Reflex increase in blood pressure induced by leg compression in man.

1. We tested the hypotheses that the increase in mean arterial pressure with the application of external leg compression in man is (i) blocked with epidural anaesthesia, and (ii) dependent upon the level of external pressure applied, the quantity of leg muscle mass compressed and the vascular volume of the leg. Fourteen healthy subjects were fitted with an anti-shock trouser garment to provide three levels (30, 60 and 90 mmHg) of leg compression, while cephalad translocation of fluid was prevented by upper-thigh cuffs inflated to a supra-systolic pressure. Cardiovascular responses were recorded during leg compression before and after the administration of epidural anaesthesia in eight subjects, while blood pressure responses from six subjects were compared with their single leg pressor response. 2. Both mean arterial and diastolic pressures were elevated with increasing leg compression, with no changes in heart rate, cardiac output, thoracic impedance, and central venous pressure. The leg compression-induced blood pressure increases were abolished by epidural anaesthesia. Furthermore, when only one leg was compressed at 90 mmHg, the pressor response was less than that elicited from compression of both legs at the same external pressure. Changes in vascular volume of the leg did not influence the pressor response to leg compression. 3. The results indicate that the mean arterial pressure increases in response to external compression of the legs and that a reflex mechanism, mediated by muscle afferent nerves, is involved. The response is dependent upon both the changes in intramuscular pressure and the quantity of muscle mass compressed.     

Changes in blood pressure and heart rate induced by movements of normal and inflamed knee joints

The effects of passive movements of normal and inflamed knee joints on blood pressure and heart rate were recorded in baroreceptor denervated cats anesthetized with halothane, and these effects were compared with those obtained by severe noxious squeezing of the hind paw. Rhythmic flexions and extensions as well as rhythmic inward and outward rotations of a normal knee joint in its physiological working range did not have any significant influence on blood pressure and heart rate. However, on the inflamed side, the same movements caused definite increases in blood pressure and heart rate (e.g. mean increases for flexion-extension movements were 13 mmHg and 4 beats/min, respectively, P less than 0.01). Static outward rotations in the normal working range were ineffective in both joints, but as soon as these static rotations were extended into the noxious range significant increases in blood pressure and heart rate were elicited. The respective mean increases induced from the normal and inflamed sides were 17 and 38 mmHg for the blood pressure and 4 and 8 beats/min for the heart rate. The increases in blood pressure and heart rate induced by noxious outward rotation of the inflamed joint regularly exceeded those elicited by noxious squeezing of the hind paw. It is concluded that impulses in articular nociceptors and possibly other fine articular afferent units activate sympathetic outflow to the cardiovascular system, and that these effects are particularly prominent when the joint receptors are sensitized by     

Effects of drug-induced changes in resting blood pressure on classically conditioned heart rate and blood pressure in restrained rats

Subsequent to receiving aversive classical conditioning, which led to a decelerative heart rate (HR) conditioned response (CR) and a pressor-depressor blood pressure (BP) CR, three separate groups of restrained rats received intravenous infusion of sodium nitroprusside (40 micrograms/mg/min) to lower baseline BP, phenylephrine (17 micrograms/mg/min) to raise baseline BP, or an equivalent volume of saline. Conditioning test trials during infusion revealed that hypotension produced by sodium nitroprusside eliminated the HR CR and transformed the BP CR into a pressor-only reaction. Hypertension produced by phenylephrine facilitated the HR CR and changed the BP CR to a pressor-only response on selected trials in which baseline BP increases and baseline HR decreases were within restricted limits. Following drug withdrawal, the HR CRs of both drug groups and the BP CR of the phenylephrine group were attenuated. The unconditioned responses to the shock unconditioned stimulus under phenylephrine were exaggerated and consisted of tachycardias and depressor BP changes, whereas under sodium nitroprusside reduced tachycardias and depressor activity occurred. The results suggested that the loss of the vagally mediated HR CR under sodium nitroprusside was due to baroreceptor-controlled inhibition of vagal discharge and that the enhancement of the HR CR under phenylephrine was due to baroreceptor-influenced facilitation of vagal discharge.     

Diurnal changes in blood pressure and heart rate in children with narcolepsy with cataplexy

The hypocretin neurons in the lateral hypothalamus are connected not only to brain alertness systems but also to brainstem nuclei that regulate blood pressure and heart rate. The premise is that regulation of blood pressure and heart rate is altered and affected by methylphenidate, a stimulant drug in children with narcolepsy with cataplexy. The changes in 24-hr ambulatory systolic and diastolic blood pressure and heart rate were compared among pre-treated narcolepsy with cataplexy patients (40 males, 10 females), with mean age 10.4 ± 3.5 years (M ± SD, range 5–17 years) with values from 100 archival age–sex–body mass index matched controls. Patients had a lower diurnal systolic blood pressure (−6.5 mmHg; p = 0.000) but higher heart rate (+11.0 bpm; p = 0.000), particularly evident in the waketime, while diastolic blood pressure was comparable. With methylphenidate (18 mg sustained release at 08:00 hours), patients with narcolepsy with cataplexy had higher systolic blood pressure (+4.6 mmHg, p = 0.015), diastolic blood pressure (+3.3 mmHg, p = 0.005) and heart rate (+7.1 bpm, p = 0.028) during wake time, but nighttime cardiovascular values were unchanged from pre-treated values; amplitude variation in cardiovascular values was unchanged over 24 hr. In conclusion, children with narcolepsy with cataplexy had downregulation blood pressure profile but a higher heart rate, and lesser non-dipping profiles. Daytime methylphenidate treatment increases only waketime blood pressure and further elevated heart rate values.     

The effect of centrally administered TRH on blood pressure,heart rate and ventilation in rat

Different doses (3, 16, 80, 400 and 2000 ng per rat) of TRH or alternatively saline were infused into the lateral ventricle of urethane-ahaesthetized rats and blood pressure, heart rate, respiration rate and tidal volume were recorded. A dose of 3 ng TRH caused a significant elevation of blood pressure and heart rate, whereas 16 ng was needed for respiration rate to be elevated. There was no change in respiratory minute volume during the experiment. We conclude that TRH has profound physiological effects and that TRH, given centrally, is a potent hypertensive, chronotropic and tachypnoeic agent.     

Age-related changes in control of blood pressure and heart rate during sleep in the rat

STUDY OBJECTIVES: The aim of this study was to determine age-related changes in the control of mean arterial pressure (MAP) and heart rate (HR) during sleep, and its relationship to the baroreflex in aging. DESIGN: MAP, HR, body temperature (TP), spontaneous activity (ACT), and sleeping/waking duration were monitored for 24 hours in groups of young (10-12 wk old) and old (23-24 mo old) rats. SETTING: The sleep laboratory at the University of Tokushima. PARTICIPANTS: Subjects were 8 young (10-12 wk old) and 7 old (23-24 mo old) Wistar rats. INTERVENTIONS: Reflex control of HR was evaluated by examining various pressure responses to an intravenous bolus injection of phenylephrine and sodium nitroprusside. MEASUREMENTS AND RESULTS: MAP and TP were recorded by a radiotelemetry system. HR was detected from the AP signal. ACT was counted by a photo-sensor system. In the case of old rats, the sensitivity of baroreflex control of HR was significantly depressed, and the spontaneous increase of MAP and HR during REM sleep and the MAP drop at the end of REM sleep were significantly enhanced. The old rats showed no large deterioration of the circadian profiles of MAP, HR, TP, and the amount of sleep. CONCLUSIONS: The baroreflex dysfunction is considered to appear in an early stage of the aging process, and to affect the control of MAP and HR during sleep.     

The effect of centrally administered TRH on blood pressure, heart rate and ventilation in rat.

Different doses (3, 16, 80, 400 and 2 000 ng per rat) of TRH or alternatively saline were infused into the lateral ventricle of urethane-anaesthetized rats and blood pressure, heart rate, respiration rate and tidal volume were recorded. A dose of 3 ng TRH caused a significant elevation of blood pressure and heart rate, whereas 16 ng was needed for respiration rate to be elevated. There was no change in respiratory minute volume during the experiment. We conclude that TRH has profound physiological effects and that TRH, given centrally, is a potent hypertensive, chronotropic and tachypnoeic agent.     

The effect of ventilation on spectral analysis of heart rate and blood pressure variability during exercise

Heart rate variability (HRV) and systolic blood pressure variability (BPV) during incremental exercise at 50, 75, and 100% of previously determined ventilatory threshold (VT) were compared to that of resting controlled breathing (CB) in 12 healthy subjects. CB was matched with exercise-associated respiratory rate, tidal volume, and end-tidal CO(2) for all stages of exercise. Power in the low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, >0.15-0.4 Hz) for HRV and BPV were calculated, using time-frequency domain analysis, from beat-to-beat ECG and non-invasive radial artery blood pressure, respectively. During CB absolute and normalized power in the LF and HF of HRV and BPV were not significantly changed from baseline to maximal breathing. Conversely, during exercise HRV, LF and HF power significantly decreased from baseline to 100% VT while BPV, LF and HF power significantly increased for the same period. These findings suggest that the increases in ventilation associated with incremental exercise do not significantly affect spectral analysis of cardiovascular autonomic modulation in healthy subjects.     

Reflex inhibition of heart rate and efferent cardiac sympathetic outflow induced by colorectal distension in anesthetized rats

Colorectal distensions of 60 and 80 mmHg significantly reduced heart rate (HR) and cardiac sympathetic nerve activity in anesthetized rats. This bradycardiac response was not influenced by the intravenous administration of atropine, but was abolished by propranolol, suggesting that it was elicited by sympathetic but not vagal efferent nerves.     

Diurnal changes of blood pressure,heart rate and body temperature during sleep in the rat

We have studied diurnal changes in mean arterial pressure (MAP), heart rate (HR) and body temperature (Tb) during wake (W), non-rapid eye movement sleep (NREMS) and REM sleep (REMS) in the rat. Although HR and Tb show a similar sinusoidal diurnal variation during all vigilance states, the diurnal profile for the MAP is vigilance-state dependent. During W, MAP values are higher during the dark phase, during NREMS, no significant diurnal change is seen, and during REMS, the MAP exhibits a reversed diurnal change, being higher during the light phase. The low frequency component (0.25–0.725 Hz) in the power spectral density of the blood pressure, an index of sympathetic activity, is also higher during the light phase than the dark phase in REMS. The present findings suggest that diurnal changes in MAP in the rat result from the wake rhythm, and that the mechanism for the diurnal control of MAP may be different from that for HR or Tb.     

Evidence that pharmacological manipulations of central L-arginine-NO pathway influence blood pressure and heart rate in rats.

In the present study we have investigated whether pharmacological manipulations of central L-arginine-nitric oxide (L-Arg-NO) pathway could affect blood pressure (BP) and heart rate (HR) in normotensive rats either untreated or pretreated with E. coli lipopolysaccharide (LPS). The intracerebroventricular injection (i.c.v.) of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, caused a fall of BP and HR in LPS-treated but not in control rats. Furthermore, the pressor responses to i.c.v. injection of N-methyl-D-aspartate (NMDA) were enhanced by L-Arg or LPS treatment and, in both cases, this potentiation was blocked by L-NAME. The present results show that in some experimental conditions, such as activation of NMDA receptors or LPS pretreatment, the central microinfusion of drugs affecting the L-Arg-NO pathway may interfere with BP and HR.     

Effect of central urotensin II on heart rate, blood pressure and brain Fos immunoreactivity in conscious rats

Central administration of urotensin II (UII) increases heart rate (HR), cardiac contractility, and plasma levels of epinephrine and glucose. To investigate the mechanisms causing these responses we examined the effects of i.c.v. administration of rat UII (10 microg) on the sympatho-adrenal and pituitary-adrenal axes in conscious rats, and we mapped the brain sites activated by UII by immunohistochemically detecting Fos expression. In six conscious rats i.c.v. UII, but not vehicle, increased HR significantly 60-90 min after treatment and increased plasma glucose at 60 and 90 min, both indicators of increased epinephrine release. Plasma corticosterone levels were significantly elevated 90 min after i.c.v. UII. Conscious rats, given i.c.v. UII (n=12) and killed after 100 or 160 min, showed increased Fos-immunoreactivity (Fos-IR) in the nucleus of the solitary tract and the central nucleus of the amygdala (CeA) at both time points, compared with vehicle (n=11). In UII-treated rats, Fos-IR in the paraventricular nucleus of the hypothalamus (PVN) was significantly elevated at 160 min, but not 100 min, compared with vehicle. There were no increases in Fos-IR in the rostral ventrolateral medulla or the A5 cell group, areas associated with sympathetic outflow to the adrenal gland. In summary, i.c.v. UII increased HR and plasma glucose and corticosterone in conscious rats. UII increased Fos-IR in the CeA and PVN, but over a longer time course in the latter. These findings indicate that UII acts on specific brain nuclei to stimulate the hypothalamo-pituitary-adrenal axis and to stimulate adrenal sympathetic nerve activity.     

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases.

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25-40) in the LHD group and 44 W (33-49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31.0 +/- 5.5 to 8.8 +/- 5.0 mmHg in the LHD group, compared with from 13.7 +/- 1.0 to 2.1 +/- 2.4 mm Hg in the controls, while ventilation/O2 intake ratio (V/VO2) and physiological dead space/tidal volume ratio (VD/VT) showed a tendency to rise, from 36.3 +/- 8.8 to 39.2 +/- 7.4, and from 0.35 +/- 0.11 to 0.39 +/- 0.09, respectively, in the LHD group, and from 27.5 +/- 3.1 to 28.7 +/- 5.3, and from 0.19 +/- 0.09 to 0.21 +/- 0.12 in the controls. Mixed venous O2 tension (PvO2) showed a marked decline from 3.60 +/- 0.33 to 3.26 +/- 0.36 kPa in the LHD group, as compared with from 3.94 +/- 0.28 to 3.71 +/- 0.29 kPa in the controls, while the calculated physiologic shunt (Qs/Qt) suggested improved alveolo-arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia-induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.     

Arterial pressure and heart rate changes during natural sleep in rat

Mean arterial pressure and heart rate data during quiet wakefulness and phases of sleep in conscious rat are sampled by a computer at a rate of 100/sec. Average values and variability expressed as standard deviation are computed for each recording session. Mean arterial pressure and heart rate and their variability decrease from quiet wakefulness to synchronized sleep. During desynchronized sleep, mean arterial pressure increases to the level of quiet wakefulness and is more variable than during synchronized sleep. Heart rate is lower and more uniform during sleep than during quiet wakefulness, and there is no difference between synchronized and desynchronized sleep except that a greater variability occurs during desynchronized sleep. The study shows that characteristic and specific cardiovascular changes accompany the phases of sleep and that a hierarchy of arterial pressure is present during the resting behavior in rat.     

Assessment of baroreflex control from beat-to-beat blood pressure and heart rate changes: A validation study

In this study, we tested the validity of a new method designed to estimate baroreflex control of heart rate from spontaneous changes in systolic pressure and pulse interval. This method was compared with a conventional method of assessing baroreflex control through measuring reflex adjustments in pulse interval associated with pharmacological manipulations of blood pressure. The estimates of baroreflex control derived from the two methods were signficantly correlated; however, only the estimate derived using pharmacological changes in pressure detected significant impairment of baroreflex control in patients with damage to baroafferents produced by radiation for oropharyngeal cancer. Analysis of spontaneous changes in pressure and pulse interval therefore provide a meaningful estimate of baroreflex control of heart rate that is, however, less sensitive than estimates obtained using pharmacological manipulations in pressure.     

Changes in blood pressure,heart rate and blood constituents during heat exposure in men with elevated blood pressure

Summary Although the vascular volume response of hypertensive men during exercise has been rather well characterized, the effect of resting heat exposure in this patient population has not been examined. This was done in the present report in seven men with high blood pressure (BP) (i. e., diastolic pressure>12 kPa (90 mmHg) upon initial interview) and 5 normotensive control subjects. 50 min after each subject had consumed an amount of water equal to 1% of his body weight, he reclined on a cot. 10 min later the subject was carried into an environmental chamber equilibrated at Tdb=45 C, Twb=28 C. Free-flowing venous blood samples were obtained from a cubital vein, and BP and heart rate were measured, before the heat exposure and at 15 min intervals during the experiment. Within 30 min systolic, diastolic and mean BP of the high BP subjects had decreased to normal levels; no BP changes were detected in normotensive subjects. Accompanying this depressor response was an exaggerated elevation in plasma glucose concentration. No alterations were found with haematocrit, plasma osmolality or electrolytes, or total protein and albumin. The data suggest that heat exposure may have been more stressful for the subjects with high BP than for their controls. This finding implies that phasic depressor responses may be as important as phasic pressor episodes in the aetiology of established essential hypertension.Training Grant HL07050 from the National Institutes of Health supported this project     

皮质下动脉硬化性脑病血压及心率变异性分析

目的和方法：采用动态检测技术观察３１例皮质下动脉硬化性脑病和对照组３１例健康人血压和心率的变异性。结果：患者均存在动态血压异常，其中平均收缩压、平均舒张压超过正常值者２７例（８７％），夜间基底血压异常升高２２例（７１％），血压异常波动２０例（６４％），昼夜节律逆转４例（１３％）。患者心率变异时域指标２４小时内全部正常心动周期的标准差、２４小时内５分钟节段平均正常心动周期的标准差、在一定时间内相邻两正常心动周期差值大于５０毫秒的个数所占的百分比均明显低于对照组，收缩压与心率无显著相关性。结论：提示血压波动及持续的夜间升压现象在该病中起着一定作用，而这种异常可能与患者植物神经系统功能失调有关