Heart-Lung interactions: The sigh and autonomic control in the bronchial and coronary circulations

1. The Darwin hypothesis that human and animal expressions of emotion are t he product of evolution and are tied to patterns of autonomic activity spec ified 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 underl ying sigh-induced changes in the bronchial and coronary circulations. 3. Awake dogs were prepared using pulsed ultrasonic flow probes on the righ t bronchial artery, parent intercostal artery and brachial artery, or on th e right, circumflex and anterior descending coronary arteries. Central veno us (CVP) and arterial pressures (AP) were measured; heart rate and flow con ductances were derived. Three spontaneous sighs were monitored before and d uring random blockade of individual and combinations of cholinoceptors, alp ha -adrenoceptors and beta -adrenoceptors using methscopolamine, phentolami ne and propranolol infusions. The data were subject to a 2(3) factorial ana lysis. 4. A spontaneous sigh is marked by a transient fall and return (< 3 s) in C VP of 18 mmHg (from 4 +/-1 to -14 +/-2 mmHg), usually followed by apnoea la sting 23 +/-2 s. There is an immediate tachycardia and small rise in AP (ph ase 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 thr ee-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 i s due to cholinoceptor withdrawal and positive beta -adrenoceptor plus beta -adrenoceptor/cholinoceptor interaction activity, in the ratio 1.75 : 1. T he phase 2 bradycardia is entirely cholinoceptor. However, only 17% of the peak rise in bronchial conductance is due to alpha-/beta -adrenoceptor inte ractions (sympathetic withdrawal); 83% is due to non-cholino/adrenoceptor m echanisms. In a separate four animals, the total sigh-induced conductance r ise 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 e ffects may be an efferent nitrergic component of an arterial chemoreceptor reflex induction of sighing. An alternative hypothesis invokes local stretc h-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 hypothes is.