SUlMMARY1. In anaesthetized cats tetanic contraction of the hind-limb muscles, elicited by stimulating the ventral roots L 6-S 1, caused a rise of arterial -blood pressure, usually accompanied by small increases in heart rate and pulmonary ventilation: in decerebrate cats, all components of the response were much increased.2. With tetani of different strengths, obtained by stimulating with different intensities at the same frequency, the pressor response increased with increasing tension.3. When muscle contraction had been abolished by gallamine, or when dorsal roots L 6-S I had been sectioned, ventral root stimulation no longer caused a pressor response. The response is therefore a reflex, initiated in the exercising limb.4. The pressor response was not affected by section of all articular nerves to knee and ankle joints, or by section of the vagi. The stimulus therefore originates in the contracting muscles alone.5. The pressor response is potentiated by occluding the circulation through the working muscles. Reasons are discussed for concluding that the stimulus is chemical rather than mechanical, and that the 'metabolic receptors' for this exercise reflex are the free endings of group III and IV sensory nerve fibres located around the blood vessels.

This review explores the fundamental neuranatomical and functional bases for integration of the respiratory and cardiovascular systems in vertebrates and traces their evolution through the vertebrate groups, from primarily water-breathing fish and larval amphibians to facultative air-breathers such as lungfish and some adult amphibians and finally obligate air-breathers among the reptiles, birds, and mammals. A comparative account of respiratory rhythm generation leads to consideration of the changing roles in cardiorespiratory integration for central and peripheral chemoreceptors and mechanoreceptors and their central projections. We review evidence of a developing role in the control of cardiorespiratory interactions for the partial relocation from the dorsal motor nucleus of the vagus into the nucleus ambiguus of vagal preganglionic neurons, and in particular those innervating the heart, and for the existence of a functional topography of specific groups of sympathetic preganglionic neurons in the spinal cord. Finally, we consider the mechanisms generating temporal modulation of heart rate, vasomotor tone, and control of the airways in mammals; cardiorespiratory synchrony in fish; and integration of the cardiorespiratory system during intermittent breathing in amphibians, reptiles, and diving birds. Concluding comments suggest areas for further productive research.

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Sympathetic stimulation increased maximum slope of restitution and electrical alternans but decreased ERP and VF threshold whilst vagus nerve stimulation had opposite effects. The interaction between action potential duration and beat-to-beat interval may play an important role in the autonomic modulation of VF initiation.

It is well recognised that stimulation of the sympathetic nervous system exerts a positive chronotropic effect on the heart, speeding the rate of discharge of the intrinsic pacemaker, which is usually the sino-atrial node, whilst parasympathetic stimulation has opposite effects (Levy & Zieske, 1969). Atrioventricular (AV) conduction is also affected, with sympathetic stimulation speeding conduction (positive dromotropy) and parasympathetic stimulation delaying conduction (negative dromotropy) (Warner et al. 1986). Autonomic stimulation also affects myocardial mechanical performance but the cause of this effect is less straightforward. Whilst it is generally accepted that sympathetic stimulation exerts a positive inotropic effect on the heart with increased contractility, the effect of vagal stimulation on cardiac mechanical performance is less well defined (Xenopoulos & Applegate, 1994). At the molecular level, the sympathetic and parasympathetic nervous systems modulate cardiac function by means of the neurotransmitters, catecholamines and acetylcholine, respectively (Levy, 1997), interacting with receptors located on the sarcolemma of the cardiac myocyte. The cellular mechanisms by which stimulation of the autonomic nervous system affect the various processes involved in excitation-contraction coupling have not been fully investigated. The ability to investigate how nerves influence these mechanisms is limited by the type of preparation available.Experimental data relating to the effect of autonomic nerve activity on cardiac function have been obtained in vivo where direct stimulation of autonomic nerves may be confounded by influences from circulating hormones and haemodynamic reflexes. On the other hand, in vitro studies on isolated heart preparations have used exogenous pharmacological agents and chemical analogues, such as isoprenaline, to mimic stimulation of autonomic nerves. The disadvantage of both of these approaches may be overcome by an isolated heart preparation in which both sets of autonomic nerves are intact and available for stimulation. In this paper we describe a novel, isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation that allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. To demonstrate the viability of the preparation, we have described the effects of direct stimulation of the sympathetic outflow and vagus nerves on the intrinsic heart rate and AV conduction at varying stimulus strengths and frequencies.Effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart -a novel model of isolated Langendorff perfused rabbit heart with intact dual autonomic innervation A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n = 10) had baseline h...

The Olympic biathlon is a very demanding physical event that requires high oxygen delivery, good cross-country skiing skills and skilful use of a rifle. Like all high-performance endurance athletes, high cardiac vagal tone is a characteristic and extends the range over which cardiac output can increase. In the biathlete, however, the enhanced vagal control of the heart also allows a strategy for better control of stability needed for accurately firing a rifle at the end of each lap of the race. The role of endurance training, central command, reflexes from muscle, and of the carotid-cardiac baroreceptor reflex in changing vagal tone during intense exercise and recovery is discussed.

It is now well accepted that the sympathetic nervous system responds to specific afferent stimuli in a unique non-uniform fashion. The means by which the brain transforms the signals from a single type of receptor into an appropriate differential sympathetic output is discussed in this brief review. The detection of and response to venous filling are used for illustration. An expansion of blood volume has been shown in a number of species to increase heart rate reflexly via sympathetic nerves and this effect is primarily an action of volume receptors at the venous-atrial junctions of the heart. Stimulation of these volume receptors also leads to an inhibition of renal sympathetic nerve activity. Thus the reflex response to an increase in plasma volume consists of a distinctive unique pattern of sympathetic activity to maintain fluid balance. This reflex is dependent on neurones in the paraventricular nucleus (PVN). Neurones in the PVN show early gene activation on stimulation of atrial receptors, and a similar differential pattern of cardiac sympathetic excitation and renal inhibition can be evoked by activating PVN neurones. Cardiac atrial afferents selectively cause a PVN GABA neurone-induced inhibition within the PVN of PVN spinally projecting vasopressin-containing neurones that project to renal sympathetic neurones. A lesion of these spinally projecting neurones abolishes the reflex. With regard to the cardiac sympathetics, there is a population of PVN spinally projecting neurones that selectively increase heart rate by the release of oxytocin, a peptide pathway that has no action on renal sympathetic outflow. In heart failure the atrial reflex becomes blunted, and evidence is emerging that there is a downregulation of nitric oxide synthesis and reduced GABA activity in the PVN. How this might give rise to increased sympathetic activity associated with heart failure is briefly discussed.

There is continuing belief that cardiac parasympathetic postganglionic fibres are sparse or absent from the ventricles. This review of the literature shows that the supposition is a myth. Early studies considered that fine silver-stained fibres coursing amongst ventricle myocardial cells were most likely cardiac parasympathetic postganglionic fibres. The conclusions were later supported by acetyl cholinesterase staining using a method that appeared not to be associated with noradrenaline nerve fibres. The conclusion is critically examined in the light of several recent histological studies using the acetyl cholinesterase method and also a more definitive technique (CHAT), that suggest a widespread location of parasympathetic ganglia and a relatively dense parasympathetic innervation of ventricular muscle in a range of mammals including man. The many studies demonstrating acetylcholine release in the ventricle on vagal nerve stimulation and a high density of acetylcholine M 2 receptors is in accord with this as are tests of ventricular performance from many physiological studies. Selective control of cardiac functions by anatomically segregated parasympathetic ganglia is discussed. It is argued that the influence of vagal stimulation on ventricular myocardial action potential refractory period, duration, force and rhythm is evidence that vagal fibres have close apposition to myocardial fibres. This is supported by clear evidence of accentuated antagonism between sympathetic activity and vagal activity in the ventricle and also by direct effects of vagal activity independent of sympathetic activity. The idea of differential control of atrial and ventricular physiology by vagal C and vagal B preganglionic fibres is examined as well as differences in chemical phenotypes and their function. The latter is reflected in medullary and supramedullary control. Reference is made to the importance of this knowledge to understanding the normal physiology of cardiac autonomic control and significance to pathology.