The effects of an intravenous nicardipine injection on baroreflex control of heart rate in man

The effects of nicardipine injection on baroreflex control of heart rate were investigated by both pressor and depressor tests in 17 adult patients. Baroreflex sensitivity was attenuated after nicardipine injection by the pressor test using phenylephrine, whereas it was not changed by the depressor test using nitroglycerine. No resetting of the baroreflex occurred after nicardipine injection. By the pressor test, the plasma norepinephrine level was decreased, indicating that parasympathetic activity increased, and by the depressor test, the plasma norepinephrine concentration was increased, indicating that sympathetic activity increased. These results suggest that it is safe to use nicardipine clinically even when reduction in blood pressure for hypovolemia or unclamping the main artery is expected, and it is disadvantageous to administer the drug when an increase in blood pressure due to cross-clamping of the main artery is forecasted.(Wajima Z, Inoue T, Ogawa R: The effects of an intravenous nicardipine injection on baroreflex control of heart rate in man. J Anesth 7: 40–47, 1993)     

Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis

Endoscopic thoracic (T2-3 or T3-4) sympathectomy (ETS) is a highly effective treatment for palmar hyperhidrosis. Because the T2-3 or T3-4 sympathetic ganglia are involved in direct sympathetic innervation of the heart, sympathectomy at this level may alter baroreflex control of heart rate. The purpose of our study was to examine the influence of ETS on baroreflex responses to pressor and depressor stimuli under small-dose sevoflurane anesthesia. We studied 40 patients with palmar or axillary hyperhidrosis who were scheduled to receive ETS. In the ETS procedure, the sympathetic trunk was identified by using thoracic endoscopy and was transected. Before and after ETS, the pressor or depressor test was performed by using an IV infusion of phenylephrine or nitroglycerin, respectively, under small-dose general anesthesia. Baroreflex sensitivity was calculated from R-R intervals and systolic blood pressure. ETS did not change heart rate and systemic blood pressure at rest, although ETS significantly altered baroreflex in both pressor and depressor tests in all patients. Baroreflex was completely suppressed in 1 of 19 patients in the pressor test and in 9 of 21 patients in the depressor test. We conclude that baroreflex responses are suppressed in patients who receive ETS. IMPLICATIONS: Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.     

Depression of baroreflex control of heart rate by halothane in growing piglets

The purpose this study was to examine the effects of halothane on baroreflex control of heart rate in developing swine. Serial tests of baroreflex function were performed over the first 2 months of life in eight piglets in the conscious state and during anesthesia with 0.45, 0.9, and 1.35% halothane. Systemic blood pressure was increased with phenylephrine (pressor test) and decreased with nitroprusside (depressor test), and stimulus-response curves relating mean blood pressure to heart rate were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Halothane markedly depressed baroreflex sensitivity at all ages in a dose-dependent manner (conscious greater than 0.45% greater than 0.9%, 1.35%). Increasing age was accompanied by decreasing baroreflex sensitivity in both the conscious and the anesthetized states. The difference in baroreflex sensitivity between conscious and anesthetized states did not change with age for the depressor test (tachycardia response), but it did change with age for the pressor test (bradycardia response). For this test, conscious values converged toward anesthetized values at higher ages; therefore, there was relatively less depression by halothane at older ages. Halothane also decreased resting heart rate and decreased the limits and narrowed the range of the baroreflex heart rate response. Increasing age was accompanied by a decreasing resting heart rate and by decreasing limits and a narrowing range of the baroreflex response. The effect of halothane on heart rate variables was similar at all ages. Halothane decreased resting blood pressure and decreased the lower limit and widened the span of the baroreflex blood pressure range.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of fentanyl on baroreceptor reflex control of heart rate in newborn infants

Baroreceptor reflex control of heart rate was studied in ten neonates and young infants before and after intravenous fentanyl (10 micrograms/kg). All infants were in stable condition while being mechanically ventilated. Mean (+/- SD) corrected gestational age was 40.1 +/- 3.7 weeks, mean weight 3120 +/- 700 g. The pressor response was tested using phenylephrine and the depressor response using nitroglycerin. Changes in heart rate (R-R interval) were plotted against changes in systolic arterial pressure, and the slope of the linear portion of this relationship expresses the baroreflex sensitivity. No significant changes in systolic arterial pressure, heart rate, and blood gas values were observed after fentanyl injection when compared to control values. Mean (+/- SEM) control phenylephrine slope was 8.44 +/- 2.05 msec/mmHg, and mean nitroglycerin slope was 2.54 +/- 0.37 msec/mmHg. Both slopes decreased significantly by 48% and 42%, respectively, after fentanyl injection (P less than 0.02). Mean plasma fentanyl concentrations measured at the end of each test were not statistically different (5.11 +/- 0.65 ng/ml and 4.28 +/- 0.58 ng/ml, respectively). This suggests that the baroreflex control of heart rate is present in term neonates and markedly depressed during fentanyl anesthesia. Changes in blood pressure occurring during fentanyl anesthesia have to be carefully considered, because cardiac output is principally rate-dependent in newborns.     

Effects of propofol on baroreflex control of heart rate and on plasma noradrenaline levels

The effects of propofol induction (2.5 mg kg-1) and of two continuous infusion rates of propofol (100 and 200 micrograms kg-1 min-1) on baroreflex control of heart rate and on plasma noradrenaline concentration were investigated in 11 unpremedicated patients. Baroreflex function was assessed using a pressor test (phenylephrine) and a depressor test (sodium nitroprusside). In addition, samples for subsequent determination of plasma noradrenaline levels and blood propofol levels were collected before each test. Baroreflex sensitivity and plasma noradrenaline concentrations were not significantly changed at any time of the study. By contrast, a significant and sustained resetting of baroreflex set point was observed, allowing unchanged heart rate at lower arterial pressure. It is concluded that the effects of propofol on baroreflex function and noradrenaline concentration are moderate.     

Large dose of flunitrazepam attenuates baroreflex control of heart rate in man

The effects of intravenous tranquilizers such as flunitrazepan, diazepam and droperidol on baroreflex control of heart rate were investigated using both pressor and depressor tests. The dose-dependency was also studied by the administration of the drugs at the usual or twofold dosage. The usual dosage caused no significant change in neuronal controlling mechanism of circulation. However, flunitrazepam at double the usual dosage produced a decrease in baroreflex sensitivity at depressor tests. The results suggest that flunitrazepam when given repeatedly might accelerate hemodynamic derangements induced by an acute decrease in blood pressure.(Wajima Z: Large Dose of Flunitrazepam Attenuates Baroreflex Control of Heart Rate in Man. J Anesth 5: 10–16, 1991)     

Sevoflurane speeds recovery of baroreflex control of heart rate after minor surgical procedures compared with isoflurane.

Volatile anesthetics attenuate arterial baroreflex functions, whereas noxious stimuli may modify baroreflex-induced circulatory responses during anesthesia. We designed the present study to compare baroreflex control of heart rate during sevoflurane and isoflurane anesthesia in young healthy surgical patients. Baroreflex sensitivity was assessed in 24 patients randomized to receive either sevoflurane (n = 12) or isoflurane (n = 12) for general anesthesia. After an 8- to 10-h fast and no premedication, measurements of RR intervals obtained from electrocardiography and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline (Awake), during end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide before incision (Anesth), during surgery at end-tidal sevoflurane 2% or isoflurane 1.2% plus 67% nitrous oxide (Surg), and 20 min after tracheal extubation (Recov). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine (100-150 micrograms) and nitroprusside (100-150 micrograms) to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating RR intervals and SBP were determined to obtain baroreflex sensitivities. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during Anesth and Surg periods compared with Awake values in both anesthetic techniques. The pressor test sensitivity during the Recov period returned to the Awake value after sevoflurane (12.9 +/- 3.7 vs 11.0 +/- 8.7 ms/mm Hg [mean +/- SD]) but was still depressed after isoflurane anesthesia (13.9 +/- 8.0 vs 4.8 +/- 3.2 ms/mm Hg; P < 0.05). The depressor test sensitivities during the Recov period remained depressed after both anesthetic techniques. We conclude that both sevoflurane and isoflurane depress arterial baroreflex function during anesthesia and surgery, but the pressor test sensitivity was restored more quickly after sevoflurane than after isoflurane anesthesia. Implications: Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. We found that baroreflex control of heart rate due to hypertensive perturbation returned to the preanesthetic level more quickly after sevoflurane than after isoflurane anesthesia.     

The recovery profile of baroreflex control of heart rate after isoflurane or sevoflurane anesthesia in humans.

Volatile anesthetics attenuate baroreflex function in a concentration-dependent manner. This study was designed to determine how long full recovery of baroreflex control of heart rate takes after isoflurane or sevoflurane anesthesia in healthy volunteers. We assessed baroreflex sensitivity in 20 subjects randomized to receive either isoflurane or sevoflurane (n = 10 each). After an 8- to 10-h fast and no premedication, mea- surements of R-R intervals obtained from the electrocardiogram (lead II) and systolic blood pressure (SBP) measured through a radial artery catheter were made at conscious baseline and 20, 60, and 120 min after the induction during end-tidal isoflurane 1.3% or sevoflurane 2.0% in air and oxygen, and 20, 60, 120, and 180 min after the emergence from general anesthesia. Baroreflex responses were triggered by bolus IV injection of phenylephrine and nitroprusside to increase and decrease SBP by 15-30 mm Hg, respectively. The linear portions of the baroreflex curves relating R-R intervals and SBP were determined to obtain baroreflex sensitivity. During anesthesia, baroreflex sensitivities of both the pressor and depressor tests were decreased by 50%-60% compared with conscious baseline values in both groups (P <0.05). Pressor test sensitivities returned to the baseline values at 120 min, whereas depressor test sensitivities returned to the baseline values at 60 min, after general anesthesia in both groups. There were no significant differences in baroreflex sensitivities between groups at any interval. Our results indicate that the recovery characteristics of baroreflex sensitivity are similar after isoflurane and sevoflurane anesthesia and that the depressor test sensitivity is restored more rapidly than the pressor test sensitivity after both anesthetic techniques. IMPLICATIONS: Arterial baroreflex function is an important neural control system for maintaining cardiovascular stability. The authors found that 2 h was required for full recovery of baroreflex function and that recovery characteristics were similar after isoflurane and sevoflurane anesthesia in healthy volunteers not undergoing surgery.     

Comparison of arterial baroreflex function in humans anesthetized with enflurane or isoflurane

To compare the depressive effects of isoflurane and enflurane on the arterial baroreflex function, we examined baroreflex control of heart rate during the entire course of clinical anesthesia. Isoflurane and enflurane were found to have similar depressive effects on the baroreflex control of heart rate when used in combination with N2O and O2. Suppression in the baroreflex sensitivity, defined by the slopes of regression line (change in msec of RR interval per mm Hg increase or decrease in systolic blood pressure) was from 7.1 +/- 3.9 to 1.8 +/- 0.7 msec/mm Hg in patients given isoflurane and from 7.8 +/- 4.3 to 3.0 +/- 1.9 msec/mm Hg in those given enflurane when evaluated by a pressor test (bolus IV phenylephrine). The slope of the depressor test (bolus IV nitroglycerin) also decreased from 4.7 +/- 2.8 to 1.9 +/- 1.5 msec/mm Hg with isoflurane and from 5.6 +/- 3.2 to 2.3 +/- 1.2 msec/mm Hg with enflurane. During surgery in which anesthetic concentration invariably needed to be increased, the suppression of the baroreflex sensitivity remained unchanged in both groups of patients. During recovery, the arterial baroreflex function in patients given isoflurane recovered more rapidly than that in patients given enflurane. This difference may be related to a more minor degree of suppression of isoflurane on the autonomic nervous system compared to enflurane.     

The concentration-dependent effects of general anesthesia on spontaneous baroreflex indices and their correlations with pharmacological gains

Beat-to-beat assessment of spontaneously occurring fluctuations in heart rate and arterial blood pressure allows noninvasive determination of cardiovagal function, but little is known regarding the effects of general anesthesia on spontaneous baroreflex (SBR) indices. We examined (a) concentration-dependent effects of sevoflurane on SBR indices, heart rate variability (HRV), and blood pressure variability and (b) correlation and agreement between pharmacological baroreflex gains and SBR indices during sevoflurane anesthesia. Continuous electrocardiogram and invasive arterial blood pressure were monitored in nine healthy volunteers before, during, and for 3 h after sevoflurane anesthesia, during which end-tidal sevoflurane was maintained at 0.7%, 1.4%, and 2.0% in random sequences. We derived three SBR indices (sequence method, alpha-index, and low-frequency transfer function) and compared them with pressor and depressor test gains by the pharmacological method. HRV and blood pressure variability were analyzed at a fixed respiratory rate (12 breaths/min) in awake and anesthetized conditions. Except for low-frequency transfer function, SBR indices were depressed by sevoflurane and remained depressed for 30 min after emergence from anesthesia, compared with the conscious baseline value. Spontaneous sequence indices and high- and low-frequency powers of HRV demonstrated concentration-dependent depression. Pharmacological gains and SBR indices during anesthesia generally correlated well, but Bland-Altman analysis revealed that SBR indices had limits of agreement as large as the baroreflex gain itself. These data suggest that spontaneous indices are inadequate estimates of, and are inconsistent with, the pharmacological baroreflex gain during sevoflurane anesthesia.     

Isoflurane attenuates baroreflex control of heart rate in human neonates

Clinical studies have suggested that baroreflex regulation of heart rate may be more affected by inhalational anesthetics in human neonates or young animals than in adults. To test this hypothesis, baroreceptor reflex control of heart rate was studied in eight neonates during administration of 1 MAC isoflurane. The neonates were hemodynamically stable and their lungs were mechanically ventilated. No other anesthetic was used. Mean (+/- SD) corrected gestational age was 39.4 +/- 2.0 weeks and mean weight was 2,710 +/- 430 g. The pressor response was tested with the use of phenylephrine and the depressor response with nitroglycerin. Changes in heart rate (R-R interval) were plotted against the changes in systolic arterial pressure, and the slope of the linear portion of this relationship was used to define the baroreflex response. Both baroresponses measured in awake neonates varied widely between patients. With administration of approximately 1 MAC isoflurane, the pretest mean systolic arterial pressure decreased by about 30% (P less than 0.001), whereas mean heart rate values remained unchanged compared with control awake values. During isoflurane administration, the mean (+/- SD) pressor response decreased to 23% of control awake values (11.2 +/- 7.7 ms/mmHg vs. 2.6 +/- 3.7 ms/mmHg; P less than 0.01) and the depressor response to 28% of control (4.3 +/- 3.2 ms/mmHg vs. 1.2 +/- 0.8 ms/mmHg; P less than 0.05). These changes can be attributed to a significant resetting of heart rate itself (calculated as the change in R-R interval at a constant pressure).(ABSTRACT TRUNCATED AT 250 WORDS)     

Difference in the effect of pancuronium and vecuronium on baroreflex control of heart rate in humans

The effects of pancuronium and vecuronium, each in doses of 0.05 and 0.08mg·kg^–1, on the baroreflex control of the heart rate were studied in 40 adult patients of either sex (21 men and 19 women) during stable nitrous oxide-oxygen-fentanyl anesthesia. The blood pressure was elevated by intravenous infusion of phenylephrine (4µg·kg^–1·min^–1) for the pressor test, and lowered by a bolus injection of nitroglycerin (0.3–0.5mg) for the depressor test. Baroreflex sensitivity was judged from the slope of the regression of the systolic blood pressure on the succeeding R-R intervals on the ECG. There was no significant difference between the baseline blood pressure at which both tests were carried out. Nitrous oxide-oxygen-fentanyl anesthesia alone suppressed the baroreflex sensitivity to a level which was at the lower limit of the physiological and non-anesthetized state. The 0.08mg·kg^–1 dose of pancuronium significantly suppressed the reflex sensitivity in both the pressor and depressor tests. However, the 0.05mg·kg^–1 dose of pancuronium and both doses of vecuronium did not cause any significant change in the test results.(Tsuchida H, Seki S, Nakae Y, et al.: Difference in the effect of pancuronium and vecuronium on baroreflex control of heart rate in humans. J Anesth 5: 255–259, 1991)     

Effects of droperidol on sympathetic activity and baroreflex control of heart rate in humans

The effects of intravenous droperidol, 0.2 mg . kg-1, on baroreflex control of heart rate and on plasma catecholamine levels were determined in 10 ASA physical status I unpremedicated patients. Baroreflex control of heart rate was assessed by a pressor test using phenylephrine. Plasma concentrations of norepinephrine and epinephrine were determined by high pressure liquid chromatography, and plasma droperidol concentrations were measured by radioimmunoassay, from blood samples withdrawn before baroreflex evaluation. All data were obtained before and 5, 10, and 15 min following droperidol administration. Baroreflex response was significantly decreased after droperidol at each time of the study with the maximal decrease (-47% from control) observed at 5 min. No resetting of baroreflex was present since the pulse interval at the reference pressure was unchanged. Plasma norepinephrine concentrations were moderately but significantly increased only at 5 min, while no significant change in epinephrine concentrations was observed. It is concluded that droperidol induces a moderate but sustained alteration of baroreflex function and a transient increase in plasma norepinephrine concentrations.     

The effects of increasing plasma concentrations of dexmedetomidine in humans

BACKGROUND: This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. METHODS: Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). RESULTS: The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. CONCLUSIONS: Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.     

The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

Background: This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans.

Methods: Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml).

Results: The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged.     

Baroreflex Sensitivity of an Arterial Wall During Rotary Blood Pump Assistance

It is well known that the baroreflex system is one of the most important indicators of the pathophysiology in hypertensive patients. We can check the sensitivity of the baroreflex by observing heart rate (HR) responses; however, there is no simple diagnostic method to measure the arterial behavior in the baroreflex system. Presently, we report the development of a method and associated hardware that enables the diagnosis of baroreflex sensitivity by measuring the responses of both the heart and the artery. In this system, the measurements are obtained by monitoring an electrocardiogram and a pulse wave recorded from the radial artery or fingertip. The arterial responses were measured in terms of the pulse wave velocity (PWV) calculated from the pulse wave transmission time (PTT) from the heart to the artery. In this system, the HR change corresponding to the blood pressure change in time series sequence was observed. Slope of the changes in blood pressure and HR indicated the sensitivity of the baroreflex system of the heart. This system could also measure the sensitivity of the baroreflex system of an artery. Changes in the PWV in response to the blood pressure changes were observed. Significant correlation was observed in the time sequence between blood pressure change and PWV change after calculating the delay time by cross-correlation. The slope of these parameter changes was easily obtained and it demonstrated the sensitivity of the baroreflex system of an artery. We evaluated this method in animal experiments using rotary blood pump (RBP) with undulation pump ventricular assist device, and PTT elongation was observed in response to increased blood pressure with RBP assistance. Furthermore, when tested clinically, decreased sensitivity of the baroreflex system in hypertensive patients was observed. This system may be useful when we consider the ideal treatment and follow-up of patients with hypertension.     

静吸复合麻醉对动脉压力反射的影响

本文对２０例病人进行加压和减压试验，比较在醒时、静吸复合麻醉下、术中及苏醒后四种状态下，动脉压力反射敏感性（即Ｒ－Ｒ间期与收缩压的线性回归方程的斜率）的变化。结果表明，麻醉后其敏感性较清醒时显著减低（Ｐ＜０．０１）。该结果提示，静吸复合麻醉一定程度地抑制动脉压力反射功能。     

Circulatory responses to baroreflexes, Valsalva maneuver, coughing, swallowing, and nasal stimulation during acute cardiac sympathectomy by epidural blockade in awake humans

Reflex circulatory responses are chiefly governed by the integrated functions of both sympathetic and parasympathetic nervous systems at any moment. To examine how sympathetic denervation of the important effector organ, the heart, modifies such reflex responses, the authors compared circulatory responses to arterial baroreflexes, the Valsalva maneuver (VM), coughing (C), swallowing (S), and nasal stimulation (NS) before and after cervical epidural blockade using 10 ml of 1.5% lidocaine in awake, healthy humans. The cervico-thoracic sympathetic denervation (sensory block of C4-T7) caused a slight suppression of the baroreflex sensitivity assessed by increases in RR intervals to increased systolic blood pressure with a pressor test (phenylephrine) in all eight subjects studied; the mean slopes of the regression lines were 29.1 +/- 9.8 ms X mmHg-1 before the blockade and 17.2 +/- 6.3 ms X mmHg-1 after the blockade (P less than 0.05). However, the baroreflex sensitivity to a depressor test (nitroglycerin) remained unchanged following the blockade. Furthermore, the responses in heart rate and blood pressure to VM (Phases II and IV) and the responses in heart rate to C, S, and NS were partially suppressed after the blockade (P less than 0.05). Despite these suppressions, the overall responses to VM, C, S, and NS remained unchanged after the blockade. No predominant parasympathetic responses such as profound hypotension and bradycardia were observed during any maneuver after the blockade.(ABSTRACT TRUNCATED AT 250 WORDS)     

EFFECTS OF FENTANYL-DIAZEPAM-NITRIOUS OXIDE ANAESTHESIA ON ARTERIAL BAROREFLEX CONTROL OF HEART RATE IN MAN

The effects of fentanyl 7.5 µg kg^–l (group I), 10.0µg kg^–1 (group Il) and 12.5 µg kg^–1(group lll) with diazepam 0.25 mg kg^–l and 70% nitrousoxide on baroreflex control of heart rate in humans were investigated.Phenylephrine (the pressor test), sodium nitroprusside (thedepressor test) and graded neck suction provoked baroreflexresponses. In group I the pressor, depressor and neck suctionbaroreflex slopes decreased during anaesthesia. In groups IIand III the depressor test slopes were also decreased duringanaesthesia. However, the slopes derived from the pressor andneck suction tests did not decrease. These data suggest thatbaroreflex control of heart rate is attenuated during low dosesof fentanyl (7.5 µg kg^–1). Baroreflex mediated tachycardiais decreased by higher doses of fentanyl (10.0 and 12.5 µgkg^–1). However, baroreflex-mediated bradycardia is maintainedduring the higher doses of fentanyl. We suggest this effectis the result of enhanced vagal efferent activity mediated byfentanyl.     

Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy

OBJECTIVES: This study was undertaken to test the hypothesis that there is a neural basis for baroreceptor deterioration during carotid endarterectomy (CEA), by investigating intraoperative hemodynamic changes induced by intraluminal carotid stretch stimulation, before and after application of local anesthetic to the adventitial layer of the carotid sinus region. METHODS: This was a prospective study of 20 patients undergoing elective CEA. During CEA, before removal of the atheroma, intraluminal stretch simulation of the carotid baroreceptors (rub test) was performed before and after injection of 1% lignocaine into adventitial tissue of the artery in the region of the carotid sinus. Continuous measurements of mean arterial blood pressure (MAP), electrocardiographic r-r intervals (R-R), heart rate, cardiac vagal tone, and carotid sinus baroreflex were recorded to determine alterations in baroreceptor function. RESULTS: Rub test before injection of lignocaine was associated with a decrease in MAP and heart rate and an increase in R-R, cardiac vagal tone, and carotid baroreflex response, indicating a functioning baroreflex. After lignocaine injection and repetition of the rub test, no significant change was seen in MAP, heart rate, R-R, cardiac vagal tone, or carotid baroreflex response, indicating a nonfunctioning baroreflex. Comparing the peak responses to the rub test stimulus before and after lignocaine injection showed significant differences for all variables (P <.05), with carotid baroreflex response and heart rate being highly significant (P <.0005). CONCLUSIONS: The baroreflex response to intraluminal stretch stimulation of the carotid sinus area is operational in patients undergoing CEA, and this response is abolished by infiltration of local anesthetic into the periadventitial tissue around the carotid sinus.