In the resting awake dog a continuous-wave Doppler flow transducer on the right bronchoesophageal artery inscribes a sharp early systolic spike and low flow in late systole and throughout diastole, indicating a highly resistive bed. An analysis of autonomic factors using intravenous, cumulative, and randomly applied cholinoceptor, beta 1- and beta 2-adrenoceptor, and alpha 1- and alpha 2-adrenoceptor antagonists indicates that the low vascular conductance is due to cholinoceptor and alpha 1- and alpha 2-adrenoceptor effects in a ratio 3.6:1. No beta-adrenoceptor tone is present. Sighing behavior invokes a transient (< 2 s) fall in intrapleural pressure (and thus rise in bronchovascular transmural pressure) of 10-30 mmHg, which is followed by a two- to threefold increase over 30 s in bronchial flow and conductance, an effect simulated in 50% of dogs when bronchovascular transmural pressure is acutely raised and maintained over 40-60 s by inflating an intra-aortic balloon distal to the origin of the bronchial artery. Autonomic blockade has no effect on bronchovascular dilatation evoked either by sighing or by balloon inflation. It is concluded that, in the resting bronchial circulation, there exists strong cholinoceptor and alpha-adrenoceptor-based vasoconstrictor activity which can be overpowered by strong nonadrenergic noncholinergic local vasodilator reflexes evoked by sudden changes in intrathoracic transmural pressure possibly acting on stretch-sensitive sensory nerve endings containing substance P, calcitonin gene-related peptide, and neurokinins. The tonic vasoconstrictor but not the sigh-evoked vasodilator effects are sensitive to pentobarbital sodium anesthesia.

The Kubicek thoracic cylinder model of impedance cardiography (IC) for measuring beat-by-beat stroke volume (SV) was evaluated in controlled studies using the electromagnetic flowmeter (FM) as the reference technique. Assuming the validity of the Kubicek equation for stroke volume calculation, IC stroke volume was found to be a linear function of EM values at any one haematocrit over a wide range of SV, but the slope of the relationship fell as haematocrit fell. Experiments using the same equation in dogs, in which blood resistivity in vivo (rho tau) was made the dependent variable, and the EM-derived value was used for stroke volume, showed that rho tau was almost constant over a wide range of haematocrits. These findings were supported by studies in man and rabbit where Fick and thermodilution-derived values were used for stroke volume. When these data were applied to normotensive and hypertensive human subjects with normal hearts and lungs in controlled studies at rest, during tilting, with drug therapy and on exercise, IC measured stroke volume and cardiac output with a variability at least as good as the 9-11% acceptable for clinical use. This conclusion applied to thoracic configurations of different sizes and shapes from adult man to the neonate. In chronic disease states, while assessments of relative changes are valuable, absolute data are questionable. Further research is required under these conditions, as it is also for other models of IC, which are based on different assumptions.

Blood resistivity (rho) values used in the Kubicek formula for stroke volume (SV) calculation by impedance cardiography are bench derived and do not take into account complex blood velocity movements and dynamic hematocrit changes in systole. In this study, the relevance of rho has been questioned. Thoracic resistivity (rho tau) has been calculated in dogs from the rearranged Kubicek formula: rho tau = (SV . ZO2)/(L2 dZ/dtmax.T), where SV was measured by the electromagnetic flowmeter (EM). Hematocrit (Hct) in the dog was varied by hemorrhage and infusion. In contrast to the direct and exponential bench rho-Hct relationship, rho tau varies inversely with Hct, but by no more than +6.3 omega . cm (at Hct 26%) and -11.8 omega . cm (at Hct 66%) about a mean rho tau of 135 +/- 1.0 omega . cm (at Hct 40%). Impedance SV calculated using rho tau over a wide range of SV bears a linear relationship to EM values with a 95% prediction limit for a single SV estimate of +/- 0.84 about a mean value of 26.9 ml. The findings suggest that rho tau is virtually constant during a variety of physiological disturbances.

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, alpha-adrenoceptors and beta-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 30s (peak at 8s). The vascular changes are absent in parent intercostal and brachial beds.

1. Previous work from this laboratory and others has shown that powerful autonomic influences modulate coronary flow. In particular, the parasympathetic nervous system produces vasodilatation when activated by baroreceptors via the vagus nerve. 2. Differences exist in baroreflex coronary vasodilator mechanisms among the right, circumflex and anterior descending coronary vascular beds in the awake chronically instrumented dog. 3. Our hypothesis is that neurogenic acetylcholine acting from the adventitial side and endothelial nitric oxide from the luminal aspect of coronary smooth muscle compete with powerful intrinsic myogenic constrictor mechanisms to regulate regional flow conductance. 4. There is also increasing evidence that heterogeneity of control systems exists in different-sized coronary vessels within an individual coronary vascular bed. 5. It is concluded that coronary vessels in vascular beds can no longer be assumed to respond in a uniform manner to neural, myogenic, metabolic or humoral factors. 6. These new perspectives of regional control mechanisms have important implications for understanding pathophysiological mechanisms inducing and sustaining tachyarrhythmias involved in ischaemic heart disease.

1. The regional coronary circulation is under the control of local metabolic and myogenic factors, but is also influenced by autonomic systems, including sympathetic and parasympathetic nerves. 2. General anaesthetic agents influence not only local control through changes in metabolic demand, but also neural control through suppression of autonomic influence. 3. Anaesthetic agents have differing effects on reflex control systems, which are dependent on coronary territory and ventricular rate. 4. Effects of anaesthesia should be taken into account when interpreting results in anaesthetized models of coronary control.

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