Activity in vagal preganglionic motoneurones running to the heart provokes a generalized cardioinhibition producing a decrease not only in heart rate (chronotropy), but also in the rate of atrioventricular (AV) conduction (dromotropy), and in the force of myocardial contraction (inotropy). These effects are secondary to, and are contingent upon, excitation of ganglion cells located in clusters on the epicardium of the dorsum of the atria, closely apposed to the sites of entry of the major veins. There is evidence that in many of the larger mammalian species, the ganglion cells are clustered into discrete zones or 'fat pads' which project to different regions of the heart and selectively control cardiac function (Ardell & Randall, 1986; Randall et al. 1986a,b;Gatti et al. 1995Gatti et al. , 1997. Several recent studies have described the anatomy of the cardiac vagal ganglia in the rat (Pardini et al. 1987;Abrahamian et al. 1991;Klimaschewski et al. 1992;Burkholder et al. 1992;deSouza et al. 1996;Cheng et al. 1999;Cheng & Powley, 2000).Although the results of some of these studies suggest the existence of a functional topography (e.g. Pardini et al. 1987), there is little clear physiological or pharmacological evidence of this in the rat. In the only previous study of a possible functional organization of rat cardiac ganglia (Burkholder et al. 1992), a brief description is given of a partial selectivity revealed by differing responses to vagal stimulation following local infiltration of hexamethonium into identified fat pads.Data from preliminary experiments in this laboratory suggest that glutamate excitation of cardiac vagal preganglionic motoneurones from different regions of the rat nucleus ambiguus results in differential chronotropic and dromotropic effects (Sampaio et al. 2000). That this may result from a different termination pattern of preganglionic axons onto ganglion cells from different ganglionic clusters is supported by the finding of restricted ganglionic innervation from motoneurones labelled with anterograde Vagal cardioinhibition is exerted through a reduction not only in the heart rate but also in the rate of propagation of the cardiac action potential and in myocardial contractility. In several species, such effects can be produced independently by selective activation of ganglia in identified 'fat pads'. In this study we investigate differential control of heart rate and atrioventricular conduction by two ganglionic clusters in the rat, a species increasingly important in studies of cardiovascular control. Epicardial sites producing low-threshold changes in P-P and P-R interval of the ECG in an arterially perfused preparation were explored with concentric bipolar stimulating electrodes. Stimulation sites centred on two principal ganglia, the sinoatrial (SA) ganglion at the junction of the right superior vena cava and right atrium, and the atrioventricular (AV) ganglion at the junction of the inferior pulmonary veins and left atrium. Stimulation of the SA ganglion decreased heart rate in all ...

ObjectivesThis study aimed to investigate the obesity prevalence in a population of Brazilian firefighters and the association of central obesity (CO) with sociodemographic, occupational, life habits, fitness and health status variables.DesignCross-sectional study.SettingsThe data were collected during annual health inspections of firefighters from the Military Fire Service of the State of Espírito Santo, a state in Southeast Brazil.ParticipantsThe study encompassed 1018 active military firefighters. After exclusion criteria, 892 male firefighters were analysed.Primary and secondary outcome measuresThe collected data included: sociodemographic, occupational, lifestyle, fitness and health status variables. The associations between these factors and CO were calculated by adjusted OR through a hierarchical logistic regression model.ResultsObesity estimation by body mass index indicated that 48.65% of the firefighters were overweight and 10.99% were obese. Concerning the body fat percentage, 26.23% of the participants were considered obese, while 18.61% of the firefighters were considered centrally obese or at risk using the waist circumference measure. After adjusted OR analysis, CO was more likely associated with the age range of 50 to 59 years old (OR 2.93; 95% CI 1.05 to 8.14), low self-reported physical activity (OR 1.95; 95% CI 1.14 to 3.34), low cardiorespiratory fitness (OR 5.15; 95% CI 3.22 to 8.23), hyperglycaemia (OR 1.70; 95% CI 1.07 to 2.72) and hypertriglyceridaemia fasting status (OR 3.12; 95% CI 1.75 to 5.55).ConclusionsOur study identified an overall high prevalence of overweight and obese individuals in the examined firefighter population. Age and cardiovascular risk factors were directly associated with CO among the firefighters. Cardiovascular risk factors should be routinely inspected within the Brazilian firefighters’ corporations in order to improve the health condition and wellness of these workers. These endeavours will improve the performance of the services provided to the population.

Cardiopulmonary reflexes are activated via changes in cardiac filling pressure (volume-sensitive reflex) and chemical stimulation (chemosensitive reflex). The sensitivity of the cardiopulmonary reflexes to these stimuli is impaired in the spontaneously hypertensive rat (SHR) and other models of hypertension and is thought to be associated with cardiac hypertrophy. The present study investigated whether the sensitivity of the cardiopulmonary reflexes in SHR is restored when cardiac hypertrophy and hypertension are reduced by enalapril treatment. Untreated SHR and WKY rats were fed a normal diet. Another groups of rats were treated with enalapril (10 mg kg -1 day -1 , mixed in the diet; SHRE or WKYE) for one month. After treatment, the volume-sensitive reflex was evaluated in each group by determining the decrease in magnitude of the efferent renal sympathetic nerve activity (RSNA) produced by acute isotonic saline volume expansion. Chemoreflex sensitivity was evaluated by examining the bradycardia response elicited by phenyldiguanide administration. Cardiac hypertrophy was determined from the left ventricular/body weight (LV/ BW) ratio. Volume expansion produced an attenuated renal sympathoinhibitory response in SHR as compared to WKY rats. As compared to the levels observed in normotensive WKY rats, however, enalapril treatment restored the volume expansion-induced decrease in RSNA in SHRE. SHR with established hypertension had a higher LV/BW ratio (45%) as compared to normotensive WKY rats. With enalapril treatment, the LV/BW ratio was reduced to 19% in SHRE. Finally, the reflex-induced bradycardia response produced by phenyldiguanide was significantly attenuated in SHR compared to WKY rats. Unlike the effects on the volume reflex, the sensitivity of the cardiac chemosensitive reflex to phenyldiguanide was not restored by enalapril treatment in SHRE. Taken together, these results indicate that the impairment of the volume-sensitive, but not the chemosensitive, reflex can be restored by treatment of SHR with enalapril. It is possible that by augmenting the gain of the volume-sensitive reflex control of RSNA, enalapril contributed to the reversal of cardiac hypertrophy and normalization of arterial blood pressure in SHR.

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The cardioinhibitory effects of cardiac vagal motoneurons (CVMs) are mediated by activation of postganglionic neurons in the epicardial ganglia which have been shown to exert functionally selective effects on heart rate and atrioventricular conduction in the rat. Here we investigate whether CVMs producing these responses may occupy different rostrocaudal positions within the nucleus ambiguus. Excitation of CVMs was attempted by microinjections of glutamate into the nucleus ambiguus of an arterially perfused preparation in a grid extending over 2 mm in the rostrocaudal plane using the obex as a reference point. Microinjections were paired, one made during pacing to measure changes in atrioventricular conduction (P-R interval) independent of changes in heart rate and the other looking for changes in heart period (P-P interval) un-paced. Although evidence of a differential distribution was found in 7 cases, in the majority (13/20), sites producing maximal effects on both variables coincided. Maximal changes in atrioventricular conduction resulted from more rostral sites in 6 cases and from a more caudal site in only one. Overall, the ratio of the change in atrioventricular conduction to the change in heart rate for a given site was significantly greater 1 mm rostral to the obex than at either end of the test grid. We conclude that while CVMs controlling atrioventricular conduction are distributed with a peak somewhat rostral to those controlling heart rate in a number of animals, there is a significant overlap and much greater variability in this distribution in the rat than in cats and dogs.

The aim of the present study was to investigate the cardiovascular activity of Scorpaena plumieri venom in both in vivo and in vitro models. In anesthetized rats, doses of the venom (14-216 microg protein/kg) induced a transient increase in the mean arterial pressure. However at higher dose (338 microg protein/kg) this effect was followed by a sudden hypotension and the animal evolved to death. The heart rate was temporarily increased and followed by bradycardia using doses > or =108 microg/kg. In isolated rat hearts the crude venom (5-80 microg protein) produced dose-dependent positive ventricular chronotropic, inotropic, lusitropic and coronary vasoconstriction responses. Partial purification of an active fraction (CF, cardiovascular fraction) which reproduced the cardiovascular effects induced by crude venom on isolated hearts was achieved by conventional gel filtration chromatography. Adrenergic blockades, prazosin and propranolol, significantly attenuated these responses. The coronary vasoconstriction response to CF was also attenuated by chemical endothelium denudation. In conclusion, the data showed that S. plumieri fish venom induces disorders in the cardiovascular system. It also suggests that alpha(1) and beta-adrenergic receptors, and the vascular endothelium, are involved at least partially, in these cardiac effects.

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Anatomical studies have demonstrated the existence of purinergic P2 receptors in the nucleus ambiguus (NA), a site containing cardiac vagal motoneurons. However, very little is known about the functional role of these receptors in central cardiac vagal regulation. The aims of our study were to evaluate the following: (1) the blood pressure and heart rate responses following purinoceptor activation within the NA; (2) the role of purinoceptors and excitatory amino acid (EAA) receptors in mediating the cardiovascular responses evoked by ATP and l-glutamate stimulation of NA; and (3) the role of NA purinoceptors in mediating the cardiovascular responses of the Bezold-Jarisch reflex. In anaesthetized rats, microinjection of l-glutamate (5.0 nmol/50 nl) into the NA induced a marked and immediate onset bradycardia with minimal change in arterial pressure. Microinjection of ATP into the NA induced a dose-dependent (0.31-6.0 nmol/50 nl) bradycardia and pressor responses. It is noteworthy that the bradycardia occurred either before or simultaneously with a pressor response (when present), indicating that it was not a baroreceptor reflex mediated response due to the rise in arterial pressure. The pressor response was prevented by α 1 -adrenergic blockade with prazosin, whereas muscarinic blockade with methyl-atropine abolished the evoked bradycardia. Ipsilateral microinjection of PPADS (a P2 receptor antagonist; 500 pmol/100 nl) into the NA significantly attenuated the ATP-induced bradycardia but spared the pressor response. In contrast, PPADS in the NA had no effect on the l-glutamate-evoked bradycardic response. Ipsilateral injection of kynurenic acid (a non-selective EAA receptor antagonist; 10 nmol/50 nl) into the NA totally blocked the bradycardia induced by l-glutamate and partly attenuated the ATP induced bradycardia. Finally, both the depressor and the bradycardic responses of the Bezold-Jarisch reflex were attenuated significantly (P < 0.01 and P < 0.05, respectively) following bilateral microinjection of PPADS into the NA. These results identify ATP and purinergic P2 receptors within the ventrolateral medulla as excitatory to cardiovagal neurons. Additionally, our data show that P2 receptors within the ventrolateral medulla are integral to the cardiovascular responses of the Bezold-Jarisch reflex.