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EVALUATION OF BRONCHOMOTOR AND PULMONARY VASOMOTOR ACTIVITY BY MEANS OF THE PERFUSED LIVING ANIMAL UNDER NEGATIVE PRESSURE VENTILATION
Author(s) -
de Burgh Daly I.,
Elsden S. R.,
Hebb Catherine O.,
Von Ludány G.,
Petrovskaia Barbara
Publication year - 1942
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1942.sp000859
Subject(s) - bronchoconstriction , medicine , vasomotor , anesthesia , perfusion , atropine , blood pressure , vagus nerve , lung , stimulation , contraction (grammar) , respiratory system , ventilation (architecture) , airway , mechanical engineering , engineering
1. A description is given of a method for blood perfusion of the entire living animal (dog) in which— ( a ) the heart ventricles are put out of action and the right auricle continues to beat and respond to vagal stimulation, its blood‐supply being intact; ( b ) the systemic and pulmonary blood‐flows, the gaseous content of the blood and the ventilation of the lungs are under separate control; ( c ) the respiratory control remains active during 3 hours' perfusion and the blood gases are maintained within normal limits; ( d ) vascular and bronchomotor responses to sensory nerve stimulations and drug injections are readily obtained; ( e ) the blood‐flows and pH values of the blood are rather lower than the corresponding values given by other workers for normal unanæsthetised dogs. 2. Stimulation of the caudal ends of the cervical vagosympathetic nerves causes changes of pulmonary arterial pressure which cannot be wholly accounted for by concomitant œsophageal contractions or by bronchomotor effects. The significance of these results in relation to pulmonary vasomotor nerve activity is discussed. 3. The bronchoconstriction due to excitation of the caudal end of the cervical vagus is potentiated by eserine and suppressed by atropine, and is also potentiated by ergotoxine in the non‐atropinised preparation. We wish to express our thanks to the Government Grants Committee of the Royal Society for defraying the expenses of the investigation by a grant to one of us (I. de B. D.).