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O Elmore

Publications and source records attributed to O Elmore.

2 recordsLinked to original sources

Does sodium pentobarbital anesthesia compromise clearance of bacteria or survival of dogs in lethal E coli shock?

Recent reports have indicated that circulating leukocytes play a prominent role in promoting survival in endotoxin and live E coli shock. Anesthesia has been reported to compromise host defense by depressing phagocytic activity. This study was designed to determine whether sodium pentobarbital would adversely affect leukocyte concentrations, E coli clearance, blood glucose concentrations, and survival of dogs in lethal E coli shock. A leukocytosis was produced in some dogs using daily sublethal intravenous injections of E coli endotoxin for 3 days. Three groups of dogs were challenged with LD100 E coli: Group A (saline-pretreated, normal leukocyte count, unanesthetized); Group B (endotoxin-pretreated, leukocytotic, anesthetized); and Group C (endotoxin-pretreated, leukocytotic, unanesthetized). Groups B and C reduced circulating E coli concentrations similarly but significantly more than Group A. All animals in Group A died, all in Group C lived, and 67% in Group B lived. The reduction in survival in Group B was probably due to the marked hemoconcentration in the anesthetized dogs which were unable to drink, rather than a compromise of their host defense. Inasmuch as phagocytic activity was similar between anesthetized and unanesthetized dogs, results suggest that barbiturate anesthesia is not deleterious to host defense.

Anesthesia↗

Preserved liver function and leukocyte response in superlethal endotoxic shock.

Recent studies reveal that endotoxin-pretreated awake dogs become markedly leukocytotic and survive superlethal endotoxin challenge without hypoglycemia. The purpose of this study was to determine if an association exists between leukocytosis, liver function, and survival in endotoxin shock. Studies were conducted on awake, conditioned adult dogs, with the experimental group (N= 5) injected intravenously with 1/1,000 LD100 E. coli endotoxin on Days 1 and 2, LD100 on Day 3, and 2 x LD100 on Day 4. A control group (N = 6) received equal volumes of saline on Days 1, 2, and 3, but on Day 4 received 2 x LD100 endotoxin. All saline-pretreated dogs died within seven hours following superlethal endotoxin challenge. Each animal in the experimental group was sacrificed at the time of its paired saline control's death for a comparison of liver pathology, since in parallel studies all endotoxin-pretreated dogs (N = 11) survived for 30 days. Animals in the experimental group exhibited a marked leukocytosis of 39,000/cu mm (mature neutrophils, 28,000/cu mm, immature neutrophils, 8,300/cu mm (P is less than 0.001) on Day 4 compared with saline-pretreated controls. At the time of death the liver enzymes, arginase, and SGPT were significantly elevated in the saline-pretreated controls compared with endotoxin-pretreated dogs (P is less than 0.02). Liver pathology in endotoxin-pretreated dogs consisted of mild necrosis, while saline-pretreated animals demonstrated massive hepatocellular necrosis. Results support the view that increased numbers of neutrophils protect liver function and enhance survival in endotoxin shock.

Alanine Transaminase↗