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Heart–Lung Interactions: The Sigh And Autonomic Control In The Bronchial And Coronary Circulations
Author(s) -
Porges William L,
Hennessy Edward J,
Quail Anthony W,
Cottee David BF,
Moore Peter G,
McIlveen Stephen A,
Parsons Gibbe H,
White Saxon W
Publication year - 2000
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2000.03370.x
Subject(s) - medicine , phentolamine , cardiology , heart rate , bradycardia , anesthesia , tachycardia , propranolol , blood pressure
SUMMARY 1. The Darwin hypothesis that human and animal expressions of emotion are the product of evolution and are tied to patterns of autonomic activity specified to progress the emotion remains under challenge. 2. The sigh is a respiratory behaviour linked with emotional expression in animals and humans from birth to death. The aim of the present study was to explore Darwin’s hypothesis with respect to tied autonomic activity underlying sigh‐induced changes in the bronchial and coronary circulations. 3. Awake dogs were prepared using pulsed ultrasonic flow probes on the right bronchial artery, parent intercostal artery and brachial artery, or on the right, circumflex and anterior descending coronary arteries. Central venous (CVP) and arterial pressures (AP) were measured; heart rate and flow conductances were derived. Three spontaneous sighs were monitored before and during random blockade of individual and combinations of cholinoceptors, α ‐adrenoceptors and β ‐adrenoceptors using methscopolamine, phentolamine and propranolol infusions. The data were subject to a 2 3 factorial analysis. 4. A spontaneous sigh is marked by a transient fall and return (< 3 s) in CVP of 18 mmHg (from 4 ± 1 to –14 ± 2 mmHg), usually followed by apnoea lasting 23 ± 2 s. There is an immediate tachycardia and small rise in AP (phase 1) then, during apnoea, bradycardia and a fall in AP (phase 2). During phase 2, bronchial and coronary blood flow and conductance rise two‐ to three‐fold over 30 s (peak at 8 s). The vascular changes are absent in parent intercostal and brachial beds. 5. The phase 1 tachycardia is entirely cholino/adrenoceptor in origin and is due to cholinoceptor withdrawal and positive β ‐adrenoceptor plus β ‐adrenoceptor/cholinoceptor interaction activity, in the ratio 1.75 : 1. The phase 2 bradycardia is entirely cholinoceptor. However, only 17% of the peak rise in bronchial conductance is due to α ‐/ β ‐adrenoceptor interactions (sympathetic withdrawal); 83% is due to non‐cholino/adrenoceptor mechanisms. In a separate four animals, the total sigh‐induced conductance rise is virtually abolished by prior infusion of N G ‐nitro‐ L ‐arginine methyl ester. 6. Therefore, the mechanism of the sigh‐induced bronchial and conductance effects may be an efferent nitrergic component of an arterial chemoreceptor reflex induction of sighing. An alternative hypothesis invokes local stretch‐sensitive C‐fibre sensory nerve endings releasing substance P–calcitonin gene‐related peptide–neurokinin A in response to cardiovascular distortion secondary to the sudden transmural pressure rise when intrapleural pressure falls. Whatever the case, these effects and the cholino/adrenoceptor base for the heart rate and broncho/coronary changes support the Darwin hypothesis.