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Biomedical subjects

A D Mason

Publications and source records attributed to A D Mason.

At least 55 records · Page 3Linked to original sources
PubMed1991

Dissociation of blood volume and flow in regulation of salt and water balance in burn patients.

The relationship between effective blood volume and related hormones in burn patients following resuscitation is not well understood. Previous reports have suggested that hormone secretion is altered by a resetting of neural control mechanisms. Serum and urine sodium, plasma renin activity, serum ADH, cardiac index, effective renal plasma flow, and total blood volume were measured in seven burn patients (mean age, total burn size, and postburn day: 32 years, 56%, and 9 days, respectively). The same values (with the exception of cardiac index and blood volume) were measured in 10 control patients (mean age, 24 years). The blood volume of patients was measured by 51chromium red blood cell (RBC) labeling and compared to normal predicted values based on body surface area and sex. Mean serum sodium and osmolality were 138 mmol/L (millimolar) and 286 mosm/kg, respectively, in both patients and control subjects. Mean +/- standard error of the mean total blood volume in the patients was low, 81% +/- 4% of predicted values. Cardiac index and renal plasma flow were significantly elevated. Plasma renin activity and antidiuretic hormone (ADH) levels were elevated and altered in the direction expected from blood volume measurements despite the findings of increased blood flow. Dissociation of organ flow and hormonal response suggests that simultaneous direct blood volume measurements are necessary to elucidate factors other than altered neural control settings to explain hormonal changes in the flow phase of injury. Depressed total blood volume appears to promote elevated ADH levels in burn patients following resuscitation. Whether there is an additional role of altered neural control settings remains to be established.

Adrenocorticotropic Hormone↗
PubMed1991

The morphology of smoke inhalation injury in sheep.

Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were exposed and evaluated at times ranging from 15 minutes to 4 weeks after exposure. Morphologic changes in the lungs were studied using light microscopy and both transmission and scanning electron microscopy. The primary, dose-responsive injury observed was acute cell membrane damage in the trachea and bronchi leading to edema, progressive necrotic tracheobronchitis with pseudomembrane formation, and airway obstruction. These inflammatory and occlusive effects were followed by congestion, alveolar space edema, atelectasis, and bronchopneumonia. Morphologic changes occurring in the alveolar epithelium following high smoke dosage included intracellular edema in type-I cells, changes in the membrane-bound vacuoles of type-II cells, and septal thickening caused by interstitial edema. No capillary endothelial changes were observed.

Animals↗
PubMed1990

Effect of prostaglandin E in multiple experimental models. IV. Effect on resistance to endotoxin and tumor necrosis factor shock.

Administration of a long-acting prostaglandin E, 16,16-dimethyl-PGE (dPGE), to rats improves their survival of bacterial peritonitis. We examined the mechanism of this protective effect with reference to its interaction with the release of cachectin (TNF). Sixty rats received saline, 20 micrograms/kg dPGE, or 80 micrograms/kg dPGE 12 hr prior to endotoxin and continuing for 48 hr. Survival rates for the saline, 20 micrograms/kg dPGE, and 80 micrograms/kg dPGE groups were 0, 40, and 85%, respectively. Forty rats received saline or 80 micrograms/kg dPGE, with the initial dose being 3 hr following endotoxin challenge and continuing for 48 hr. Survival rates for both groups were 0%. Sixty rats received saline or 80 micrograms/kg dPGE at 12 and 1 hr prior to endotoxin. Two hours after challenge, they were sacrificed and plasma TNF levels were assayed. The plasma TNF level in saline-treated rats was 22.72 +/- 0.83 ng/ml and in the dPGE-treated group, 16.03 +/- 1.13 ng/ml (P less than 0.001).

Animals↗
PubMed1990

Effect of prostaglandin E in multiple experimental models. VII. Effect on resistance to sepsis.

The immunosuppression seen following burn injury has frequently been attributed to elevated prostaglandin E levels. We evaluated the contribution of elevated prostaglandin E levels on susceptibility to infectious complications utilizing multiple mouse models. The administration of 100 micrograms/kg of the long-acting derivative of prostaglandin E, 16,16-dimethyl-prostaglandin E, was found to improve survival in C3/HEN mice challenged with 1 x 10(8) Escherichia coli organisms intraperitoneally. The administration of indomethacin was found to decrease survival in the same model. With C3/HEJ (endotoxin-resistant) mice, indomethacin was found to increase mortality rates in animals challenged with 1 x 10(8), 1 x 10(9) or 1 x 10(10) Escherichia coli organisms. These findings suggest that elevated prostaglandin E levels seen in burn patients may not be responsible for the postburn increased susceptibility to infectious complications.

Animals↗
PubMed1990

Smoke inhalation injury and the effect of carbon monoxide in the sheep model.

The role of carbon monoxide (CO) in causing the physiologic and anatomic changes characteristic of smoke inhalation injury was evaluated in 34 sheep. The smoke-exposed group received a dose of smoke known to produce mild inhalation injury. The CO group received a pure gas mixture that contained concentrations of oxygen, carbon dioxide, and CO similar to those in the smoke. Cardiopulmonary function was measured immediately after exposure, and 24 and 72 hours after exposure. The CO group showed a transient increase in cardiac output, but the smoke group showed no such response. The CO group maintained normal PaO2 levels during the 72-hour study period; the smoke group gradually developed hypoxemia. The lungs of the CO exposed animals had no discernible histologic changes; lungs of the smoke group showed progressive inflammatory changes. These results indicate that CO per se is not the primary etiologic agent of smoke inhalation injury.

Animals↗
PubMed1990

Multiple graft harvestings from deep partial-thickness scald wounds healed under the influence of weak direct current.

The time required for wound healing, contraction, and hypertrophic scarring often limit the use of deep partial-thickness burn wounds as donor sites for split-thickness grafts. We have examined the effects of weak direct current and silver nylon dressings on the healing of partial-thickness scald burns, split-thickness grafts taken from these wounds when healed, and the resulting donor sites in a guinea pig model. Dorsal scald wounds treated with weak direct current reepithealized by 12 days postinjury. Split-thickness grafts taken from healed scald wounds showed more rapid revascularization with direct current treatment than did control grafts. Grafts and donor sites treated with direct current showed more rapid reepithelialization, decreased contraction, improved hair survival, and decreased dermal fibrosis when compared to controls not treated with direct current. Only donor wounds treated with weak direct current were reusable as donor sites.

Animals↗
PubMed1990

Evaluation and management of patients with inhalation injury.

Inhalation injury, present in approximately one third of burned patients treated at burn centers, increases mortality by a maximum of 20% in relation to age and extent of burn. The development of animal models of inhalation injury has made possible the identification of both the airway and vascular responses evoked by smoke inhalation. Inflammatory occlusion of terminal bronchioles and necrosis of the endobronchial mucosa render the airway and pulmonary parenchyma susceptible to infection and the resulting pneumonitis further increases mortality. Early diagnosis, best achieved by endoscopic bronchoscopy and 133xeon ventilation perfusion scan, permits timely application of high-frequency ventilation that appears to reduce the incidence of pneumonia and to decrease mortality. Pharmacologic agents give promise of ameliorating the deleterious changes of the vasculature. The recent advances in understanding inhalation injury have identified the research needed to further improve patient salvage.

Animals↗
PubMed1990

Wound endotoxin is not a principal mediator of postburn hypermetabolism in rats.

Localized bacterial colonization of a 30% total body surface burn (TBSB) wound raises the resting metabolic rate of rats. To determine whether endotoxin (LPS) released in the burn wound contributes to this response, the metabolic rates and colonic temperatures of male Sprague-Dawley rats were monitored before and for 1 week after thermal injury. Wounds were seeded with non-virulent P. aeruginosa (NVP), or S. epidermidis (SE) or were left unseeded at the time of injury. Non-bacteremic SE-seeded rats were as hypermetabolic as the NVP-seeded animals on postburn days (PBDs) 3-4 and 7-8, indicating that wound LPS is not an obligatory mediator of postburn hypermetabolism. Continuous subcutaneous infusion of NVPlps (2.6 and 12.6 micrograms/100 gm/hr) beneath unseeded burn wounds did not raise metabolic rates above those of burned, unseeded controls. Neither NVP seeding nor LPS infusion resulted in measurable endotoxemia on PBDs 7-8. These results indicate that the LPS released in the colonized burn wound does not serve as either a circulating mediator or the principal inducer of other mediators of postburn hypermetabolism in rats.

Animals↗
PubMed1990

Effect of blood transfusions on immune function. Part VI. Effect on immunologic response to tumor.

Transfusions are reported to increase the incidence of tumor metastasis in clinical studies and primary tumor growth in animal studies. We evaluated the effect of transfusions on immunologic response to primary and metastatic tumors in multiple rat models. One half of the animals were administered lactated Ringer's solution and one half ACI rat blood at the time of tumor challenge. In 80 rats a slow-growing colon tumor was implanted subcutaneously. At 4 months there were no significant differences in tumor size or leukocyte infiltration of the tumor. Similar results were obtained with a rapidly growing colon cancer. Analysis of T-lymphocyte subpopulations in both groups showed no differences. Rats transfused at the time of intravenous challenge with a suspension of 1 x 10(6) tumor cells had a mean survival time of 38.3 +/- 0.8 days and the control group had a mean survival time of 41.1 +/- 0.8 days (p = 0.016). One week after transfusion, natural killer cell lysis of tumor cells at a 100:1 effector/target cell ratio was 18.0% +/- 1.8% in the transfusion group and 23.0% +/- 1.3% in the control group (p = 0.034). In conclusion, transfusions in multiple rat cancer models did not affect primary tumor growth or the host's immunologic response to it but did significantly impair natural killer cell function and survival with tumor metastases.

Adenocarcinoma↗
PubMed1989

Excision of the burn wound in patients with large burns.

The known major determinants of survival for patients with burn injury are age, burn size, inhalation injury, and infection. The clinical courses of 210 patients with burns of 30% of the body surface or greater treated from Jan 1, 1983, through Dec 31, 1985, were reviewed to determine whether excision of the burn wound could be identified as a factor in survival after massive burn injury. The predominant site of infection changed from the burn wound to the lung, with pneumonia being the most common bacterial infection in patients whose wounds were treated as described. Effective topical control of bacterial proliferation and excision of the burn wound have resulted in replacement of invasive bacterial wound infection by nonbacterial burn wound infection. The apparent advantages of excision, particularly in large burns, may reflect only patient selection, since only those patients who are considered to be physiologically stable and able to tolerate the physiologic stress of excision are considered for operation.

Adolescent↗
PubMed1989

What's in a name? Is methicillin-resistant Staphylococcus aureus just another S aureus when treated with vancomycin?

Methicillin-resistant Staphylococcus aureus (MRSA) strains, principally resistant to penicillinase-resistant penicillins and aminoglycosides, are increasingly common hospital isolates. We have examined the significance of MRSA colonization and infection in 1100 consecutively admitted, seriously burned patients in whom vancomycin was used to treat all staphylococcal infections. Colonization with S aureus (SA) was identified in 658 patients, in 319 of whom MRSA colonization was identified. Two hundred fifty-three SA infections occurred in 178 patients; of these infections, 58% were pulmonic and 38% were bacteremic. Methicillin-resistant SA infections occurred in 58 of the SA-infected patients. A severity index, based on multiple-regression analysis of mortality as a function of burn size and age in the study population, was used to estimate expected mortality. We demonstrated no measurable increase in mortality attributable to MRSA in this population of burned, SA-infected patients. The results question the clinical and economic value of added control practices, such as closing of units, refusal of transfer or admission, added isolation, treatment of carriers, furlough of colonized staff, and other expensive measures that are specifically directed at prevention of MRSA infections in critical care areas.

Burns↗
PubMed1989

The effect of PGE in multiple experimental models. II. Effect on steady-state levels of plasma and brain amino acids and transmitters.

Elevations in prostaglandin E (PGE) have been documented in tumor and trauma patients. The physiologic significance of this elevation is not fully established. Utilizing a long-acting derivative of PGE, 16,16-dimethyl-prostaglandin E (dPGE), in a rat model, we evaluated its effects on metabolic rates, amino acid, and neurotransmitter metabolism. dPGE was not found to significantly alter resting metabolic rate. It did decrease the plasma level of three amino acids, including tyrosine. Although dPGE also decreased brain tissue levels of tyrosine, no significant alterations were observed on amine neurotransmitters or metabolites.

Amino Acids↗
PubMed1989

Effect of prostaglandin E in multiple experimental models. VI. Effect on T-cell subsets.

Burn injuries have been shown to impair immune function. One of the hypotheses for the etiology of the immunosuppression is that burn injuries result in an elevation of prostaglandin E (PGE) levels which then impair leukocyte function. We evaluated the effect of PGE levels on immune function in multiple animal models utilizing T cell subset levels for our immunologic measurements. Elevations in PGE levels were achieved by administering 16,16-dimethyl-prostaglandin E (dPGE) and reductions by administering indomethacin. The animal models included burned rats, burned-septic rats, and nonburned rats. Neither indomethacin nor dPGE administration resulted in alterations of any of the T cell subset populations in our models.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Metabolic and thermoregulatory responses to burn wound colonization.

This study was designed to determine whether there is a relationship between bacterial colonization of the burn wound and resting oxygen consumption (VO2) and colonic temperature (Tc) in burned rats. Resting VO2, Tc, and blood, spleen, and wound cultures were monitored for 2 weeks after 30% total body surface full-thickness burns. The wounds of 53 animals were seeded with 10(8) nonvirulent P. aeruginosa (NVP) at the time of injury, while the wounds of 33 rats were allowed to colonize spontaneously. The seeded wounds contained 10(6) colony forming units/gm (CFU/gm) by the fourth postburn day (PBD), while the unseeded wounds did not reach this level of colonization until after the first week postinjury. Wound seeding accelerated the metabolic and thermoregulatory responses to injury. Average VO2 and Tc of the seeded group were above the unseeded group on PBD's 3-4 and 7-8, but there were no significant differences between groups on PBD's 14-15. Although the unseeded animals were hypermetabolic during the first week, they remained afebrile. There was a significant correlation between wound bacterial counts and the increase in resting VO2 of 44 nonbacteremic animals, but variations in the data suggest that factors other than number of viable wound bacteria affect this relationship. Changes in Tc were unrelated to wound bacterial count but were correlated with changes in VO2. Taken together, the data suggest that bacteria in the burn wound contribute to the rise in energy expenditure following thermal injury.

Animals↗
PubMed1989

Relationship of transfusion and infection in a burn population.

The relationship between the number of red blood cell transfusions and major infectious complications was evaluated in 594 thermal injury patients admitted between 1982 and 1986 who had burns over 10% or more of total body surface area and survived more than 10 days. The mean age of this group was 32.9 years, with a mean burn size of 36% of total body surface area; 83% were male. Of the 594 patients, 23.7% died and 38.7% had documented inhalation injury. The mean number of red blood cell transfusions received was 19.7, with a range of 0 to 201. Two hundred fourteen patients (36%) had major infectious complications, defined as pneumonia or invasive burn wound infection. A cross-tabulation of predicted mortality, number of transfusions, and infectious complications revealed a significant positive correlation between transfusion number and infectious complications in patients with predicted mortalities between 10 and 70%. Per cent total burn, patient age, presence of inhalation injury, and number of transfusions were identified by discriminant function analysis as significant variables (p less than 0.05) in discriminating between patients with and without infections (85% accuracy). Logistic regression analysis confirmed the above findings, showing a relationship between the number of transfusions received and infectious morbidity which was independent of age or burn size, but no significant relationship between number of transfusions and mortality.

Adolescent↗
PubMed1988

Lymphocyte phenotype and function changes in burn patients after intravenous IgG therapy.

The effects of prophylactic administration of intravenous IgG on immune-cell phenotype and function in burn patients were compared with those of patients receiving standard therapy. Intravenous IgG infusions were given twice weekly for three weeks postburn or until wound closure. Intravenous IgG had no effect on the proportion of total T-lymphocytes, T-helper lymphocytes, or T-suppressor lymphocytes, but the proportion of B-lymphocytes decreased 40% in treated patient samples. Lymphocytes from treated patients incorporated less thymidine when stimulated with concanavalin A or pokeweed mitogen, but not with phytohemagglutinin. The amount of IgM secreted by pokeweed mitogen-stimulated cultures from treated patients increased by 24%, while the amount of IgG remained constant. The changes in beta-lymphocyte number and functional response may have been induced by the increased serum IgG levels in the intravenous IgG-treated patients.

Burns↗
PubMed1988

Lymphoid subpopulation changes after thermal injury and thermal injury with infection in an experimental model.

Subpopulation analysis of peripheral blood lymphocytes is a frequently used measure of immunocompetence. Yet, little is known about the lymphocyte subpopulations in the circulation and lymphoid organs after severe trauma. Blood, spleen, and lymph node (LN) subpopulations were compared in a rat model of burn injury (B) and burn injury with infection (BI). B and BI rats received 30% total body surface scald burns. Infection was induced by seeding wounds with Pseudomonas aeruginosa. Subpopulations were identified by flow cytometry 48 hours after burn. Helper lymphocytes were selectively depleted from the circulation of BI but not B animals, which caused the ratio of helper to suppressor cells (HSR) in BI animals to decrease significantly compared with the unburned controls. Both LN helper and suppressor cells were decreased in BI animals and the HSR was unchanged, but a selective reduction in suppressor cells in B LN increased the HSR relative to unburned controls. Spleen subpopulations were unchanged for both B and BI groups. Subpopulation changes after trauma and infection were different for each tissue examined.

Animals↗