Search PubMed⌕ Search

Biomedical subjects

M E Webster

Publications and source records attributed to M E Webster.

At least 37 records · Page 2Linked to original sources
PubMed1968

Kinins, beta-adrenergic receptors and functional vasodilatation in the submaxillary gland of the cat.

1. The close arterial infusion of bradykinin into the submaxillary gland of the cat produced a pronounced hyperaemia that could be blocked by simultaneous perfusion of the gland with blood containing carboxypeptidase B. Carboxypeptidase B, however, failed to reduce the vasodilatation of chorda tympani nerve stimulation suggesting that the kinins are not involved in the regulation of submaxillary gland blood flow.2. Isoproterenol injections produced pronounced salivary gland vasodilatation. Beta-adrenergic blocking drugs reduced or abolished the hyperaemia of isoproterenol and reduced that of chorda tympani nerve stimulation. The combination of beta-blocking drugs and atropine could abolish or reduce further this nerve induced hyperaemia.3. The above results suggest that stimulation of cholinergic and beta-adrenergic receptors could account for the chorda tympani induced hyperaemia. Conclusive proof of this possibility remains to be determined.

Animals↗
PubMed1967

Respiratory function during thermal tachypnoea in sheep.

1. Four Merino wethers were exposed to dry bulb temperatures ranging from approximately 20 to 60 degrees C, and the concurrent changes in respiratory frequency, tidal volume, respiratory minute volume, alveolar ventilation, dead space ventilation, carbon dioxide output, rectal temperature, and arterial and mixed venous blood, CO(2) content, CO(2) partial pressure and pH were established.2. The respiratory response to heat exposure showed two phases. Respiratory minute volume was initially increased by a rise in the respiratory frequency, while tidal volume decreased. After more prolonged exposure there was a second phase in which respiratory minute volume was further increased by an increase in the tidal volume; respiratory frequency was now slower than in the first phase but was still well above control values.3. The increase in respiratory minute volume during the first phase of the response was restricted almost entirely to the respiratory dead space; changes in blood CO(2) and pH were slight. In the second phase, respiratory minute volume showed a much greater increase, and a change of alveolar ventilation to about 5 times the control level resulted in severe respiratory alkalosis.4. Contrary to findings in cattle, the slower, deeper form of respiration could be elicited even with rectal temperature in the normal range. This change in respiration appears to be the result of either peripheral thermoreceptor function or mechanical demands of the respiratory system. The neglect of control of acid-base balance during the second phase indicates the existence of a dominant thermal stimulus or modification of respiratory control mechanisms.

Animals↗