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 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.

Effects of anaesthesia on regional coronary control mechanisms.

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.

Recent views on integrated coronary control: significance of non-uniform regional control of coronary flow conductance.

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.

Baroreflex control of coronary blood flow varies regionally in awake dogs.

1. Baroreflex responses to changes in aortic pressure were measured simultaneously in three main coronary regions of awake dogs. 2. Pulsed Doppler flow probes were mounted at prior surgery on the right, circumflex and anterior descending coronary arteries; the animals were placed in complete heart block and the left ventricle was paced. After 2-4 weeks recovery, baroreflexes were evoked by inflating a balloon catheter placed in the mid-thoracic aorta via the femoral arteriotomy. Flow and pressure data were collected at rest, and during acute (8s) and steady-state (25s) baroreflex challenge. 3. Changing ventricular rate alone caused a fall in aortic pressure at low rates; however, over the range 60 to 180 b.p.m., circumflex and anterior descending coronary flow and conductance changed directly with ventricular rate, but right coronary flow and conductance remained unchanged. 4. Acute aortic pressure elevation increased flow at 8s in all beds at all rates. Conductance effects at 60 b.p.m. were negligible in all three beds, but rose at 100 and 180 b.p.m. in the right and circumflex beds. 5. Sustained aortic pressure elevation (25s) caused flow to return towards control in all beds ventricular rates, but in the right coronary at 60 b.p.m. flow fell below control. Conductance at this time was unchanged at all rates in the anterior descending bed, fell modestly in the circumflex, and decreased to below resting in the right coronary bed. 6. Baroreflex control of coronary flow and conductance thus varies between territories, and within territories, depending on ventricular rate. The right coronary bed appears to be regulated by a bidirectional, baroreflex-linked mechanism, which is functionally opposite in action to that found in most vascular beds.

Impedance cardiography for cardiac output measurement: an evaluation of accuracy and limitations.

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.

Central nervous system opiate and 5-hydroxytryptamine influences on baroreflex control of the coronary circulation.

The effect of intravenous infusion of fentanyl (an opiate receptor agonist, 0.55 microgram kg-1 min-1) on the control of the circumflex coronary circulation was examined in unsedated dogs at rest and during baroreceptor stimulation evoked by acute rises in aortic pressure (balloon inflation in thoracic aorta). Circumflex flow was measured using Doppler flow transducers in dogs with experimental complete heart block and with ventricles paced at a constant rate. Studies were also performed before and one week after intracisternal injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), to examine the role of CNS 5-hydroxytryptamine (5-HT) in any sympathetic vasoconstrictive effects. Fentanyl infusion caused after a few minutes a progressive rise in resting aortic pressure and a significant fall in circumflex conductance; circumflex flow usually fell. Atrial rate also fell. The gain of the baroreflex control of circumflex conductance was enhanced by fentanyl. One week after intracisternal 5,7-DHT, the gain of the baroreflex in each dog was diminished. When fentanyl was infused into these preparations, no consistent changes in resting atrial rate, aortic pressure and circumflex conductance could be observed, but all dogs showed a recovery of the coronary baroreflex gain towards values observed before intracisternal 5,7-DHT. These data suggest that the gain control of coronary baroreflexes is influenced by CNS opiate and 5-HT dependent mechanisms.

Thoracic resistivity for stroke volume calculation in impedance cardiography.

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.

Baroreflex control of coronary conductance in normotensive and renal hypertensive conscious dogs with complete heart block.

1. The autonomic and local control of the circumflex coronary bed evoked through acute rises in aortic pressure (aortic balloon inflation) was analysed in conscious, normotensive and hypertensive dogs in complete heart block with ventricles paced at 100 beats/min. 2. In normotensive dogs there was an initial rise (6-12 s) in circumflex conductance preceding a fall in conductance as aortic pressure increased and was sustained. The initial rise, but not the later fall, in circumflex conductance was partly due to a cholinoreceptor and partly due to alpha-adrenoreceptor mechanisms. Local constrictor mechanisms were responsible for the later fall in conductance. 3. The initial cholinoreceptor component of the rise in circumflex conductance is initiated through arterial baroreflex mechanisms. 4. The initial autonomic mechanisms regulating circumflex conductance appear to be absent in renal hypertension. 5. The absence of the transient autonomic rise in circumflex flow and conductance in response to rapid elevations in aortic pressure in certain forms of hypertension, e.g; during tachyarrhythmias and behavioural disturbances, may result in myocardial ischaemia when it is least appropriate.

Leptospiral agglutinins in dogs in Sydney.

From June 1971 to June 1972, sera from 600 dogs in Sydney were tested for leptospiral agglutinins by a rapid slide agglutination method. The end-point titre was taken at 50 percent agglutination of the live organisms. Forty-one samples (6.8 percent) had a significant leptospiral titres (100 or greater) and 5 of these reacted to 2 serotypes. Thirty serums (5 percent) contained agglutinins against L. copenhageni, and 6 (1 percent) against L. pomona, while a few samples reacted against hardjo, tarassovi, australis, grippotyphosa or pyrogenes serotypes. No significant titres were found to L. canicola, L. hebdomadis, L. autumnalis or L. bataviae.