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Biomedical subjects

D D Holmes

Publications and source records attributed to D D Holmes.

18 recordsLinked to original sources
PubMed1977

Glucose utilization and role of blood in endotoxin shock.

The present study was conducted to explore influences modifying glucose uptake in canine blood administered LD100 E. coli endotoxin. Particular emphasis was given to assay the role of the white blood cell (WBC) in glucose utilization. Significant increases in glucose uptake and lactic acid production, attributed to increased activity of the WBC, were observed 1-3 h after endotoxin was added to blood in vitro. Although a net increase in glucose utilization was noted, endotoxin simultaneously exerted adverse effects by depressing glucose uptake below predicted values (Q10 = 2.12 with LD100 endotoxin vs. 2.78 in saline controls) and increasing WBC mortality rate. Blood from dogs pretreated with sublethal doses of endotoxin in vivo utilized glucose at an accelerated rate when subjected to endotoxin in vitro. Excess glucose was consumed because of elevated numbers of white blood cells although additional glucose requirements after endotoxin were independent of temperature between the ranges of 34-41 degrees C. All animals pretreated with daily sublethal injections of endotoxin for 3 days survived superlethal doses of endotoxin.

Animals↗
PubMed1977

Leukocyte response and hypoglycemia in superlethal endotoxic shock.

This laboratory has documented a progressively developing hypoglycemia associated with systemic hypotension, hepatosplanchnic pathology, and death in endotoxin-shocked dogs. Recent data documented accelerated uptake of glucose in blood following endotoxin, with certain components of the buffy coat responsible for the increased uptake. The present study utilizing the awake dog assayed a possible protective role of leukocytes against the lethal effects of endotoxin. Animals were divided into paired groups: saline controls (Group I) and endotoxin experimentals (Group II). Group II animals were injected intravenously with sublethal doses of E. coli endotoxin on 2 successive days (Days 1 and 2), LD100 on the third day, and 2 X LD100 on Day 4. The control group received equal volumes of saline on Days 1, 2, and 3, but on Day 4 received a superlethal dose of endotoxin identical to the experimental group. The awake dog became febrile and exhibited initial leukopenia with subsequent marked leukocytosis in response to endotoxin. Lethal hypoglycemia was not seen in animals demonstrating initial leukocytosis (zero time) on the day of superlethal endotoxin challenge, while animals with initial normal leukocyte counts died with low glucose concentrations (mean, 40 mg%). Results suggest that an initial leukocytosis and sustained gluconeogenic function are important factors in survivability to endotoxin shock.

Animals↗
PubMed1977

Physiologic changes in the dog anesthetized with thiamylal and enflurane.

Enflurane anesthesia with thiamylal induction in the dog produced only slight, statistically insignificant, changes in the heart rate and the mean systemic blood pressure. A significant depression of the respiratory rate with an associated significant increase in the arterial partial pressure of CO2 was produced, accompanied by a decrease in the blood pH. Progressive drop of the body temperature occurred throughout anesthesia. Significant hematologic changes included a reduction in the packed cell volume and the erythrocyte and leukocyte counts. The only significant change in the blood chemistry was an increase in alkaline phosphatase at 24 and 48 hours after induction of anesthesia.

Alkaline Phosphatase↗