Head-torso coordination in police officers wearing loaded tactical vests during running.

BACKGROUND: The influence of load carriage in operational police officers is not well understood despite a relatively high injury rate. Assessing load related changes in head and torso coordination may provide valuable insight into plausible injury mechanisms. RESEARCH QUESTION: Do typical police tactical vest loads alter head and torso coordination during running? METHODS: Thirty-eight UK police officers ran at a self-selected pace (>2 ms-1) on a non-motorised treadmill in four vest load conditions (unloaded, and low, high and evenly distributed loads). Peak head and torso tilt, and peak vest displacement were compared between all four conditions. Timings between vest and torso change of direction were compared between the three loaded conditions. The coupling angle between the head and torso calculated using modified vector coding were compared between unloaded and each loaded conditions using Statistical Parametric Mapping. RESULTS: No significant differences were found between conditions for peak head or torso tilt alone (p > 0.05). Loading equipment low on the vest led to significantly greater mediolateral vest displacements (38 mm) away from the torso than a high (34 mm) or evenly distributed (30 mm) conditions. The vest was found to change direction vertically before the torso in the anterior-posterior direction, and then influence torso motion. The loaded conditions changed the head-torso coupling from in-phase (with head-dominancy) to anti-phase (with torso dominancy) between 55% and 77% stance. Anti-phase with a relatively stationary head and the torso rotating forward likely places a greater concentric demand on the posterior neck muscles relative to unloaded running. SIGNIFICANCE: Current tactical vest designs allow significant extra displacement of load away from the body during running, altering coordination at the head and torso.

Effects of insulation on the temperature within farrowing huts and the weaning weights of piglets reared on a commercial outdoor pig unit.

The air temperatures inside uninsulated and insulated huts were recorded on an outdoor pig unit in the south of England between September 1997 and September 1998, and the herd's production parameters were also recorded. During the summer the temperatures inside some of the uninsulated huts exceeded 45 degrees C, but the temperatures inside the insulated huts were lower and fluctuated less. Despite the high temperatures, the weaning weight of piglets reared in the uninsulated huts were often higher than those of the piglets reared in the insulated huts, possibly as a result of the higher mortality of small piglets in the uninsulated huts, especially during the winter. The weaning weights of the piglets were higher during the summer.

A study of the availability of emergency dental services in Birmingham.

The study reported here was undertaken to ascertain the efficiency and adequacy of the Emergency Dental Services in Birmingham. Even after the inception of the new contract in 1990, too many registered patients appeared to be attending the Birmingham hospitals or contacting their doctors for dental treatment which could and should have been provided by their own dentist. Overall, the results showed that the service provided by Birmingham dentists before 10.30 p.m. is more than adequate, and that most dentists are acting in accordance with the FHSA guidelines relating to the new contract.

Vascular alpha-1 adrenergic receptor subtypes in the regulation of arterial pressure.

Alpha 1 (alpha 1)-adrenoceptors can be found at numerous end organs in the autonomic nervous system, especially vascular smooth muscle. The tonic sympathetic activation of vascular alpha 1-adrenoceptors maintains vascular resistance and is vital to the regulation of arterial pressure. Recent evidence clearly demonstrates that alpha 1-adrenoceptors are a heterogenous class of receptors and that each subtype may subserve specific cardiovascular functions. Elucidation of the physiological role of each subtype in the regulation of vascular resistance and arterial pressure will enhance our understanding of the cardiovascular system and may facilitate the development of therapeutics with improved efficacy and tolerability.

Role of vascular alpha-1 adrenoceptor subtypes in the pressor response to sympathetic nerve stimulation in the pithed rat.

Previous studies suggest that systemic arterial pressure is tonically regulated by the interaction of peripheral sympathetic nerves with vascular alpha-1A adrenoceptors in vivo. To explore this relationship further, the present study examined the inhibitory effect of selective alpha-1A [5-methylurapidil (5-MU) and nifedipine (NIF)] and alpha-1B [chloroethylclonidine (CEC)] antagonists on the pressor response to electrical stimulation (ES) of the spinal cord in pithed rats. Diastolic pressure changes were measured in the presence of 5-MU or CEC and compared with control responses. Pretreatment with 5-MU (0.5 mg/kg i.v.) significantly suppressed the ES pressor response (50-80% inhibition) at all stimulation frequencies. Likewise, NIF (inhibitor of calcium influx associated with alpha-1A adrenoceptor activation) selectively inhibited the pressor response to ES to the same degree as did 5-MU. CEC (25 mg/kg i.v.) also significantly shifted the ES response curve; however, this effect was mediated by activation of presynaptic alpha-2 receptors on sympathetic terminals because prior administration of idazoxan (5 mg/kg) prevented the inhibitory effect of CEC. Based on the potent inhibitory effects of 5-MU and NIF on the ES pressor response in the pithed rat, it was concluded that vascular alpha-1A adrenoceptors reside in the synaptic region of neurovascular junction where they are primarily activated by neuronal norepinephrine release.(ABSTRACT TRUNCATED AT 250 WORDS)

A hemodynamic excitatory response to veratridine in the in utero lamb.

The inhibitory hemodynamic effects of the Bezold-Jarisch reflex in the adult animal, which play a role in the response to disease states, are elicited by veratridine and are mediated by vagal afferents. We tested whether the reported excitatory response to veratridine in the fetal animal may be caused by a maturational phase in the Bezold-Jarisch response. The effects of proprananol and atropine on the hemodynamic response to veratridine were examined at 124-141 d (mean, 133 d) of gestation in 11 fetal lambs instrumented long-term (instrumentation, 111-129 d of gestation). Seven lambs had intact vagal nerves, and four had bilateral cervical vagotomies. Veratridine injected into the superior vena cava (0.3 to 2.8 micrograms/kg) and the left atrium (0.2 to 0.8 microgram/kg) increased heart rate, arterial pressure, and left ventricular output, with the responses to left atrial injections occurring more rapidly. Propranolol markedly inhibited the increase in arterial pressure; atropine had no effect. Neither carbocaine, perfused around the cervical vagi, nor bilateral transection of the vagal nerves altered the hemodynamic excitatory response to veratridine. These findings demonstrate that the fetal excitatory response to veratridine is not mediated by vagal afferents, indicating the Bezold-Jarisch reflex does not undergo a maturational change from an excitatory reflex to an inhibitory one and suggesting the maturational loss of a sympathetically mediated hemodynamic reflex.

Cardiovascular effects of chloroethylclonidine, an irreversible alpha 1B-adrenoceptor antagonist, in the unanesthetized rat: a pharmacological analysis in vivo and in vitro.

The role of vascular alpha 1B-adrenergic receptors in the regulation of arterial pressure (MAP) and heart rate (HR) was examined by assessing the effect of i.v. chloroethylclonidine (CEC; irreversible alpha 1B antagonist) in unanesthetized, normotensive Long-Evans rats. MAP, HR and the pressor response to i.v. phenylephrine (PE) were monitored for 24 hr after saline or CEC (15 mg/kg and 25 mg/kg) injection. Neither i.v. saline nor CEC affected MAP or HR throughout the course of the study, yet the PE response was maximally inhibited (> 75% at 15 min) by both doses of CEC. The PE response recovered by 2 hr at the 15-mg/kg dose but remained inhibited up to 4 hr at 25 mg/kg. At 24 hr, all cardiovascular parameters returned to control levels. CEC (100 microM, 30 min) produced irreversible blockade of norepinephrine-induced contractions in rat aortic rings; prazosin (10 nM) and sodium thiosulphate (1 mM, a reagent that inactivates aziridinium ions) reversed CEC's inhibitory effect. Precyclized CEC and its hydrolysis product beta-hydroxyethylclonidine (beta-HEC) poorly antagonized aortic alpha 1B-receptors. Ex vivo analysis of aortic rings from saline and CEC-treated rats showed that PE-induced contractions were shifted to the right and maximally depressed in a dose-dependent manner after 24 hr. These results suggest that 1) CEC produces long lasting blockade of alpha 1B-adrenoceptors in vitro and in vivo via formation of an aziridinium ion intermediate and 2) vascular alpha 1B-adrenoceptors are not coupled to the tonic physiological regulation of MAP in the rat.

Intracoronary PGE2 and veratrine inhibits renin release in conscious dogs via chemosensitive ventricular afferents.

1. Prostaglandins (PG) and veratrum alkaloids stimulate ventricular sensory receptors with non-myelinated vagal afferents and mediate inhibitory circulatory responses. 2. The present study in conscious instrumented dogs was carried out to determine the effects of intracoronary artery infusions of veratrine (Ver-IC) and PGE2 (PGE2-IC) on plasma renin activity (PRA). 3. A 15-20 mmHg decrease in arterial pressure was produced during Ver-IC (0.2-0.8 micrograms/kg per min) and PGE2-IC (10-50 ng/kg per min), but there was no change in PRA or heart rate. 4. In contrast, significant increases in PRA (+3.51 +/- 0.37 ng angiotensin I/mL per h; P less than 0.01) and heart rate (+38.5 +/- 6.2 beats/min; P less than 0.001) were elicited in response to a 15-20 mmHg decrease in arterial pressure produced by intravenous infusions of nitroprusside. 5. Pharmacological blockade of afferent fibres in the pericoronary region of the left main coronary artery during Ver-IC resulted in significant hypotension-induced increases in PRA (P less than 0.001) and heart rate (P less than 0.001), thus removing the inhibitory influence of chemosensitive ventricular afferents. 6. Therefore, intracoronary veratrum alkaloids and prostaglandins inhibit hypotension-induced increases in PRA and heart rate in the conscious dog. This is mediated by chemosensitive receptors located in the left ventricular myocardium along with afferent nerves in the pericoronary region and cervical vagi.

Intracoronary veratrine and acute aortic stenosis modify renal responses to hypotension in conscious dogs.

The present study was undertaken to determine whether intracoronary (left circumflex) veratrine (ICV) infusions and increases in left ventricular (LV) systolic pressure influence renal circulatory and excretory function in chronically instrumented conscious dogs (n = 19). Thirty minutes of ICV infusions decreased arterial pressure by 15-20 mmHg, but heart rate, urine flow, sodium excretion, and free water clearance did not change. Intravenous nitroprusside infusions, which also lowered arterial pressure by 15-20 mmHg, increased heart rate while urine flow, sodium excretion, and free water clearance were significantly decreased. Heart rate and renal excretory function also did not change during a 15- to 20-mmHg decrease in arterial pressure when LV systolic pressure was simultaneously raised to approximately 170 mmHg by ascending aortic occlusion. The topical application of a local anesthetic in the region of the left main coronary artery abolished the Bezold-Jarisch reflex and the attenuation of hypotension-induced salt and water retention and tachycardia by ICV. Renal plasma flow and glomerular filtration rate were not altered during any of the above experimental treatments. These results suggest that in the conscious dog chemical and mechanical stimulation of LV sensory receptors with afferents in the pericoronary region can modulate the neurohumoral reflex control of renal excretory function independent of local filtration effects.

Reflex inhibition of plasma renin activity by increased left ventricular pressure in conscious dogs.

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.(ABSTRACT TRUNCATED AT 250 WORDS)

Vagal afferents inhibit the antidiuresis and antinatriuresis secondary to bilateral carotid occlusion in the chloralose-anesthetized dog.

It has been reported that bilateral carotid occlusion (BCO) does not alter renal excretory function in conscious dogs on a high-salt diet with intact vagi provided renal perfusion pressure (RPP) is held constant. In contrast, low carotid sinus pressures in chloralose-anesthetized dogs with severed vagi elicit significant reductions in renal excretory function which were mediated by renal sympathetic nerves. The purpose of the present study was to investigate the influence of BCO on renal function in chloralose-anesthetized, volume expanded dogs with and without intact cervical vagi and with RPP held constant. A total of 10 dogs, volume expanded with hypotonic saline, were prepared to measure systemic arterial pressure (SAP), carotid sinus pressure (CSP), RPP, and urine flow. With the cervical vagi intact, BCO elicited an increase in SAP from 132 +/- 4 mm Hg to 172 +/- 5 mm Hg (p less than 0.01). This was associated with significant and paradoxical increases in urine flow (+35%), sodium excretion (+63%), osmolar clearance (+32%), and free water clearance (+33%). These changes were also accompanied by small but significant increases in ERBF (+11%) and GFR (+12%). Bilateral cervical vagotomy alone (Vx) increased SAP (129 +/- 6 mm Hg to 146 +/- 5 mm Hg, p less than 0.05). Urine flow and free water clearance were decreased but sodium excretion and osmolar clearance were increased. No change in ERBF or GFR was measured. BCO after Vx elicited a greater increase in SAP as compared to BCO alone (194.5 +/- 6.2 mm Hg) which was accompanied by significant decreases in urine flow (-60%), sodium excretion (-55%), osmolar clearance (-43%), ERBF (-13%), and GFR (-19%). Therefore, the results of this study demonstrate that the contrasting influences of BCO on renal function reported previously in conscious and anesthetized animal models may be due to the presence or absence of the inhibitory influences of afferent fibers contained in the cervical vagi, probably cardiac in origin.

Use of a counterpulsation balloon as a substitute for the pulmonic valve: a new application.

An inflatable, 3-ml balloon positioned within the distal right ventricular outflow tract was used to restore pulmonic valve function in 8 dogs that had undergone open-chest valvectomy. Balloon inflation and deflation were accomplished with a counterpulsation console. Valvectomy produced loss of the pulmonic incisura, a decrease in pulmonary artery diastolic pressure (PADP; mean +/- standard error) (9.5 +/- 1.3 versus 4.4 +/- 0.6 mm Hg, p less than 0.01), and an increase in pulmonary artery pulse pressure (PAPP) (8.6 +/- 0.7 versus 19.1 +/- 1.9 mm Hg, p less than 0.01) without significantly affecting forward cardiac output (CO) (1,750 +/- 110 versus 1,880 +/- 230 ml/min, p is not significant). Properly timed counterpulsation restored the pulmonic incisura, raised the PADP from 6.1 +/- 0.8 to 9.5 +/- 0.8 mm Hg (p less than 0.01), lowered the PAPP from 15.1 +/- 1.4 to 10.6 +/- 1.0 mm Hg (p less than 0.01), and raised the forward CO from 1,850 +/- 260 to 1,920 +/- 260 ml/min (p less than 0.01). The injection of glass beads, 40 to 150 microns in diameter, into the right ventricular outflow tract increased pulmonary vascular resistance from 383 +/- 87 to 730 +/- 150 dyne . sec cm-5 (p less than 0.05) and decreased forward CO from 1,850 +/- 260 to 1,570 +/- 230 ml/min (p less than 0.05). Following this injection, counterpulsation again restored the pulmonic incisura, raised the PADP from 9.3 +/- 1.4 to 16.0 +/- 1.8 mm Hg (p less than 0.01), lowered the PAPP from 25.0 +/- 2.5 to 18.2 +/- 2.5 mm Hg (p less than 0.01), and raised the forward CO from 1,570 +/- 230 to 1,720 +/- 220 ml/min (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Imparied atrial receptor modulation or renal nerve activity in dogs with chronic volume overload.

Left atrial receptors with vagal afferents are reset and become less sensitive in dogs with chronic high output congestive heart failure (Zucker et al J Clin Invst 1977;60:323). We determined if the normal reflex inhibition of renal sympathetic nerve activity (RNA) which occurs in response to left atrial distension is altered in dogs with chronic volume overload produced by an aorto-vena caval fistula (AVF). In addition, we examined the ability of the arterial baroreflex to alter RNA. In normal dogs, left atrial distension decreased RNA by 6.8 +/- 1.8% per mmHg change in left atrial pressure (LAP). After carotid sinus denervation (CSD), this inhibition was increased to 10.9 +/- 1.4% per mmHg change in RNA in response to left atrial distension. Vagotomy completely abolished any change in RNA in response to left atrial distension. In contrast, dogs with chronic AVF's demonstrated an increase in RNA in response to left atrial distension by 4.5 +/- 3.9% per mmHg change in LAP. The response of the AVF dogs was significantly different from the normal dogs (P less than 0.005). This was also the case after CSD. Loading and unloading of the arterial baroreceptors with norepinephrine and nitroprusside demonstrated that the modulation of RNA by arterial baroreceptors was similar in AVF dogs compared with normal dogs. The present study demonstrates that chronic volume overload results in a decrease in the peripheral sympathetic inhibitory effects of left atrial receptor stimulation at a time when arterial baroreceptor function is preserved.

Pulmonary artery balloon counterpulsation for right ventricular failure: I. Experimental results.

The effects of pulmonary artery balloon counterpulsation (PABC) as a circulatory assist for the failing right ventricle were investigated. Sixteen anesthetized dogs underwent instrumentation to measure cardiac output and to record pressures in both ventricles, the pulmonary artery, and the aorta. Autonomic control of the heart was surgically and pharmacologically ablated. A specially designed counterpulsation balloon was inserted through the right ventricular (RV) outflow tract into the pulmonary artery. Pulmonary hypertension, induced acutely by the microembolization of the pulmonary circulation with glass beads combined with infusion of serotonin, served as a model for development of acute RV failure. Immediate effects of PABC were investigated in 10 dogs during normal function and failure of the right ventricle at different levels of preload. After further embolization which caused progressive cardiogenic shock, the effects of 10 minutes of PABC, and of its withdrawal, were examined. In all cases, PABC immediately decreased RV preload and afterload. In the failing right ventricle, counterpulsation also significantly increased cardiac output. Progressive cardiogenic shock was successfully reversed by PABC; after 10 minutes of counterpulsation, increases in cardiac output (+53%), arterial pressure (+55%), and RV minute work (+62%) were observed, paralleled by a fall in RV preload (-22%). After PABC was discontinued, the circulatory status again began to deteriorate. We conclude that PABC effectively improves function of the failing right ventricle caused by acute pulmonary hypertension.

Pulmonary artery balloon counterpulsation for right ventricular failure: II. Clinical experience.

The use of pulmonary artery balloon counterpulsation (PABC) provided immediate salvage following cardiac surgical procedures in 2 patients with biventricular failure in whom inotropic drugs and intraaortic balloon counterpulsation did not provide sufficient support to allow weaning from cardiopulmonary bypass. Although both patients eventually died, the hemodynamic effectiveness of PABC was documented. The various clinical settings for right ventricular as well as biventricular failure are reviewed, the currently available options for treatment are summarized, and the directions for future laboratory investigation and possible clinical applications are presented.

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog.

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Renal and iliac vascular responses to left ventricular receptor stimulation in conscious dogs.

The purpose of the present study was to investigate the relative responses of the renal and iliac vascular beds to the selective chemical stimulation of left ventricular receptors in the conscious dog. Twenty dogs were chronically instrumented to obtain measurements of arterial blood pressure, renal blood flow, and iliac blood flow before and after a bolus intracoronary injection of veratridine (0.4-1.0 micrograms/kg in 0.5-ml vol) with the heart paced. The responses to intracoronary veratridine were a significant reduction in arterial blood pressure averaging 25 mmHg accompanied by a simultaneous reduction in renal blood flow of 25%. Renal resistance did not change throughout the course of the response analyzed (50 s). Iliac blood flow, however, increased, reaching a peak of 35% above control due to a 51% decrease in iliac resistance. After sinoaortic denervation, renal resistance still failed to show a decrease, although the recovery of arterial blood pressure and iliac resistance was prolonged. After a mild hypotensive hemorrhage (20 ml/kg), a greater decrease in iliac resistance occurred with intracoronary veratridine injections, but renal resistance still did not change. The reduction in iliac resistance with intracoronary veratridine was significantly attenuated after phentolamine administration (2 mg/kg iv) but not after atropine alone (0.2 mg/kg iv). A significant cholinergic receptor component of iliac vasodilation was observed only after prior alpha-adrenergic-receptor blockade. The results of this study are consistent with the conclusion that in the conscious dog, left ventricular receptors exert a preferential neural control over skeletal muscle vascular resistance and do not influence renal vascular resistance.

Renal nerve and blood pressure responses to stimulation of cardiac receptors in dogs and cats by bradykinin.

It has been recently demonstrated in anesthetized, sinoaortic denervated-vagotomized (SAD + Vx ) cats that epicardial or intracoronary (IC) bradykinin (BK) evokes an increase in efferent renal nerve activity (RNA) and a pressor response which is mediated by the cardiac sympathetic afferent nerves. The purpose of this study was to compare the effect of epicardial, IC, and left atrial (LA) administration of BK on arterial blood pressure (ABP) and RNA in intact and SAD + Vx cats and dogs. A total of seven cats and eight dogs anesthetized with chloralose were prepared with a left circumflex coronary arterial catheter (dogs) or a LA catheter (cats). Changes in ABP and RNA were determined in both dogs and cats when 1 to 100 micrograms/ml of BK was applied to the anterior surface of the left ventricle or injected IC or LA (0.3 and 3.0 micrograms/kg BK) in the intact and SAD + Vx state. In both the intact and SAD + Vx cat, a pressor response was consistently elicited with epicardial BK. In the SAD + Vx state, epicardial BK increased ABP by 33.4 +/- 4.7 mm Hg (p less than .001). RNA followed this same trend showing a consistent and significant increase with both LA and epicardial BK (+24.8 +/- 8.4% in the SAD + Vx state; P less than .05). Changes in RNA in dogs were highly variable with epicardial and IC BK in intact and in SAD Vx dogs, resulting in insignificant changes in this parameter. The results of this study demonstrate that the reflex effects of stimulation of cardiac sympathetic afferents by BK are species specific and need not evoke an increase in peripheral sympathetic outflow.

Mechanisms producing tachycardia in conscious baboons during environmental heat stress.

The involvement of changes in sympathetic activity, changes in cardiac efferent vagal activity, and nonautonomic mechanisms in producing the rise in heart rate (HR) during heat stress-induced hyperthermia was studied in seven unanesthetized, chronically instrumented baboons (Papio anubis and P. cynocephalus). The experimental protocol consisted of subjecting the baboon to environmental heating (EH) of sufficient intensity (40-45 degrees C) to raise arterial blood temperature (Tbl) 2-3 degrees C in 1-2 h while in one of four states: 1) normal (control), 2) beta-adrenergic receptor blockade induced by propranolol, 3) cholinergic receptor blockade induced by atropine, and 4) combined beta- and cholinergic receptor blockade induced by propranolol and atropine together. HR rose linearly with Tbl during EH in all four states (correlation coefficient greater than or equal to 0.97 in all cases) with average HR-Tbl regression coefficients (slopes) being 20.5 +/- 1.2 (SE) beats X min-1 . degrees C for the normal state, 12.2 +/- 0.5 beats X min-1 . degrees C-1 for the beta-blockade state, 13.3 +/- 1.1 beats X min-1 . degrees C for the cholinergic blockade state, and 8.4 +/- 0.8 beats X min-1 . degrees C-1 for the combined beta- and cholinergic receptor blockade state. Thus nonautonomic mechanisms account for about 40% of the tachycardia in heat-stressed baboons with the remaining 60% produced by combined vagal withdrawal and sympathetic activation. Furthermore application of a multiplicative model of autonomic control of HR to these data suggests that about 75% of the autonomic component is produced by vagal withdrawal.

Influence of left ventricular receptor stimulation on plasma vasopressin in conscious dogs.

The current study was undertaken to determine whether receptors in the left ventricle are capable, when stimulated, of inhibiting plasma arginine vasopressin (AVP) in the conscious dog. Dogs were instrumented to measure aortic pressure and heart rate. In addition, a catheter was implanted in the left circumflex coronary artery. Left ventricular receptors were stimulated by the intracoronary infusion of veratrine, which evoked a hypotension and bradycardia. Control experiments consisted of intravenous infusion of veratrine. Plasma AVP, osmolality, and sodium and potassium concentrations were measured at intervals following the infusion. Similar experiments were done during the intravenous infusion of sodium nitroprusside (NP) to lower aortic pressure to the same extent as that seen with intracoronary infusion of veratrine. Experiments were also performed in chronic sinoaortic-denervated dogs. Intracoronary infusion of veratrine resulted in a significant decrease in aortic pressure from 93.9 +/- 2.8 to 70.5 +/- 4.5 mmHg. Control plasma AVP averaged 2.13 +/- 0.25 pg/ml and did not change significantly during this time. NP infusion lowered aortic pressure to a similar degree, and plasma AVP rose to 21.17 +/- 3.79 pg/ml after 5 min. There were no significant changes in any other plasma constituents. The results were similar in sinoaortic-denervated dogs. We conclude from the results of this study that receptors in the left ventricle are not capable of decreasing plasma AVP from low basal levels or from augmented levels.