason

Publications and source records attributed to A D Mason.

At least 145 records · Page 8Linked to original sources
PubMed1976

Insulin response to glucose in hypermetabolic burn patients.

Fifty-four intravenous glucose tolerance tests were performed in 12 normal individuals and 21 thermally injured patients. In the 17 hypermetabolic burn patients studied between the 6th and 16th days postinjury, fasting blood glucose was elevated (111 +/- 7 mg/100 ml, mean +/- SE compared to 85 +/- 3 in controls, P less than 0.001), but the instantaneous proportionality constant for glucose disappearance (k) was similar to that obtained in normal individuals (5.27 +/- 0.51, 100/min vs 4.01 +/- 0.58 in normals, NS). Fasting serum insulin concentrations were comparable in the 12 normals and 17 hypermetabolic burn patients (22 +/- 3muU/ml in normals vs 22 +/- 2), as was fasting insulin corrected for fasting glucose (24 +/- 3 in normals vs 21 +/- 3, NS), initial insulin response (0-10 min delta insulin, 58 +/- 13 in normals vs 67 +/- 10, NS) or total insulin response corrected per unit glycemic stimulus (insulinogenic index, 0.48 +/- 0.10 in normals vs 0.52 +/- 0.07, NS). With time following injury, the proportionality constant for glucose disappearance and insulin response decreased, and these alterations were related to the posttraumatic weight loss. In the 5 convalescent patients studied between the 37th and 90th days postinjury, glucose and insulin dynamics appeared similar to those observed in starved man. In these burn patients, hypermetabolism and negative nitrogen balance occurred in association with a normal insulin response to glucose. Increased hepatic gluconeogenesis appears to be characteristic of the catabolic response to this stress, directed by increased glucagon and catecholamines, not a decrease in fasting insulin or dampened insulin response.

Blood Glucose↗
PubMed1976

Use of 133xenon in early diagnosis of inhalation injury.

133Xenon lung scanning post-thermal injury was used to detect inhalation injury in 86 patients admitted to the United States Army Institute of Surgical Research during 1974. Inhalation injury was indicated by the 37 (43%) positive scans. Based on all available clinicopathologic evidence, 11 (13%) of the scans were erroneous with seven (8%) falsely positive and four (5%) falsely negative. Eighty-six per cent of the scans were "appropriate." Addition of bronchoscopy and/or pulmonary function testing appeared to improve diagnostic accuracy. By using any pair of tests, falsely negative diagnoses were virtually eliminated. Inhalation injury, as expected, had an adverse effect on survival rates. The group of patients whose expected mortality lay between 40 and 59% were most notably affected. One hundred per cent (five of five) of those with inhalation injury died; only one of eight without inhalation injury died.

Bronchoscopy↗
PubMed1976

The pathophysiology of acute electric injuries.

Results of the present investigation indicate that an electric burn is simply a thermal injury. The tissue damage associated with an electric injury occurs when electric energy is converted to thermal energy or heat. An electric burn is self limiting: once the current arcs, no further skin and muscle damage is possible because amperage falls to zero. Tissue temperature is the critical factor in determining the magnitude of tissue injury before the current arcs. With the exception of skin resistance, resistances of individual tissues seem not relevant to amount of tissue damage in electric injuries. Living tissue acts as a volume conductor; once skin resistance has been overcome all internal tissue resistance, with the exception of bone, is negligible to current flow. In the present study the volume of tissue traversed by the electric current was more closely related to the extent of tissue injury than the internal resistance of the individual tissues. Muscle injury occurred at the time of initial thermal insult and progressive or de novo muscle necrosis was not seen in this model.

Acute Disease↗
PubMed1976

Protein metabolism in burned rats.

Incorporation of [2-14C]glycine was used to estimate serum protein synthesis in four groups of rats. These were the control (group C); 20% body surface burn (group B); 20% burn, seeded with Pseudomonas aeruginosa (group BI); and burned-infected treated topically with mafenide (alpha-amino-p-toluenesulfonamide) acetate (group BIS), a treatment which controls P, aeruginosa burn-wound infection in humans. On the 6th day postburn the relative specific activities of all fractions were increased in the order BI greater than BIS greater than B greater than C, as were the concentrations of the globulins; Serum albumin concentration fell, being lowest in BI. Tissue albumin contents, measured by radioimmunoassay, of eviscerated blood-free bodies of rats were (mg/100 g rat wt): C, 207; B, 294; BI, 256. Analyses of individual tissues showed that the difference was due to increased albumin content in the burn-wound area. The tissue albumin was of normal molecular size and was immunologically reactive. We conclude that the prolonged hypoalbuminemia following burn injury is not a consequence of impaired albumin synthesis, but a result of altered compartmentation.

Animals↗
PubMed1976

The quantitative swab culture and smear: A quick, simple method for determining the number of viable aerobic bacteria on open wounds.

The quantitative swab culture is a reliable method for quantifying the number of viable bacteria colonizing open wounds. For open wounds in burn patients, the swab bacterial count is linearly related to biopsy quantification of viable bacteria in the underlying tissue. This technique is simple and requires no surgical manipulation of the wound. For a wound of uniform appearance, the standard deviation of a single swab culture from the mean log bacterial count for a series of cultures from widely spaced areas on the wound is +/- 0.85 logs; 95% confidence limits are +/- 1.7 logs from the mean. A Gram-stained smear from a wound swab requires less than 10 minutes to prepare. Visualization of bacteria on the smear indicates that 106 or more bacteria per swab are present. The value of the smear and swab techniques for predicting safe wound closure may be inferred from the published reports of others and the direct relationship between the swab and biopsy counts of viable bacteria for open wounds.

Bacterial Infections↗
PubMed1976

Impaired glucose flow in burned patients with gram-negative sepsis.

Fifteen thermally injured patients with positive blood stream cultures for gram-negative organisms demonstrated a decreased mass flow of glucose through the glucose space when compared with 17 patients without sepsis studied at a comparable time after injury. Amino acid concentrations determined in ten burned patients with sepsis and nine burned patients without sepsis revealed an increase in the gluconeogenic precursors alanine, glycine, methionine and phenylalanine in those patients with sepsis. The administration of alanine consistently increased serum glucose in seven patients without sepsis but exerted no effect on glucose concentrations in six person with sepsis. These data, taken together, indicate that gram-negative sepsis in burned patients impairs the increased rate of glucose production and flow to peripheral tissue which characteristically occurs after thermal injury.

Adolescent↗
PubMed1975

Suppression of leukocyte chemotaxis in vitro by chemotherapeutic agents used in the management of thermal injuries.

Polymorphonuclear leukocytes from burned patients exhibit suppressed chemotaxis possibly related to the susceptibility of such patients to opportunistic infection. This study assesses the effect of normal serum upon burn-suppressed leukocytes and the effects of three commonly used topical chemotherapeutic agents upon the chemotaxis exhibited by granulocytes from normal controls. In vitro incubation with normal serum restored chemotaxis to normal in the suppressed granulocytes from burned patients. The serum factor responsible for this restoration was heat labile. Serum albumin alone did not exhibit this effect. Both mafenide and silver sulfadiazine suppressed the chemotactic function of granulocytes obtained from normal controls, while silver nitrate exhibited no such activity. Studies of the chemotactic function of control granulocytes after incubation with sera from burned patients yielded similar results; only the sera from patients treated with silver nitrate failed to suppress normal leukotaxis. The chemotactic impairment found in leukocytes from burned patients, however, while related to burn size and predictive of prognosis, did not vary with the agent used for the topical therapy. These data suggest the presence of a reversible intrinsic defect in leukotaxis consequent to burn injury, related to some factor deficient in burn serum. In addition, extrinsic impairment of normal granulocyte leukotaxis by two commonly used chemotherapeutic agents is demonstrated.

Administration, Topical↗
PubMed1975

Ventilatory patterns following burn injury and effect of sulfamylon.

Seven burn patients treated with silver nitrate dressings were studied during the first 10 days after injury. Minute ventilation, oxygen consumption, and ventilatory equivalent were measured. Minute ventilation was increased two- to threefold, as was oxygen consumption. Ventilatory equivalent was only slightly increased. THree patients were initially treated with silver nitrate, and then, when clinically stable, were switched to Sulfamylon. They showed a 50% rise in ventilation, tidal volume, ventilatory equivalent, and a slight increase in respiratory rate and VD/VT. In addition, their PO2 increased and base excess fell. Five normal subjects were then given Diamox, and their minute ventilation, O2 consumption, and ventilatory equivalent were measured at rest, with a standard exercise, and with an added dead space. Diamox produced only a 25% increase in minute ventilation and ventilatory equivalent. The results suggest that, although some of the increased ventilation of Sulfamylon is due to carbonic anhydrase inhibition, another factor, such as pain casued by the topical agent, also plays a role.

Acetazolamide↗
PubMed1975

Alterations in hypothalamic function following thermal injury.

Nine burn patients with a mean burn size of 39% (range, 23-65%) and five normal individuals studied in an environmental chamber selected optimal comfort temperature by regulating a bedside temperature control unit. The normal individuals selected 27.8 degrees C plus or minus 0.6 (SE) as the comfort temperature and their mean skin temperature was 33.4 plus or minus 0.6 and core temperature 36.9 plus or minus 0.1 while in this environment. In contrast, the burn patients maintained a higher ambient comfort temperature (mean 30.4 plus or minus 0.7, p less than 0.05 when compared to controls) associated with an elevated core (38.4 plus or minus 0.3, p less than 0.01) and surface temperature (35.2 plus or minus 0.4, p less than 0.05). Human growth hormone response to insulin hypoglycemia and arginine infusion was measured in nine additional burn patients (mean burn size, 52%; range, 23-90%) and five normals. Fasting HGH was significantly elevated (1.7 plus or minus 0.2 ng/ml, n = 18, versus control of 0.9 plus or minus 0.1, n = 10, p less than 0.001), despite fasting hyperglycemia in the burn patients (123 plus or minus 5 mg/100 glycemia in the burn patients (123 plus or minus 5 mg/100 ml versus 91 plus or minus 2, p less than 0.001). HGH response to insulin hypoglycemia was diminished in the burn patients with peak HGH value in patients averaging 12.6 ng/ml compared to 27.8 in the recovered patients and 32.6 in the controls (p less than 0.01). Patients receiving an arginine infusion also demonstrated diminished HGH response following injury. The HGH response to known stimuli returned toward normal with time and recovery in the surviving patients. Alterations in comfort temperature, fasting blood glucose, and glucose-HGH interaction occur following thermal trauma. These changes taken together suggest that metabolic responses to injury may be the consequence of homeostatic readjustment within the hypothalamus.

Adolescent↗
PubMed1975

The effect of early surgical excision and homografting on survival of burned rats and of intraperitoneally-infected burned rats.

The effects of early and delayed surgical excision and skin homografting on survival in burned, uninfected rats and in burned rats infected with Pseudomonas aeruginosa, intraperitoneally, has been studied. The survival rate in animals treated with surgical excision and no coverage was significantly worse than in the animals who were simply burned. Immediate excision of the burn wound followed by prompt coverage with skin homografts resulted in decrease in the mortality rate from subsequent intraperitoneal infection of Pseudomonas. The beneficial effects of early surgical excisions and immediate skin homograft coverage were also achieved when formalin-fixed skin homografts were used.

Animals↗
PubMed1975

Effect of ambient temperature on heat production and heat loss in burn patients.

Four controls and eight burned patients with thermal injury ranging from 7 to 84% total body surface were studied in an environmental chamber at 25 and 33 degrees C ambient temperature and a constant vapor pressure during two consecutive 24-h periods. Hypermetabolism was present in the burn patients in both ambient temperatures and core and skin temperatures were consistently higher than in the normal men despite increased evaporative water loss. The higher environmental temperature decreased metabolic rate in patients with large thermal injuries in whom the decrement in dry heat loss produced by higher ambient temperature exceeded the increase of wet heat loss. In patients with burns smaller than 60%, these changes equaled one another and higher environmental temperature exerted no effect on metabolic rate. Core-skin heat conductivity increased with burn size; patients with large burns were characterized by inadequate core-skin insulation when exposed to the cooler environment, necessitating the compensatory increase of metabolic rate. This increase, however, was small and of the order of 5-8 kcal times m-2 times h-1.

Adolescent↗
PubMed1974

Catecholamines: mediator of the hypermetabolic response to thermal injury.

Hypermetabolism characterizes the metabolic response to thermal injury and the extent of energy production is positively related to the rate of urinary catecholamine excretion. Alpha and beta adrenergic blockade decreased metabolism from 69.6 +/- 5.3 Kcal/m(2)/hr to 57.4 +/- 5.2 (p < 0.01), and infusion of 6 microgm epinephrine/minute in normal man significantly increased metabolic rate. Twenty noninfected burned adults with a mean burn size of 45% total body surface (range 7-84%) and four normal controls were studied in an environmental chamber at two or more temperatures between 19 and 33 C with vapor pressure constant at 11.88 mm Hg. All burn patients were hypermetabolic at all temperatures studied and their core and mean skin temperatures were significantly elevated above control values. Between 25 and 33 C ambient, metabolism was unchanged in controls and burns of less than 40% total body surface (48.9 +/- 4.6 Kcal/m(2)/hr vs. 48.9 +/- 4.5), but metabolic rate decreased in larger burns in the warmer environment (72.0 +/- 1.9 vs. 65.8 +/- 1.7, p < 0.001). At 21 C, metabolism and catecholamines increased, except in four nonsurvivors who became hypothermic with decreased catechol elaboration. Metabolic rate in ten patients with bacteremia was below predicted levels while catecholamines were markedly elevated suggesting interference with tissue uptake of the neurohormonal transmitters. Feeding burn patients or administering glucose and insulin improved nitrogen retention and altered substrate flow but did not significantly reduce urinary catecholamines or metabolic rate. Burned patients are internally warm, not externally cold, and catecholamines appear to mediate their increased heat production. Hypermetabolism may be modified by ambient temperature, infection, and pharmacologic means. Alterations in hypothalamic function due to injury, resulting in increased catecholamine elaboration, would explain the metabolic response to thermal injury.

Adolescent↗