Effects of supine floating on heart rate,blood pressure and cardiac autonomic nervous system activity

It is known that heart rate, oxygen uptake and body temperature during exercise in water are affected by water temperature, buoyancy and so on. Relaxation in water (supine floating) has been performed in hydrotherapy and aqua exercise. But there were few reports about supine floating (Schulz and Kaspar 1994). The purpose of this study was to make clear the effects of supine floating on heart rate, blood pressure and cardiac autonomic nervous system activity in males.     

The autonomic component in blood pressure and heart rate effects of tilting in the three-toed sloth

1. This study attempts to elucidate unique heart and blood pressure responses seen in sloths in response to tilting by blocking autonomics with atropine, propranolol, or a combination of these. 2. Atropine produces less heart rate increase in sloths than in other mammals but blocks reflex bradycardia as expected. 3. Propranolol reduces heart rate to about the same degree as in man and completely blocks all cardiac responses to tilting, both direct and reflex. 4. Atropine slightly diminishes blood pressure responses to tilting whereas propranolol tends to augment the already marked increases.     

糖尿病植物神经病变病人心率变异的非线性定量分析

目的：研究糖尿病人植物神经病变与心率变异的关系。对象：正常对照组和根据临床有无糖尿病神经病变（ＤＡＮ）分组的糖尿病病人,方法：应用２４小时动态心电图对正常和糖尿病人进行心率变异的线性,非线性散点图和非线性定量参数分析,结果：单纯糖尿病组ＳＤＮＮ,ＳＤＡＮＮ和ＰＮＮ５０低于正常组（Ｐ〈０．０５）;糖尿病＋ＤＡＮ组各项线性时域分析指标均低于正常和单纯糖尿病组（Ｐ〈０．０１－０．００１）,散点图分析结果     

Concurrent reductions in blood pressure and metabolic rate during fasting in the unrestrained SHR

Arctic ground squirrels (Spermophilus parryii) overwinter in hibernaculum conditions that are substantially below freezing. During torpor, captive arctic ground squirrels displayed ambient temperature (T(a))-dependent patterns of core body temperature (T(b)), metabolic rate (TMR), and metabolic fuel use, as determined by respiratory quotient (RQ). At T(a) 0 to -16 degrees C, T(b) remained relatively constant, and TMR rose proportionally with the expanding gradient between T(b) and T(a), increasing >15-fold from a minimum of 0.0115 +/- 0.0012 ml O(2). g(-1). h(-1). At T(a) 0-20 degrees C, T(b) increased with T(a); however, TMR did not change significantly from T(b) 0 to 12 degrees C, indicating temperature-independent inhibition of metabolic rate. The overall change in TMR from T(b) 4 to 20 degrees equates to a Q(10) of 2.4, but within this range of T(b), Q(10) changed from 1.0 to 14.1. During steady-state torpor at T(a) 4 and 8 degrees C, RQ averaged 0.70 +/- 0.013, indicating exclusive lipid catabolism. At T(a) -16 and 20 degrees C, RQ increased significantly to >0.85, consistent with recruitment of nonlipid fuels. RQ was negatively correlated with maximum torpor bout length. For T(a) values <0 degrees C, this relationship supports the hypothesis that availability of nonlipid metabolic fuels limits torpor duration in hibernating mammals; for T(a) values >0 degrees C, hypotheses linked to body temperature are supported. Because anterior body temperatures differ from core, overall, the duration torpor can be extended in hibernating mammals may be dependent on brain temperature.     

Effect of autonomic blockers on the heart rate of intact rats and animals with artificial hyperthyroidism.

The effect of various autonomic blockers on the heart rate (from the ECG recording) of intact rats and of animals with experimental hyperthyroidism induced by the administration of dried thyroid was studied. In intact rats, the heart rate fell significantly (by 22%) during the first week after the peroral administration of propranolol (0.05% in food), but trimepranol (0.02%), reserpine (0.001%) and guanethidine (0.1%) had no effect (in a suplementary experment, a small, but statistically significant decrease was also found after trimepranol). In experimental hyperthyroidism, using the same blocker doses, the heart rate fell significantly after propranolol (by 23%), trimepranol (22%), reserpine (16%) and, in a preliminary experiment, guanethidine (19%). On injecting 0.05 mg propranolol intravenously, the maximum drop in the heart rate in intact rats was 22%, while in hyperthyroidism it was hardly more than half this value (at all the intervals from 2 to 30 minutes the decrease was statistically significant). Practolol, in a dose of 0.3 mg i.v., was less effective -- in intact rats the heart rate fell by not more than 12% (at all the intervals from 2 to 30 minutes the decrease was significant), but in hyperthyroidism the drop was slower and statistically non-significant. The results do not furnish an unequivocal answer to the question of the role of adrenergic regulation of the heart rate under physiological conditions and in experimental hyperthyroidism in rats.     

Effects of nNOS antisense in the paraventricular nucleus on blood pressure and heart rate in rats with heart failure

Using neuronal NO synthase (nNOS)-specific antisense oligonucleotides, we examined the role of nitric oxide (NO) in the paraventricular nucleus (PVN) on control of blood pressure and heart rate (HR) in conscious sham rats and rats with chronic heart failure (CHF). After 6-8 wk, rats with chronic coronary ligation showed hemodynamic and echocardiographic signs of CHF. In sham rats, we found that microinjection of sodium nitroprusside (SNP, 20 nmol, 100 nl) into the PVN induced a significant decrease in mean arterial pressure (MAP). SNP also induced a significant decrease in HR over the next 10 min. In contrast, the NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 200 pmol, 100 nl) significantly increased MAP and HR over the next 18-20 min. After injection of nNOS antisense, MAP was significantly increased in sham rats over the next 7 h. The peak response was 27.6 +/- 4.1% above baseline pressure. However, in the CHF rats, only MAP was significantly increased. The peak magnitude was 12.9 +/- 5.4% of baseline, which was significantly attenuated compared with sham rats (P < 0.01). In sham rats, the pressor response was completely abolished by alpha-receptor blockade. HR was significantly increased from hour 1 to hour 7 in sham and CHF rats. There was no difference in magnitude of HR responses. The tachycardia could not be abolished by the beta(1)-blocker metoprolol. However, the muscarinic receptor antagonist atropine did not further augment the tachycardia. We conclude that NO induces a significant depressor and bradycardiac response in normal rats. The pressor response is mediated by an elevated sympathetic tone, whereas the tachycardia is mediated by withdrawal of parasympathetic tone in sham rats. These data are consistent with a downregulation of nNOS within the PVN in CHF.     

Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise

This study examined the acute effects of caffeine on thecardiovascular system during dynamic leg exercise. Ten trained,caffeine-naive cyclists (7 women and 3 men) were studied at rest andduring bicycle ergometry before and after the ingestion of 6 mg/kgcaffeine or 6 mg/kg fructose (placebo) with 250 ml of water. Afterconsumption of caffeine or placebo, subjects either rested for 100 min(rest protocol) or rested for 45 min followed by 55 min of cycleergometry at 65% of maximal oxygen consumption (exercise protocol).Measurement of mean arterial pressure (MAP), forearm blood flow (FBF),heart rate, skin temperature, and rectal temperature and calculation offorearm vascular conductance (FVC) were made at baseline and at 20-minintervals. Plasma ANG II was measured at baseline and at 60 minpostingestion in the two exercise protocols. Before exercise, caffeineincreased both systolic blood pressure (17%) and MAP (11%) withoutaffecting FBF or FVC. During dynamic exercise, caffeine attenuated theincrease in FBF (53%) and FVC (50%) and accentuated exercise-inducedincreases in ANG II (44%). Systolic blood pressure and MAP were alsohigher during exercise plus caffeine; however, these increases weresecondary to the effects of caffeine on resting bloodpressure. No significant differences were observed inheart rate, skin temperature, or rectal temperature. These findingsindicate that caffeine can alter the cardiovascular response to dynamicexercise in a manner that may modify regional blood flow andconductance.

     

Effects of midodrine on exercise-induced hypotension and blood pressure recovery in autonomic failure.

We tested the hypothesis that the oral alpha1-adrenergic agonist, midodrine, would limit the fall in arterial pressure observed during exercise in patients with pure autonomic failure (PAF). Fourteen subjects with PAF underwent a stand test, incremental supine cycling exercise (25, 50, and 75 W), and ischemic calf exercise, before (control) and 1 h after ingesting 10 mg midodrine. Heart rate (ECG), beat-to-beat blood pressure (MAP, arterial catheter), cardiac output (Q, open-circuit acetylene breathing), forearm blood flow (FBF, Doppler ultrasound), and calf blood flow (CBF, venous occlusion plethysmography) were measured. The fall in MAP after standing for 2 min was similar ( approximately 60 mmHg; P = 0.62). Supine MAP immediately before cycling was greater after midodrine (124 +/- 6 vs 117 +/- 6 mmHg; P < 0.03), but cycling caused a workload-dependent hypotension (P < 0.001), whereas increases in Q were modest but similar. Midodrine increased MAP and total peripheral resistance (TPR) during exercise (P < 0.04), but the exercise-induced fall in MAP and TPR were similar during control and midodrine (P = 0.27 and 0.14). FBF during cycling was not significantly reduced by midodrine (P > 0.2). By contrast, recovery of MAP after cycling was faster (P < 0.04) after midodrine ( approximately 25 mmHg higher after 5 min). Ischemic calf exercise evoked similar peak CBF in both trials, but midodrine reduced the hyperemic response over 5 min of recovery (P < 0.02). We conclude midodrine improves blood pressure and TPR during exercise and dramatically improves the recovery of MAP after exercise.     

树鼩血压和心率的无创测定

目的建立健康树鼩的心率、血压正常值参考范围,并探讨不同来源、不同性别、不同年龄树鼩心率、血压的差异。方法随机挑选实验树鼩180只,按来源分为野生成年组、F1代自繁成年组和青幼年组三个组,每组雌雄各半,共60只。采用智能无创血压计（鼠仪）逐只测定HR（心率）、SBP（收缩压）、DBP（舒张压）和MBP（平均动脉压）。结果野生成年树鼩、自繁成年树鼩和青幼年树鼩心率分别为394.33±37.74 BPM、351.61±72.76 BPM和378.19±69.04 BPM,野生和自繁成年树鼩组差异有显著性（P〈0.05）。自繁成年树鼩收缩压、舒张压和平均动脉压均明显低于青幼年树鼩,差异有极显著性（P〈0.01）。野生成年树鼩和自繁成年树鼩相比,收缩压、舒张压和平均动脉压差异均无显著性（P〉0.05）。结论大鼠无创血压计适合于树鼩的血压、心率的测量。通过测定,获得了野生成年树鼩、F1代自繁成年树鼩和青幼年树鼩的心率和血压参考值范围,丰富了树鼩基础生理数据,可为相关研究提供科学参考。     

Central muscarinic modulation of fetal blood pressure and heart rate

It has previously been demonstrated that the fetal lamb cardiovascular system can respond to peripheral muscarinic stimulation. However the role of central muscarinic mechanisms in modulating fetal cardiovascular function has not been described. Pilocarpine is a muscarinic agonist that readily crosses the blood-brain barrier and was therefore employed to examine both central and peripheral muscarinic mechanisms in modulating fetal cardiovascular function. Fetal lambs were prepared for chronic intrauterine recording of fetal blood pressure (FBP) and heart rate (FHR). Direct administration of pilocarpine to the fetus resulted in an immediate dose-dependent decrease in both systolic and diastolic blood pressure and a rapid fall in FHR. The initial phase of hypotension was very short-lived (1-2 min) and was subsequently followed by a significant increase in systolic, diastolic and pulse pressures (30-60 min). Fetal heart rate gradually returned to control levels by 30 min after pilocarpine administration. Atropine pretreatment was effective in completely blocking the cardiovascular actions of pilocarpine, while methylatropine was only able to block the initial hypotensive and bradycardiac response. A prolonged tachycardia was also unmasked by methylatropine pretreatment. These data suggest that the initial hypotension and bradycardia in response to pilocarpine administration are mediated via peripheral muscarinic receptors, while stimulation of central muscarinic receptors result in hypertension and tachycardia. These data confirm that, as in the adult, central cholinergic mechanisms are involved in the modulation of cardiovascular function in the developing fetus.     

The blood pressure and heart rate chronome of centenarians.

Rhythm characteristics of blood pressure (BP) and heart rate (Hr) of 11 healthy centenarians and 66 medical students are described. Each subject ambulatorily monitored measured BP and HR around the clock at 15-min intervals for 48 hours. Least-squares spectra were obtained by the fit of cosine curves (cosinor) and compared between the two populations. Confounding by geographic differences seems to be ruled out by comparisons with results from international data bases. A shift in prominence from the circadian domain to higher frequency harmonics was found for the BP but not for the HR of centenarians. In clinically mostly healthy centenarians, markers of primary aging may consist of a relatively low circadian BP and HR amplitude and a tendency toward internal and external desynchronization. Whether these chronobiologic changes with age are desirable, indifferent or undesirable can now be elucidated by outcome studies, in the light of the reference standards provided herein.     

急性低氧对家兔血压心率微血管反应性及自由基的影响

目的 :探讨不同急性低氧下的血压、心率、微血管反应性和自由基的影响。方法 :实验采用家兔人工吸入含氧量为 12 .5 %和 8.5 %氮氧混合气体 (模拟 4 0 0 0m和 6 5 0 0m高原急性低氧 )。急性低氧时间分别为 5、10、15、2 0min ,观察血压、心率、微血管反应性和自由基影响。结果 :①急性低氧 5min时收缩压略有升高 ,以后变为降低 ;舒张压在急性低氧 2 0min后明显降低 (P <0 .0 5 ) ;②心率随急性低氧时间的延长变慢 ,尤其含氧量 8.5 %急性低氧组明显 (P <0 .0 5 )。③眼结膜微血管管径随急性低氧时间延长呈现扩张 (P <0 .0 5 ) ,血细胞流速减慢 (P <0 .0 5 ,P <0 .0 1)。④急性低氧 2 0min后SOD活力明显降低 (P <0 .0 5 ) ,MDA含量升高 (P <0 .0 5 )。结论 :急性低氧可使血压降低 ,心率减慢 ,微血管管径变大和血细胞流速减慢 ,同时体内自由基产生增加。     

Effect of ethanol on heart rate and blood pressure in nonstressed and stressed rats

The effect of ethanol on the cardiovascular system (ECG, heart rate, blood pressure) was studied in anesthetized, nonstressed or stressed rats. In anesthetized rats, ethanol showed no effect on heart rate or ECG. In nonstressed rats, ethanol sedated the animals but increased heart rate significantly. This ethanol induced tachycardia seemed the result of a direct stimulation of the sympathetic nerves to the heart. Blood pressure was not significantly affected by ethanol in these nonstressed rats. In stressed rats, marked behavioral excitation and significant increases in heart rate and blood pressure were noted. Ethanol pretreatment calmed the animals considerably during restraint. Ethanol did reduce slightly the stress-induced tachycardia but markedly reduced or antagonized stress-induced blood pressure increases. No major changes in the ECG were noted during these studies with the exception of a few individual animals which showed pathologic ECG responses to ethanol. These data show that ethanol affects cardiovascular functions differently in anesthetized, nonstressed or stressed rats, and that ethanol can significantly reduce or antagonize stress-induced behavioral excitation, tachycardia and hypertension.     

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.