Spontaneous arterial baroreflex control of the heart rate during head-down tilt in heat-stressed humans

The purpose of this study was to elucidate the effect of raised body temperature per se during acute heat stress on the spontaneous arterial baroreflex control of heart rate (f _c) in humans. To investigate whether unloading of cardiopulmonary baroreceptors during whole-body heating would alter the arterial baroreflex control of f _c, we controlled loading of the cardiopulmonary baroreceptors by head-down tilt (HDT) at angles of 5°, 10°, 15°, and 30° during heat stress produced by hot-water-perfused suits. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and f _c. As an index of cardiopulmonary baroreceptor loading, the left atrial diameter (LAD) was measured by echocardiography. During whole-body heating, the LAD decreased with the rising body core temperature and increased with the HDT. The decreased LAD during heating almost recovered to the normothermic control level by 10° HDT. In the supine position, cardiac baroreflex sensitivity remained unchanged during heating. Arterial pressure, f _c and cardiac baroreflex sensitivity were not changed by HDT ranging from 5° to 30° during heating. These results suggest that cardiac baroreflex sensitivity remain unchanged during graded loading of the cardiopulmonary baroreceptors in heat-stressed humans. Also, we conclude that the sensitivity of the spontaneous arterial baroreflex controlling the f _c is not influenced by raised body temperature per se during acute heat stress. Electronic Publication     

Reversibility of abnormal arterial baroreflex control of heart rate in heart failure

The reversibility of the abnormalities in arterial baroreceptor control of heart rate in heart failure was examined in an experimental model of canine high-output biventricular failure produced by an arteriovenous fistula that could be later surgically corrected by ligation. Marked attenuation of arterial baroreceptor control of heart rate in response to both hypertensive and hypotensive stimuli was seen in this model of heart failure. After surgical correction the heart rate response to a hypertensive stimulus did not return to normal but remained severely blunted for up to 8 mo of follow-up. The lack of reversibility after surgical correction suggests that permanent structural changes in arterial baroreceptors may occur after heart failure of short duration.     

Central and baroreflex control of heart rate during the wake-sleep cycle in rat.

Spontaneous fluctuations in Heart Period (HP) and Mean Arterial Pressure (MAP) make it possible to evaluate baroreceptor-heart rate reflex sensitivity (BRS). 30-s sequences of HP and MAP beat-to-beat values were considered in the different wake-sleep states (Wake, W; Quiet Sleep, QS; Active Sleep, AS) in rats to assess whether 1) BRS changes between states and 2) the different indexes supply consistent BRS measures. BRS indexes were calculated according to validated literature procedures as regression coefficients of HP vs. MAP 1) within all ramps of increasing or decreasing MAP of four beats or more, with HP and MAP changing in the same direction (baroreflex-mediated fluctuations, BRSp), 2) within all such ramps irrespective of the relative direction of HP and MAP changes (baroreflex + non-baroreflex, i.e. non-homeostatic centrally driven, fluctuations, BRSA). HP vs. MAP regression coefficient along the entire 30-s sequence (bHPMAP) was also calculated. RESULTS: BRSp did not change among states, BRSA decreased from QS to W to AS, bHPMAP decreased from QS to W and became negative in AS. CONCLUSIONS: 1) as indicated by BRSp, baroreflex sensitivity is state independent, 2) BRSp to BRS(A) to bHPMAP are increasingly affected by non-baroreflex fluctuations, BRSp being most apt to measure BRS, 3) non-homeostatic MAP and HP fluctuations increase from QS to W and prevail in AS. These potentially harmful fluctuations are normally buffered by baroreflexes: in the case of baroreflex impairment, circulatory risk may arise in conditions like AS, when they prevail.     

Left atrial receptors in arterial baroreflex control of heart rate

We have studied the influence of left atrial receptor stimulation on arterial baroreflex control of heart rate with a view to determine the role of cardiac efferent sympathetic and parasympathetic pathways in any interaction observed. Experiments were performed on anaesthetized, artificially ventilated, and thoracotomised cats and dogs. The sensitivity of baroreflex heart rate response was found to be higher in dogs as compared to cats. Both the sympathetic and parasympathetic effects contributed to the reflex chronotropic effects observed during changes in mean arterial blood pressure. The reflex tachycardia response during left atrial receptor stimulation was more pronounced in dogs than in cats. Stimulation of left atrial receptors caused slight inhibition of the baroreflex tachycardia response and potentiation of the bradycardia response.     

Histamine release during the induction of anesthesia with propofol in allergic patients: A comparison with the induction of anesthesia using midazolam-ketamine

OBJECTIVE: A prospective randomized controlled study was performed for patients with a history of allergy to evaluate the effect of the induction of anesthesia with propofol against histamine release, skin reactions, hemodynamic changes and other clinical symptoms, while also comparing these parameters during the induction of anesthesia with midazolam-ketamine for patients with a history of allergy. SUBJECTS: We examined 40 patients undergoing oral surgery, who had a history of allergy and/or the percentage of eosinophils in the leukocytes was more than 3%. METHODS: Forty patients were randomly allocated into two groups and thus received either midazolam-ketamine (M-K group, n = 20) or fentanyl-propofol (propofol group, n = 20) for the induction of anesthesia. Venous blood samples (4 ml each) were obtained before induction as a control and at 0.5, 1, 3, 5 minutes after the administration of each induction agent, and then furthermore at 0.5, 1, 3, 5 minutes after tracheal intubation in order to measure the plasma histamine level by using the HPLC post-label system. In addition, the blood pressure and heart rate were also simultaneously recorded. Skin reactions were also evaluated by two anesthesiologists. RESULTS: The incidence of 50% histamine release during the induction of anesthesia with propofol occurred in 15% of the patients with a history of allergy. Sixteen patients out of 20 (80%) showed a decrease in the systolic blood pressure after the administration of propofol without any evidence of histamine release. The incidence of 50% histamine release, skin reactions and an increase in the heart rate between the two groups were not statistically significant after the administration of each anesthetic agent. Moreover, some patients also demonstrated histamine release after tracheal intubation. Hemodynamic changes after tracheal intubation showed a similar tendency in both groups. No significant difference was observed regarding the incidence of histamine release, skin reactions and hemodynamic changes between both groups after tracheal intubation. CONCLUSIONS: Propofol was found to show a similar incidence of histamine release during the induction of anesthesia using midazolam-ketamine, and thus was also found to be a useful induction agent against histamine release for patients with a history of allergy when hydroxizine was used as a premedication.     

Suspected anaphylactic reaction associated with microemulsion propofol during anesthesia induction

Although rare, intraoperative anaphylaxis can lead to significant morbidity and mortality. Aquafol® (Daewon Pharmaceutical Co. Ltd., Seoul, Korea), a microemulsion propofol, was developed to eliminate lipid solvent-related adverse events, and was used in clinical anesthesia since 2009 with little data about severe side effects such as anaphylaxis. A healthy 16-yr-old male patient who had past medical history with two previous operations of no complications developed cardiovascular shock with generalized erythema following administration of microemulsion propofol during anesthesia induction. Intravenous injection of epinephrine and steroid rescued him. He remained in a stable state without any problems postoperatively and was discharged. Clinicians should consider this rare but serious complication during induction of anesthesia with propofol.     

Effect of posture on arterial baroreflex control of heart rate in humans

Summary Altered baroreflex function may contribute to the cardiovascular changes associated with weightlessness. Since central blood volume (CBV) increases during simulated weightlessness, we have examined the possibility that acute changes in CBV may modify baroreceptor function. We used graded head-up tilt (HUT) and head-down tilt (HDT) to induce changes in CBV, and neck suction to stimulte carotid baroreceptors, in 6 subjects. The increase in pulse interval induced by a negative pressure of 8.2 kPa (62 mm Hg) imposed for 10 s while supine was compared with the increase while tilted for 8 min at ± 15, ± 30 and ± 45. During HDT at 15 the pulse interval over the first 5 cardiac cycles following suction onset was 51 ± (SEM) 18 ms longer (p<0.05), at 30 it was 61±20 ms longer (p<0.05), and at 45 it was 74±35 ms longer (p<0.01), compared with supine. During HUT at 15 the pulse interval was 25±9 ms shorter (p<0.05) than when supine, but was not significantly different at 30 and 45. These responses occurred independently of changes in brachial blood pressure. Attenuation was also observed after 5 min (56±17 ms; <0.05), and after 40 min (25±9 ms; p<0.05) of 60 HUT compared with supine. We conclude that posture does modify arterial baroreflex control of heart rate. If this occurs primarily as a result of a change in CBV, then the acute effect of weightlessness may be an accentuation, not an attenuation, of baroreflex function.M. H. Harrison was a National Research Council postdoctoral research fellow on leave from the Ministry of Defence, UK     

小剂量艾司洛尔对丙泊酚麻醉诱导静脉注射疼痛的影响

目的 研究小剂量艾司洛尔对丙泊酚麻醉诱导静脉注射疼痛的影响.方法 选择2007年6月至2008年3月全身麻醉下行择期手术的患者80例,随机分为对照组(A组)和艾司洛尔组(B组),每组40例.A组进行常规麻醉诱导,B组先静脉注射艾司洛尔0.5 mg/kg,30 s后再进行常规麻醉诱导.采用4分制对两组的丙泊酚注射痛进行评分,比较麻醉前、诱导完毕、气管插管完成即刻、气管捅管后2、4、6、8与10 min的血压和心率变化及诱导期间注射痛的发生率.结果 两组麻醉前和诱导期间各时点血压和心率的变化差异无统计学意义(均P>0.05).诱导期间丙泊酚总的注射疼痛发生率A组为65%(26/40),B组为23%(9140)(P<0.01).其中重度疼痛发生率A组为20%(8/40),B组为3%(1/40)(P<0.05);而轻度和中度疼痛发生率两组间差异无统计学意义(P>0.05).结论 小剂量艾司洛尔可减轻丙泊酚麻醉诱导的静脉注射疼痛.     

Effect of enflurane on the baroreflex control of heart rate in decerebrate rats

Volatile anesthetics alter the arterial baroreflex (BRX) but its mechanisms are poorly understood. This study was designed to determine the effect of 1 and 2 minimal alveolar concentrations (MAC) of enflurane on the BRX parameters in unanesthetized brain stem-intact and decerebrate rats. Under enflurane anesthesia, the femoral artery and both femoral vein were catheterized for pressor (phenylephrine) and depressor (nitroprusside) drug delivery and continuous blood pressure measurements. Decerebration was performed at midcollicular level. BRX tests were performed in 3 time periods; before enflurane (conscious brain-intact), during 1 or 2 MAC enflurane exposure 1 hour after a sham operation or a decerebration operation, and 2 hours after the termination of enflurane (zero enflurane). Mean arterial pressure (MAP) and heart rate (HR) were fitted to a sigmoid logistic equation, the Boltzman equation. The curve of best fit was obtained with a computer program. 1 MAC and 2 MAC of enflurane shifted MAP-HR baroreflex curves to the left in the all groups and significantly attenuated the baroreflex range. The slope of conscious intact period and zero enflurane period of each group did not change significantly, but during the enflurane period the slope was significantly lowered. Enflurane depressed the baroreflex sensitivity (slope) and the HR range in a similar dose-dependent manner in both brain stem-intact and decerebrate rats. Such results draw into question whether the suprapontine sites contribute to enflurane's actions on cardiovascular autonomic regulation.     

Effect of central venous pressure on arterial baroreflex control of heart rate.

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.     

麻醉期心率变异性的非线性动力学分析

采用非线性动力学分析指标,分形维数,近似熵,复杂度分析44例受试者麻状态和清醒状态心率变异性的变化。分析结果表明,麻醉状态心率变异性的复杂度（P＜0．05）和近似熵均低于清醒状态（P＜0．1）,而麻醉状态的分形维数明显高于清醒状态（P＜0．001）,提示了心率变异性的非线性动力学变化可以作为麻醉深度监测的一项重要指标。     

全麻诱导时丙泊酚滴定给药与传统给药对患者血流动力学的影响

 目的：比较丙泊酚全麻诱导时滴定给药和传统给药对患者血流动力学的影响,以探求更安全、合理的麻醉诱导方案。方法：60例美国麻醉医师学会（American Society of Anesthesiology,ASA）分级Ⅰ~Ⅱ级、拟气管插管全麻下行择期手术的患者,随机分成2组,每组30例。Ⅰ组为传统给药组,按丙泊酚传统量2 mg·kg^-1以250 mg·min^-1的速度静脉泵注;Ⅱ组为滴定给药组,丙泊酚以1 mg·kg^-1·min^-1的速度静脉泵注,滴定至患者镇静警觉（OAA/S）评分1分,改为1  mg·kg^-1·h^-1维持。2组均在泵注丙泊酚的同时,给予芬太尼4 μg·kg^-1以注射泵注入。传统组给丙泊酚后1 min、滴定组入睡后给予顺阿曲库铵2  mg·kg^-1静推,4 min后行气管插管。记录诱导插管期间各个时点的收缩压（SBP）、舒张压（DBP）、平均血压（MBP）、心率（HR）和脉搏氧饱和度（SpO₂）。记录血压下降超过30%的例数。术后第2 d询问患者对插管过程是否有记忆。结果：2组均在一次试插即完成气管插管,术后随访均对插管过程无记忆。Ⅱ组SBP和MBP在给药后1 min、3 min及DBP在给药后1 min下降幅度均较Ⅰ组小（P<0.01）。Ⅱ组血压下降超过30％的例数较Ⅰ组少（P<0.01）。结论：和传统的给药方法相比,全麻诱导时丙泊酚滴定给药既能满足气管插管所需要的麻醉深度,又能避免血流动力学的剧烈波动。     

全身麻醉状态下心率变异性的连续小波分析

为更准确地通过分析心率变异性(HRV)判断麻醉深度随时间的变化,需要密切关注麻醉状态下HRV低频(LF)和高频(HF)成分随时间的变化情况,采用连续小波变换(CWT),将CWT中的尺度转换为频率,对患者麻醉前后的HRV信号(RR间期序列)进行了时频分析。其时频能量图以及LF、HF能量值都表明麻醉后HRV信号的LF和HF成分受到了抑制,LF/HF值也由麻醉前的9.021 9降为麻醉后的3.557 3。CWT和传统的时频分析方法在分析同一麻醉后HRV的时频分布表明,CWT可以更准确地定位HRV时域信号中出现突变的时间以及引起频率变化的频段范围。因此,CWT作为分析麻醉状态下HRV的一种新方法,能提供HRV更为准确的时频定位,进而提供更为准确的麻醉深度监控结果。     

Age-dependent effects of captopril on the arterial baroreflex control of heart rate in conscious lambs

To test the hypothesis that angiotensin (ANG) II modulates the arterial baroreflex control of heart rate (HR) in an age-dependent manner, various parameters governing the arterial baroreflex control of HR were assessed before and after removal of endogenously produced ANG II by administration of the angiotensin-converting enzyme (ACE) inhibitor, captopril, to conscious, chronically instrumented lambs aged approximately 1 week (8 +/- 1 days; n = 8) or approximately 6 weeks (46 +/- 5 days; n = 8). After administration of captopril, systolic, diastolic and mean arterial pressures decreased significantly from control levels and HR increased; however, the effects were greater in 1- than in 6-week-old lambs. In 1-week-old lambs, after administration of captopril, there was also a significant increase in the slope coefficient, a decrease in minimum HR and a decrease in the point of maximum gain. In 6-week-old lambs, there were no effects of captopril on any of the parameters governing the arterial baroreflex. Therefore, we accept our hypothesis and conclude that the role of ANG II in modulating cardiovascular homeostasis appears to be more predominant in the newborn than later in life.     

Self-biofeedback control of heart rate during exercise.

To improve cardiac adjustment to exercise, we developed a new self-biofeedback heart rate (HR) controller. Using this device, we analyzed time courses of HR, running speed (RS), stride length (ST) and pitch of gait (PI) in response to various preset HR levels in 7 normal human subjects. When HR was preset at 80 bpm, HR increased rapidly in response to exercise and exceeded the preset level at 12. 1 s with overshoot. At the preset HRs of 100, 120, 140 and 160 bpm, the HRs increased to each preset level at 39.2, 64.5, 58.5 and 83.0 s after the onset of exercise, respectively, and the HRs were adjusted with a range of +/- 4%. For all preset HRs, RS, ST and PI increased more rapidly than the HR and reached the maximum values within 30 s. During exercise, RS, ST and PI remained constant within 1.5-5.5 min. HR, RS, ST and PI increased in proportion to the preset HR. The increases in PI against HR (DeltaPI/DeltaHR) decreased with the higher HR level, and at HRs of 160-170 bpm, HR and PI showed identical rhythm. The increases in RS were produced by 18-59% increases in PI and by 12-44% increases in ST. We concluded that, using our newly developed self-biofeedback HR control system, we could control HR to a given preset value by a change in RS due to PI and ST.     

Instructed heart rate control in a high heart rate population

Forty college students were selected from a large number of introductory psychology students on the basis of high heart rate during an initial screening session. Subjects were then contacted and participated in two additional sessions during which heart rate, respiration rate, and skin conductance measures were obtained. Each session consisted of a baseline period followed by five trial periods during which subjects attempted to control their heart rate or performed a visual tracking task. Subjects were randomly assigned to one of four groups. One group served as a control and monitored a visual feedback display driven by their own heart rate but received no instructions to decrease their heart rate. In contrast, the three heart rate control groups were instructed to decrease heart rate during the trial periods by utilizing a relaxation procedure, proportional biofeedback, or proportional biofeedback plus criterion information. No group differences were present during the baseline periods. During feedback trials, however, all the training groups differed from the control in heart rate but did not differ from each other. It is suggested that feedback displays may not facilitate heart rate reduction beyond the level achieved by instructing subjects to use a general relaxation procedure.     

Respiratory sinus arrhythmia and carotid baroreflex control of heart rate in endurance athletes and untrained controls

The purpose of this study was to compare the magnitude of the respiratory sinus arrhythmia, an index of cardiac vagal tone, and carotid baroreflex control of heart rate in endurance-trained athletes (n = 12, aged 20 +/- 1 years, means +/- SE) and untrained control subjects (n = 12, aged 22 +/- 1 year). Average R-R interval (ECG) and its variability were determined at rest under controlled breathing conditions, and the changes in R-R interval in response to brief applications of suction (-10, -25, -40 mmHg) and pressure (10 and 30 mmHg) to the carotid sinus region of the neck were also measured. The average R-R interval at rest was greater in the athletes vs. controls (1150 +/- 45 vs. 854 +/- 44 ms, P less than 0.001), but the standard deviation of the R-R intervals was similar in the two groups (72 +/- 15 vs. 70 +/- 9 ms). The magnitude of the tachycardia in response to neck pressure was also similar in the athletes and controls. Although the heart rate responses to neck suction were not significantly different between the two groups, there was a strong trend for attenuated bradycardic responses in the athletes at the two highest stimulus levels (70 +/- 14 vs. 97 +/- 25 ms and 86 +/- 14 vs. 145 +/- 38 ms for the -25 and -40 mmHg levels, respectively, P greater than 0.1). The results of this study do not support the postulate that cardiac vagal tone is enhanced in the endurance-trained state.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.