PubMed Health⌕ Search

Biomedical subjects

B Grubb

Publications and source records attributed to B Grubb.

22 records · Page 2Linked to original sources
PubMed1977

Effect of arterial carbon dioxide on cerebral blood flow in ducks.

The purpose of this study was to determine the effect of arterial PCO2 on blood flow to the avian brain. Cerebral blood flow was measured on curarized, artificially ventilated Pekin ducks by the rate at which intra-arterially injected xenon-133 was cleared from the duck's brain. A two-component clearance curve resulted: the blood flow calculated from the fast and slow components was similar to the blood flow to mammalian grey and white matter, respectively. Hypercapnia markedly increased the fast component of blood flow, whereas hypocapnia had no effect on this component. These effects were not due to changes in blood pressure, which was independent of arterial PCO2. Blood flow calculated from the slow component was independent of arterial PCO2. We conclude that the lack of response to hypocapnia may contribute to the exceptional tolerance of birds to high altitude by maintaining normal cerebral blood flow.

Animals↗
PubMed1976

De novo synthesis of alanine by the perfused rat hindlimb.

Due to the disproportionately large production of alanine by muscle, it has been suggested that part of the alanine released by muscle is synthesized de novo by the transamination of glucose-derived pyruvate. This glucose-alanine conversion was quantitated in the isolated rat hindlimb perfused with a solution of bicarbonate buffer containing 2% albumin, 2.4% dextran, 2.5-15.9 mM glucose, 32-34% dog erythrocytes, and 0.05 muCi/ml [14C]glucose. Measurement of labeled alanine production allowed quantitation of de novo alanine synthesis. De novo derived alanine accounted for an average of 33% of the total alanine released by the perfused tissue (perfusate glucose concentration 8.3 mM), concurrently 2.7% of the glucose taken up by the limb was converted to alanine. By increasing the glucose concentration perfusing the muscle, both the rate of glucose uptake and de novo alanine release were increased. Addition of insulin to the perfusate (700 muU/ml) resulted in a significant increase in the rate of glucose uptake and de novo alanine production, but the rate of total alanine release was significantly decreased by the hormone. It was concluded that de novo alanine production accounts for a sizeable portion of the total alanine released by muscle, nevertheless a comparatively small fraction of the glucose carbons are actually transformed to alanine.

Alanine↗
PubMedDate not supplied

Syncope due to autonomic insufficiency syndromes associated with orthostatic intolerance.

Recurrent syncope may be either a sign or a symptom and may occur due to a wide variety of very different causes. Extensive investigations into the nature of this disorder soon uncovered that it represents only one aspect of a broad, heterogenous group of disturbances of the autonomic nervous system (ANS) that can result in hypotension, orthostatic intolerance, and often syncope. Disorders of orthostatic regulation may be subgrouped into both primary and secondary forms. In primary autonomic failure syndromes, as opposed to the intermittent periods of hypotension seen in the reflex syncopes, patients could develop orthostatic intolerance due to a failure of the ANS to function under normal circumstances. Chronic autonomic insufficiency has two entities: Pure Autonomic Failure (PAF) and Multiple System Atrophy (MSA). Over the last several years, it has become apparent that a milder form of autonomic insufficiency occurs that is now referred to as the Postural Orthostatic Tachycardia Syndrome (POTS). The secondary forms of autonomic failure occur in association with a particular disease process. One of the most important things to remember are the vast number of pharmacologic agents that may either cause or worsen orthostatic hypotension. The principal feature that all of these conditions share is that normal cardiovascular regulation is disturbed resulting in postural hypotension. The comerstone of evaluation is a detailed history and physical examination. One of the physician's most important tasks is to identify whether hypotensive syncope is primary or secondary in nature, and to determine if there are any potentially reversible causes (i.e., drugs, anemia, volume depletion). It is equally important to educate the patient. Nonpharmacologic therapies are useful. Pharmacotherapy should be used cautiously in selected cases.

Autonomic Nervous System↗