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T Adams

Publications and source records attributed to T Adams.

At least 109 records · Page 6Linked to original sources
PubMed1983

Role of lymphocytes in the ovine response to endotoxin.

The involvement of thymocytes in the cardiopulmonary response to endotoxin was studied in chronically instrumented sheep. Four hours after the administration of 0.75 microgram/kg of endotoxin the blood levels of thymocytes were less than 25% of the control value, at a time when there was a marked fall in the cardiac index and a rise in pulmonary lymph flow. In a second series of experiments sheep were depleted of their thymocytes by the administration of antithymocyte serum. When endotoxin was given to these animals the cardiac output did not fall to the same extent, nor did the hematocrit rise as much as it did in the intact animal. It thus appears that the thymocyte may play a contributing role in the cardiopulmonary response to endotoxin.

Animals↗
PubMed1983

Effect of naloxone treatment on the cardiopulmonary response to endotoxin in sheep.

The administration of small dosages of endotoxin to sheep results in cardiopulmonary changes characterized by an elevation in pulmonary lymph flow, vascular resistance, and hemoconcentration, and a reduction in cardiac output. These changes are not as great when the narcotic antagonist, naloxone (2 mg/kg/h for 5 h), is infused prior to and during the endotoxin response. The present study evaluates the ovine response to endotoxin when naloxone is administered 1 h after the endotoxin infusion. Sheep were prepared by implanting cardiopulmonary and lung lymphatic catheters. One week following the last surgical procedure, the sheep, in the awake state, were given 0.75 micrograms/kg of endotoxin and the variables were measured. Three days later, a second dose of endotoxin was administered and variables were again measured. An infusion of naloxone was given with one of the dosages of lipopolysaccharide. Two dosages of the narcotic antagonist were used. One group received 2 mg/kg bolus + 2 mg/kg/h for 5 h; another group was given twice this amount. Both dosages were started 1 h after endotoxin. The response to endotoxin was essentially the same whether or not the sheep were treated with naloxone. If naloxone pretreatment is effective and posttreatment is not, then it is possible that an opiatelike substance might be released by endotoxin which in turn results in the ultimate release of the lesion-producing substance.

Animals↗
PubMed1982

Kappa light chain nephropathy without evidence of myeloma cells. Response to chemotherapy with cessation of maintenance hemodialysis.

A rarely diagnosed nodular glomerulopathy is presented arising secondary to kappa light chain deposition and clinically characterized by hypertension, congestive heart failure, massive proteinuria and slowly progressive azotemia. Kappa light chains were detected in the urine, the glomerular nodules, and the basement membranes of both glomeruli and tubules. A malignant proliferation of plasma cells could not be detected. Two morphologic features were unusual: the presence of microaneurysms, and the deposition of immunoglobulin and complement in a similar pattern to the kappa light chains. Noteworthy clinical aspects included the elusiveness of the proper diagnosis, the massive proteinuria in the absence of amyloid deposits, and the remarkable improvement in renal function following intermittent chemotherapy.

Aged↗
PubMed1982

Is endotoxin responsible for the cardiopulmonary lesions seen during acute burn wound sepsis?

Acute burn wound sepsis is a common clinical entity resulting from a showering of the circulation with gram-negative organisms which grow abundantly in the burn. We duplicate this state in our laboratory by creating 40%, third degree burns (anesthetic burns) in chronically instrumented sheep. Three days following the thermal insult, the burn wound is infected by injecting gram-negative organisms (3 X 10(10)) into it. Cardiopulmonary variables and pulmonary lymph flux data are monitored two hours prior to the injection of organisms and for three hours following it. Three different organisms were used in this study; Pseudomonas aeruginosa (N = 12), Escherichia coli (N = 9), and Klebsiella pneumoniae (N = 2). The injection of all three organisms resulted in a similar response; an early marked pulmonary hypertension and a late increase in microvascular permeability. These changes occur concomitantly with an elevation in hematocrit and an early marked fall in neutrophils. The cardiac output gradually falls over the period of observation despite vigorous body shivering associated with a febrile response. The data from the sheep were compared to similarly instrumented animals (N = 12) which were not burned, but received a very small dosage of E coli endotoxin (0.75 micrograms/kg). The cardiopulmonary response was qualitatively identical to that seen with live organisms. However, the quantitative changes in several of the cardiopulmonary variables were much more marked with endotoxin. It is concluded that the cardiopulmonary response noted with burn wound sepsis is produced by endotoxin.

Animals↗
PubMed1982

The effects of a prostaglandin synthetase inhibitor, ibuprofen, on the cardiopulmonary response to endotoxin in sheep.

Prostaglandins released during inflammatory reactions cause increases in microvascular hydrostatic pressure, a primary cause of edema. Ibuprofen, a nonsteroidal, anti-inflammatory agent that reduces prostaglandin synthesis via inhibition of cyclooxygenase, was used to investigate the possible role of prostaglandins in the cardiopulmonary responses during sepsis. Sheep, surgically prepared for cardiopulmonary studies and collection of lung lymph, were given 0.75 micrograms/kg per 30 min of E. coli endotoxin iv. Ibuprofen (14 mg/kg) was given 15 min before and 1 h 45 min after the administration of endotoxin. We had previously noted a triphasic character to the hypovolemia encountered in endotoxin sepsis. The initial phase occurs during the first hour after endotoxin administration; it is characterized by decreases in PaO2, neutrophil count, and lymph-to-plasma (L/P) protein concentration ratios and by increases in mean arterial pressure, body temperature, hematocrit, lymph flow, and total plasma protein concentration. In the second phase these variables return toward their baseline values. In Phase 3 the same changes are observed an in Phase 1 except for a decrease in total plasma protein concentration and an increase in L/P ratios. Ibuprofen administration results in a statistically significant reduction in magnitude of Phase 1 changes, without notable effect on Phase 2 or Phase 3 values. These observations support the hypothesis that prostaglandins released during inflammatory reactions contribute to the extravascular fluid movement. Ibuprofen appears to lessen the severity of microvascular hydrostatic pressure-induced edema and the hypovolemia that occurs in the early stages of endotoxin.

Animals↗
PubMed1981

Pain relief.

Explore the source record for details and available documents.

Buprenorphine↗
PubMed1981

Hemodynamic consequences of endotoxemia in sheep.

Sheep which have been previously prepared for cardiopulmonary studies and collection of lung lymph were given 0.75 micrograms/kg of E coli endotoxin iv. This induced sepsis produced a triphasic response. Phase 1 occurs during the first hour after endotoxin administration and is characterized by a decreased cardiac output, lymph to plasma protein ratio, neutrophil count, and an increased hematocrit, total plasma protein concentration, lymph flow, and pulmonary artery pressure. During phase 2 these variables tend to return toward their baseline values. Phase 3 begins 2.5 hr after the administration of endotoxin and shows many of the same changes that were observed in phase 1. Also during the late phase, the plasma protein concentration and lymphocyte count were reduced and the lymph to plasa protein ratio was increased. It is concluded that (1) An early fall in cardiac output occurs as a consequence of hypovolemia. The decreased volume is the result of fluid movement from the vascular compartment to the interstitial space consequent to a microvascular pressure increase. Since the changes occur coincidentally with a drop in neutrophil count, these cells may bear some causal relationship to the response. (2) The late fall in cardiac output in phase 3, also the result of a diminished vascular volume, occurs secondarily to extravasular fluid movement as a consequence of both an elevated microvascular pressure and an increased permeability to protein. The latter may be causally related to a fall in lymphocytes.

Animals↗
PubMed1980

Thermodynamic technique for the quantification of regional blood flow.

A method is described to quantify regional blood flow by thermal analysis. A weak temperature field is established in a tissue and for a thermal steady state, unidirectional heat flux and the associated temperature gradient are measured simultaneously across a small fixed segment of the tissue. This information is evaluated with probe calibrations for homogeneous isotropic fluids, with data from ancillary measurements in the nonperfused tissue and with values of specific heat and density of blood to express local blood flow in heat transfer [effective thermal conductivity (W. degrees C-1 . cm-1 x 10(-3) and/or in perfusion (ml . min-1 . cm-3)] terms. The technique measures local perfusion in small tissue volumes and is usable in acute or chronic experiments. Its accuracy is not a function of the absolute steady-state temperature of the tissue or of its metabolic heat production.

Animals↗
PubMed1976

Bleeding times, platelet adhesion, and aspirin.

The effects of aspirin on well-standardized commercially produced platelet adhesiveness devices and template bleeding times were simultaneously studied in 19 normal volunteers. As expected, there was significant prolongation of the bleeding time after aspirin, but there was no change in platelet adhesion. Reason for the different effects of aspirin on the two tests are discussed. In addition, the normal range of platelet adhesion was further defined utilizing commercially prepared glass-bead columns.

Adult↗
PubMed1975

Epidermal thermal conductivity and stratum corneum hydration in cat footpad.

Epidermal thermal conductivity (k) was calculated for the cat footpad by measuringtransepidermal heat flux and temperature gradient (¿T) while changes in stratum corneum water content were produced by "internal hydration" (IH; eccrine sweat gland activity by nerve stimulation) or by "external hydration" (HH; exposure to air saturated with water vapor). In some experiments, cutaneous vasoconstriction accompanying IH was prevented by an alpha-adrenergic receptor blocking agent, phenoxybenzamine (POB), 3.52 mg/kg iv. For dry skin k=0.167 plus or minus 0.023 (SE) W.m (-1) degree C (-1). With and without POB, IH produced 49.5% and 17.2% increases in k, respectively; HH after IH did not increase k more. With POB, IH increased k more than did HH alone (49.5% and 15.5%, respectively) and at a higher rate (4.22 times 10 minus 3 and 0.63 times 10 minus 3 W.m minus 1.degree C minus 1. min minus 1, respectively.) As k increased, usually deltaT decreased. Increasing k and decreasing deltaT with skin hydration explain the phenominon that air temperature is felt to be lower the more humid a cold exposure, since the temperature of thermoreceptors at the dermoepidermal junction is closer to that of the skin surface when the corneum is hydrated than when it has a low water content.

Animals↗