Biomedical subjects

A G Britten

Publications and source records attributed to A G Britten.

5 recordsLinked to original sources

PubMed1990

Rapid sequence anesthesia induction for emergency intubation.

Emergency intubations are done for a variety of reasons in the emergency department (ED). In some patients, a rapid, controlled induction of anesthesia is useful to facilitate intubation and to reduce the complications of intubation. This is referred to a rapid sequence induction (RSI) in the anesthesia literature. Atropine, thiopental, fentanyl, diazepam, ketamine, vecuronium, succinylcholine, other drugs and their applications for RSI are described. The purpose of this article is to describe the use of RSI in the airway management of ED patients. Nineteen pediatric patients requiring emergency intubation were intubated using RSI with vecuronium and thiopental. Actual intubation difficulty using RSI was significantly less than the anticipated intubation difficulty without RSI. There were no complications caused by intubation or RSI that had a significant impact on patient outcome. We feel that a sedative in combination with vecuronium represents the most optimal means of achieving RSI in the ED setting. Although the induction of general anesthesia is best done by anesthesiologists, emergency physicians are often the most experienced physicians immediately available to manage an airway in a critical emergency. An objective protocol such as that described will make it easier for emergency physicians to perform this procedure when needed.

Adolescent↗

PubMed1985

Interaction of CO2 and ammonia on cerebral blood flow and O2 consumption in dogs.

Studies of acutely induced hyperammonemia and chronic hyperammonemia associated with liver dysfunction suggest that cerebral blood flow (CBF) and O2 consumption (CMRO2) become uncoupled and that CMRo2 may depend on arterial CO2 tension (PaCO2). We examined CBF (radiolabeled microspheres) and CMRO2 during hypercapnia (PaCO2 congruent to 74 Torr) and hypocapnia (PaCO2 congruent to 21 Torr) both before and during intravenous ammonium acetate infusion in pentobarbital-anesthetized dogs. Continuous infusion over 120 min produced stable increases of arterial ammonia levels (1,400 mumol/l) by 30 min, whereas CBF, CMRO2, and O2 extraction (measured at sagittal sinus) remained unchanged when PaCO2 was held constant (congruent to 35 Torr). Acute hyperammonemia attenuated the increase in CBF during hypercapnia by 44% and abolished the decrease in CBF during hypercapnia. Regional blood flow to pons and midbrain increased under normocapnic conditions, and midbrain blood flow increased further during hypocapnia. Sodium acetate infusion did not affect CBF responses to CO2. Thus we failed to observe an uncoupling of global CBF and CMRO2 during normocapnic hyperammonemia, or an interaction of CO2 and ammonia on CMRO2, although the increased pons and midbrain blood flow may reflect regional effects of ammonia on reticular activating system metabolism. On the basis of the literature, we suggest that the attenuated hypercapnic CBF response may arise from impaired glial regulation of extracellular potassium and bicarbonate concentrations and that lactic acid production, enhanced by combined alkalosis and hyperammonemia, may contribute to the abolition of hypocapnic vasoconstriction.

Acetates↗

PubMed1976

Recovery in rats after spinal cord injury.

Previous studies from this laboratory have shown evidence of regeneration of long descending spinal motor tracts in rats after spinal cord transection and treatment to modify the animals' immune response. In this study, less extensive surgical lesions were combined with the most favorable drug treatment (75 mg per kilogram of cyclophosphamide in a single dose) in an effort to improve the prospects for regeneration. Less than complete spinal cord transections in the rat were frequently followed by clinical and electrophysiologic evidence of return of function. Such return of function appears to depend on a reorganization of the nervous system that results in the use of the few remaining fibers to transmit motor information rather than on regeneration. Immunosuppressive treatment had no effect on these results.

Animals↗

PubMed1975

Dental abnormalities in rats after a single large dose of cyclophosphamide.

Delayed drug-related mortality in rats treated with a single high dose (75 mg/kg) of cyclophosphamide complicated experiments using this drug treatment. We observed that this delayed mortality was due to dental abnormalities including broken teeth, absent teeth, extra long teeth, and/or supernumerary teeth. These dental abnormalities developed about 140 days after treatment and, if left untreated, interfered with eating. Eventually, the untreated rats starved. Clipping their long teeth and feeding the rats powdered chow eliminated the deaths. Researchers should be aware that high doses of cyclophosphamide may result in dental abnormalities several months after the treatment.

Animals↗

PubMed1971

Acetylcholine binding to Torpedo electroplax: relationship to acetylcholine receptors.

Binding of [(3)H]acetylcholine to a particulate fraction of Torpedo electroplax was measured by equilibrium dialysis. Two high-affinity sites present on phospholipoproteins bound acetylcholine reversibly, and binding was blocked by nicotinic drugs. Characteristics of this binding suggest that these phospholipoproteins may be acetylcholine receptors.

Acetylcholine↗