Bolus Administration Of Phenylephrine Research Articles

Ephedrine and phenylephrine induce opposite changes in cerebral and paraspinal tissue oxygen saturation, measured with near-infrared spectroscopy: a randomized controlled trial.

While the effects of phenylephrine (PE) and ephedrine (E) on cerebral oxygen saturation (rScO2) already has been studied, the effect on paraspinal oxygen saturation (rSpsO2) is still unexplored. This study aims to assess the effect of PE and E on rScO2 and rSpsO2, measured with near-infrared spectroscopy. A randomized 4-treatment cross-over trial was designed in 28 patients under BIS-titrated anaesthesia with sevoflurane. If MAP decreased more than 20% from baseline, incremental doses of PE and/or E were given according to the randomization (group I: E-PE-E, group II: PE-E-PE, group III: E-E-E, group IV: PE-PE-PE). rScO2 and rSpsO2 on T3-T4, T9-T10 and L1-L2 were recorded. Differences in rSO2 (post-pretreatment) within each group were analyzed with paired Student's t test. Differences in effects of PE and E on rScO2 and rSpsO2 were analyzed with linear mixed-modelling. Following PE administration, rScO2 decreased significantly (- 2.7% ± 3.5), while it remained stable following E (- 0.6% ± 3.6). Contrastingly, rSpsO2 at T3-T4, T9-T10 and L1-L2 slightly increased following PE (0.4% ± 2.5, 0.7% ± 2.0 and - 0.1% ± 1.4, respectively), while it decreased after E administration (- 1.3% ± 3.4%, - 0.7% ± 2.6% and - 1.3% ± 2.7%, respectively). Compared to E, PE administration was associated with a significant decrease in rScO2 (- 2.1%, 95% CI [- 3.1%, - 1.2%], p < 0.001). In contrast, compared to PE, E was associated with a significant decrease in rSpsO2 at T3-T4, T9-T10 and L1-L2 (- 2.0%, 95% CI [- 2.8, - 1.1], p < 0.001; - 1.4%, 95% CI [- 2.4%, - 0.4%], p = 0.006; and - 1.5%, 95% CI [- 2.3%, - 0.8%], p < 0.001, respectively). An opposite effect on rScO2 and rSpsO2 was observed after bolus administration of PE and E.

Localized WR-1065 Delivery to Murine Salivary Glands has Radioprotective Effect and Hemodynamic Benefit Over Systemic Administration

There are over 50,000 cases of head and neck cancer (HNC) diagnosed each year in the United States. Approximately 75% of these patients will undergo radiation at some point during their treatment, and of those patients over 50% will go on to develop permanent xerostomia. Amifostine is the only FDA approved drug for use in xerostomia radioprophylaxis, but suffers from a narrow therapeutic window and systemic toxicities including severe nausea and hypotension that severely limit its clinical utility. To overcome challenges of systemic administration and potentially increase effectiveness, local delivery via Wharton’s duct of WR-1065 (the active metabolite of Amifostine) was utilized. Our hypothesis is that retroductal delivery of WR-1065 to the murine submandibular gland (SMG) will improve salivary gland function while reducing drug side effects such as hypotension at 90 days following a single xerogenic dose (15.0 Gy) of irradiation. All studies used n = 5 C57BL/6 female mice per treatment group. To assess blood pressure response, anesthetized mice underwent bilateral femoral catheterization and aortic placement of a pressure transducer. Mice received either IV or retroductal doses of Amifostine or WR-1065. Baroreflex was subsequently measured by bolus administration of phenylephrine. For radiation studies, mice received unilateral SMG injection with WR-1065 or saline. A single dose of 15.0 Gy was then delivered to the submandibular glands using a Cs137 irradiator with a slit collimator. Study endpoints include volume of stimulated saliva secretion 90 days post irradiation, SMG histology, and immunohistochemical staining compared to irradiated and nonirradiated control groups. Hemodynamic data show retained baroreflex sensitivity and mean arterial pressure following retrograde WR-1065 injection. Furthermore, mice receiving retrograde WR-1065 show significantly higher volumes of stimulated saliva secretion (61±29 μL) compared to irradiated (14±8 μL) and saline treated controls (19 ±7 μL) at 90 days (p<0.05). Furthermore, no significant difference exists in gland secretion between irradiated WR-1065 treated mice and non-irradiated mice. Preliminary data shows improvement in stimulated saliva secretion and gland histology in WR-1065 retroductally treated mice 90 days post irradiation. Hemodynamic data further supports development of this drug delivery modality for SMG radioprotection, as blood pressure and baroreflex sensitivity are retained following retrograde WR-1065 injection.

Hemodynamic effects of ephedrine and phenylephrine bolus injection in patients in the prone position under general anesthesia for lumbar spinal surgery.

Ephedrine and phenylephrine (PE) are vasoconstrictors commonly used to restore the blood pressure (BP) to normal values. The aim of the present study was to investigate the effects of ephedrine and PE bolus administration on intra-arterial systolic BP (ISBP), intra-arterial diastolic BP (IDBP) and cardiac output (CO) in patients undergoing lumbar spine surgery in the prone position under general anesthesia (GA). In this prospective, randomized, and double-blind study, a total of 60 patients aged 20-60 years and undergoing elective lumbar spine surgery were administered either a single dose of ephedrine (0.1 mg/kg) or PE (1 µg/kg) through a central venous catheter as a bolus injection following the achievement of a stable hemodynamic status for ≥10 min. Following bolus injection of ephedrine or PE, a significant increase in ISBP was observed in the two experimental groups compared with pre-ephedrine and pre-PE values. The duration of the increment in ISBP however was significantly longer in the ephedrine group compared with the PE group. A similar response was observed in IDBP. A significant increase in CO began 1 min following ephedrine injection and lasted for the entire observation period, whereas the increase was only sustained for 3 min following bolus injection in the PE group. The results of the present study demonstrated that bolus ephedrine produces a more persistent pressor response and durable increase in CO and CI compared with PE when patients are in the prone position with GA for spine surgery.

6% Hydroxyethyl starch (130/0.4) vs Ringer's lactate preloading before spinal anaesthesia for Caesarean delivery: the randomized, double-blind, multicentre CAESAR trial

Vasopressor administration is recommended to prevent hypotension during spinal anaesthesia (SA) for elective Caesarean delivery. We aimed to test the superior efficacy and ensure safety of a hydroxyethyl starch (HES) vs a Ringer's lactate (RL) preloading, when combined with a phenylephrine-based prophylaxis. A total of 167 healthy parturients undergoing elective Caesarean delivery under SA were included in this multicentre, randomized, double-blind study. Patients received 500 ml of 6% HES (130/0.4)+500 ml of RL (HES group) or 1000 ml of RL (RL group) i.v. before SA. After SA, i.v. phenylephrine boluses were titrated when systolic arterial pressure (SAP) was below 95% of baseline. The primary outcome was the incidence of maternal hypotension (SAP <80% of baseline). The incidence of both hypotension and symptomatic hypotension (i.e. with dizziness, nausea/vomiting, or both) was significantly lower in the HES group vs the RL group: 36.6% vs 55.3% (one-sided P=0.025) and 3.7% vs 14.1%. There was no significant difference in total phenylephrine requirements [median (range): 350 (50-1800) vs 350 (50-1250) µg]. The decrease in maternal haemoglobin value the day after surgery was similar in the two groups [1.2 (1.0) vs 1.0 (0.9) g dl(-1)]. There was no detectable placental transfer of HES in six umbilical cord blood samples analysed in the HES group. Neonatal outcomes were comparable between the groups. Compared with a pure RL preloading, a mixed HES-RL preloading significantly improved prevention of both hypotension and symptomatic hypotension based on early phenylephrine bolus administration and did not induce adverse effects. NCT00694343 (http://clinicaltrials.gov).

Phenylephrine versus ephedrine on cerebral perfusion during carotid endarterectomy (PEPPER): study protocol for a randomized controlled trial

BackgroundIntraoperative arterial hypotension can lead to severe complications in patients undergoing carotid endarterectomy, in particular if cerebral auto-regulation is impaired. Short-acting agents, such as phenylephrine or ephedrine, commonly used to correct intra-operative hypotension, have different hemodynamic effects. Recently, it was reported that, in healthy anesthetized subjects with intact cerebral auto-regulation, frontal lobe cerebral tissue oxygenation declined after phenylephrine bolus administration, while it was preserved after ephedrine use (Br J Anaesth 107:209–217, 2011; Neurocrit Care 12:17–23, 2010). However, the effect of both agents in patients undergoing carotid endarterectomy is unknown. The aim of this study is to assess the effect of two routinely used vasopressors (phenylephrine and ephedrine) on the cerebral hemodynamics during carotid endarterectomy.Methods/designPatients undergoing carotid endarterectomy will be prospectively included and randomized for correction of intraoperative hypotension with either phenylephrine (50 to 100 μg) or ephedrine (5 to 10 mg). If hypotension persists for more than five minutes after treatment, the patient will be classified as a non-responder and escape medication as preferred by the anesthesiologist will be administered. Changes in cerebral hemodynamics will be quantified by changes in transcranial Doppler-derived middle cerebral artery blood velocity and near infra-red spectroscopy-derived frontal lobe cerebral tissue oxygenation, when intra-operative hypotension is treated with phenylephrine or ephedrine in patients who undergo carotid endarterectomy with or without an adequate functioning cerebral auto-regulation.To quantify whether the intra-operative cerebral auto-regulation is impaired or not, a decrease in breathing frequency from the normal 12 breaths per minute to 6 breaths per minute for an episode of three minutes will be performed.DiscussionPhenylephrine and ephedrine are two of the most commonly used short-acting agents to increase blood pressure in clinical anesthesiologic practice. Monitoring of middle cerebral artery blood velocity with transcranial Doppler and frontal lobe cerebral tissue oxygenation with near infra-red spectroscopy are part of the standard of care. Furthermore, there are no reports that the three-minute modification in breathing frequency described in the “intervention”-section is harmful. Therefore, the risks for participating patients are negligible and the burden minimal.Trial registrationClinical trials.gov: NCT01451294

Blood pressure management and regional cerebral oxygen saturation during surgery in beach chair position

It was interesting to read the paper by Ko et al. [1] regarding cerebral oxygen saturation monitoring in patients undergoing an arthroscopic shoulder surgery in beach chair position (BCP). While mostly agreeing with their conclusion, one may also raise a few concerns, such as the timely determination of baseline values and the proper use of vasopressors. As to whether blood pressure should be corrected to account for the level difference between the site of measurement (most commonly a non-invasive cuff on the non-operative arm) and the brain in BCP is under debate [2]. They indeed evaluated whether measured at the level of the brain or at the level of the heart correlated with regional cerebral oxygen saturation (rSO2) in patients undergoing BCP surgery, and found that measured at the brain, but not at the heart level, correlated with rSO2. Nevertheless, they stated in the conclusion that Monitoring cerebral rSO2 and at the level of brain can be helpful to detect the possibility of cerebral deoxygenation earlier [1]. To admit their observation, it would be proper to state that MAP measured at the brain but not at the heart level reflects rSO2 in patients undergoing surgery in BCP. They also mentioned that Baseline mean arterial pressure, ---, BIS, and left and right rSO2 were recorded while the patient's condition was stable over 5 minutes before induction. However, the induction of anesthesia and the use of high inspired oxygen fraction per se may significantly decrease BIS and increase rSO2 values [3]. As such, we believe that these parameters measured after (i.e., immediately before patients were raised into BCP) the induction of anesthesia better represents the baseline values. Phenylephrine, an α-agonist, and ephedrine, an α- and β-agonist, are both commonly used to maintain and thus, cerebral perfusion pressure in neurosurgical patients who develop hypotension. However, in healthy anesthetized subjects with intact cerebral autoregulation, a bolus administration of phenylephrine reduced the rSO2 measured by a near-infrared spectroscopy device under intravenous anesthesia with propofol/remifentanil, whereas ephedrine maintained it [4,5]. In this context, phenylephrine and ephedrine may have differentially affected rSO2 in their study. Moreover, they did not use equipotent dosages of the two vasopressors. Would it not be better for them to have included it as one of the limitations of the study?

Chronic AT1‐receptor blockade does not alter cerebral oxygen supply/demand ratio during cardiopulmonary bypass in hypertensive patients

The angiotensin II receptor type 1 antagonist candesartan has been hypothesized to alter vasopressor requirements and brain-blood flow by changing cerebrovascular autoregulation. Therefore, we assessed the effects of a pre-anaesthetic treatment course with candesartan on cerebral arterial-jugular bulb oxygen content difference, middle cerebral artery blood velocity, and vasopressor requirements in hypertensive patients undergoing elective on-pump coronary artery bypass graft surgery. In a randomized, double-blind, placebo-controlled study, we evaluated the effects of candesartan (8 mg po/d, given for 6-8 days before surgery) in 35 hypertensive patients. The mean arterial pressure was maintained above 60 mmHg by bolus administration of phenylephrine, if required, and dosages were recorded. Candesartan did not significantly alter oxygen content difference across the cerebral circulation, mean middle cerebral artery blood velocity during cardiopulmonary bypass, or phenylephrine requirements either before (0.0067 microg/kg/min+/-0.0042 vs. 0.0056 microg/kg/min+/-0.0049, P=0.48) or during cardiopulmonary bypass (0.0240 microg/kg/min+/-0.0240 vs. 0.0250 microg/kg/min+/-0.0190, P=0.97) compared with placebo. Thus, a 6-8-day treatment course with candesartan does not alter global cerebral perfusion and oxygen supply/demand ratio during cardiopulmonary bypass, or vasopressor requirements in hypertensive patients undergoing on-pump coronary artery bypass graft surgery, and no deleterious consequences of AT1-receptor blockade were detected.

Modulation of arterial baroreflexes by antisense oligodeoxynucleotides to NMDAR1 receptors in the nucleus tractus solitarius

An antisense oligodeoxynucleotide which specifically blocked the production of the glutamate receptor subtype NMDAR1 was administered to the nucleus tractus solitarius (NTS) in order to examine the role of this receptor in baroreflex control of heart rate. Baseline blood pressure and heart rate were unchanged by NTS treatment with the antisense oligodeoxynucleotide to the NMDAR1 receptor subunit. However, the reflex bradycardia evoked in response to the hypertension induced by bolus administration of phenylephrine was significantly attenuated following bilateral NTS antisense oligodeoxynucleotide treatment. Administration of the corresponding mismatched antisense oligodeoxynucleotide did not significantly alter the reflex bradycardia. These data indicate that NMDAR1 receptors are involved in neurotransmission in the baroreflex arc at the level of the NTS. The specificity of antisense oligodeoxynucleotides may prove to be a useful technique to analyze the role of receptor subtypes mediating neurotransmission in central pathways.

976-12 Reduced Reflex Vagal Activity in Patients with AV Nodal Reentrant Tachycardia Compared to Patients with Atrioventricular Reentrant Tachycardia

Decreased heart rate variability, a manifestation of reduced tonic vagal activity. has been reported following radiofrequency catheter ablation (RFCA) for AV nodal reentrant tachycardia (AVNRT). Disruption of parasympathetic fibers in the posteroseptal region is the proposed mechanism. Baroreflex sensitivity (BRS). an index of reflex vagal activity. has not been evaluated in patients with AVNRT. We studied BRS prior to and immediately following RFCA in 20 patients with AVNRT(age 13–65 years, mean 42; 15 females. 5 males). Fourteen patients with atrioventricular reentrant tachycardia (AVRT) and free wall accessory pathways (age 14–46 years. mean 25; 6 females. 8 males) were evaluated as controls (RFCA site far from posteroseptal region I. BRS (msec/mmHg) was assessed with continuous femoral artery blood pressure (BP) and ECG recordings during the bolus administration of phenylephrine (400 μg). BRS was calculated as the slope of the change in cycle length vs the change in systolic BP during the first sustained rise in BP. At baseline. prior to RFCA. mean BRS for patients with AVNRT was significantly less than for patients with AVRT (8.3 ± 5.9 vs 22.1 ± 10.3; P &lt; 0.0002). This difference remained significant when controlled for age (p &lt; 0.0002) and male gender (p &lt; 0.0003). but not for female gender (p &lt; 0.09). Following RFCA there was no significant change in BRS for patients with AVNRT (9.3 ± 7.6) or AVRT (17.3 ± 9.6) compared to pre-RFCA values. This comparison remained insignificant when controlled for age or gender. These results suggest that in the baseline state, patients with AVNRT have lower reflex vagal activity than patients with AVRT. Reduced reflex vagal activity may contribute to the development of sustained AVNRT in patients with dual AV nodal physiology. RFCA did not alter BRS in either patient group.

Effect of phenylephrine bolus administration on left ventricular function during postural hypotension in anesthetized patients

Study Objective: To investigate the effect of intravenous (IV) phenylephrine (PHE) bolus administration on left ventricular function in patients who developed postural hypotension during isofurane anesthesia in the head-up tilt (reverse Trendelenburg) position. Design: Prospective “before-after” trial. Setting: Operation theater of a university medical center. Patients: 15 ASA physical status I and II patients without cardiovascular disorders. Interventions: The anesthetized patients were tilted from a supine horizontal to a 30-degree reverse-Trendelenburg position. Once a steady state was achieved, PHE 3 μg/kg was administered as an IV bolus dose. Measurements and Main Results: Transesophageal echocardiography was used to assess left ventricular function. We measured blood pressure (BP); heart rate; left ventricular end-systolic and end-diastolic area, diameter, and wall thickness; and ejection time at baseline and after tilt, immediately before and for a period of 3 minutes after PHE injection. We calculated fractional area change (FAC), mean velocity of circumferential fiber shortening (mVcf), and end-systolic wall stress. Head-up tilt caused a reduction of mean arterial pressure [from 68 to 54 mmHg (mean)], end-systolic and end-diastolic left ventricular area (from 9.7 to 6.5 cm 2 and from 19.2 to 13.1 cm 2, respectively) and end-systolic wall stress (from 56 to 33 10 3 · dyne/cm 2). FAC and mVcf remained unaltered. PHE administration restored baseline values or overcompensated the changes caused by tilt. FAC slightly decreased in response to PHE (from 0.51 to 0.43), end-systolic wall stress increased to 83 10 3 · dyne/cm 2, and mVcf remained unchanged. Conclusion: PHE bolus administration effectively restored BP and cardiac filling which were reduced after head-up tilt, without causing a relevant impairment of left ventricular function or an increase in end-systolic wall stress above the upper normal limit.

The Effect of Phenylephrine Bolus Administration on Left Ventricular Function During Isoflurane-Induced Hypotension

The Effect of Phenylephrine Bolus Administration on Left Ventricular Function During Isoflurane-Induced Hypotension

Effect of phenylephrine bolus administration on left ventricular function during high thoracic and lumbar epidural anesthesia combined with general anesthesia.

The effect of phenylephrine (PHE) boluses on left ventricular (LV) function was examined in patients without cardiovascular disease who developed arterial hypotension during high thoracic epidural anesthesia (TEA) combined with general anesthesia (GA) (group 1) or lumbar epidural anesthesia (LEA) combined with GA (group 2). LV function was assessed by transesophageal echocardiography (TEE) before and after central venous injection of 1 microgram/kg PHE. Fractional diameter shortening (FDS), end-systolic wall stress (ESWS), and rate-corrected velocity of circumferential fiber shortening (mVcfc) were determined. PHE effectively restored arterial blood pressure in both groups with a peak effect between 30 and 45 s after injection. FDS was reduced from 38% to 25% (mean, P < 0.01) in group 1 and remained unchanged in group 2. ESWS increased from 70 to 143 x 10(3) dyne.cm-2 (P < 0.01) and from 57 to 86 x 10(3) dyne.cm-2 (P < 0.05), in groups 1 and 2, respectively. mVcfc was significantly reduced from 1.11 to 0.80 circ/s (P < 0.05) in group 1 and was not altered in group 2. The authors conclude that PHE given as an intravenous bolus to patients under high TEA plus general anesthesia causes a transient impairment of LV function.

Calcium Channel Modulation of α1- and α2-Adrenergic Pressor Responses in Conscious and Anesthetized Dogs

The influence of halothane and isoflurane on alpha-adrenergic-mediated vasoconstriction before and following calcium channel modulation was investigated in chronically instrumented dogs. After ganglionic, cholinergic, and beta-adrenergic blockade, systemic hemodynamic responses following equieffective pressor doses of phenylephrine (0.6 micrograms/kg iv), a selective alpha 1 agonist, and azepexole [B-HT 933] (20 micrograms/kg iv), a selective alpha 2 agonist, were obtained. The calcium channel stimulator Bay k 8644 (0.5 and 1 micrograms.kg-1.min-1) was infused intravenously for 10 min and phenylephrine and azepexole administered at the end of each infusion. On different days, each dog was subsequently anesthetized with equihypotensive concentrations of halothane (1.7%) or isoflurane (2%) in oxygen and the same pharmacologic interventions were repeated in the presence of halothane or isoflurane. Twenty-one experiments (three groups) using seven chronically instrumented dogs were completed. Halothane and isoflurane produced significant (P less than 0.05) attenuation of the increase in arterial pressure after bolus administration of phenylephrine and azepexole. Bay k 8644 augmented the pressor responses mediated by both phenylephrine and azepexole in all three groups. Thus, halothane and isoflurane nonselectively reduced the pressor response to both alpha 1- and alpha 2-adrenergic receptor stimulation and this was probably not mediated by inhibition of transmembrane calcium flux through dihydropyridine sensitive channels.

Opiate receptor inhibition improves the blunted baroreflex function in conscious dogs with right-sided congestive heart failure.

The endogenous opiate system is activated in congestive heart failure. because endogenous opioids are known to depress the baroreflex function, we conducted studies to determine whether the increased endogenous opioids play a role in causing the reduced baroreflex function that occurs in heart failure. Right-sided congestive heart failure was produced in 16 dogs by tricuspid avulsion and progressive pulmonary artery constriction. Seven sham-operated dogs were included for comparison. Baroreflex function was measured in the conscious dogs after pretreatment with either normal saline or an opiate-receptor antagonist by bolus administration of phenylephrine. The slope of the regression line relating systolic blood pressure to cardiac cycle (R-R) interval was taken as an index of baroreflex sensitivity. Plasma beta-endorphin was elevated in the dogs with heart failure (15.3 +/- 2.5 pmol/l) compared with the sham-operated dogs (4.2 +/- 0.4 pmol/l, p less than 0.001). The dogs with heart failure also exhibited a reduced baroreflex sensitivity (3.84 +/- 0.19 msec/mm Hg) after saline pretreatment when compared with the sham-operated dogs (10.86 +/- 1.20 msec/mm Hg, p less than 0.001). Administration of naloxone hydrochloride increased the baroreflex sensitivity of dogs with heart failure to 5.16 +/- 0.26 msec/mm Hg (p less than 0.01) but produced no significant effects in sham-operated dogs (11.36 +/- 1.42 msec/mm Hg). To further study the site of action for the effect of naloxone, we measured baroreflex sensitivity in the dogs with heart failure after pretreatment with naloxonazine, a selective mu-receptor antagonist, with ICI 154,129, a selective delta-receptor antagonist, or with naloxone methobromide, a quaternary analogue of naloxone that does not penetrate the blood-brain barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Influecne of nifedipine on arterial baroreflex modulation of heart rate control during dynamic increases in arterial pressure: Studies in normal man

Studies in animals have demonstrated that calcium channel blocking agents exert important influences on autonomic mechanisms in addition to their direct vascular effects. Previous studies in our laboratory showed that clinical doses of nifedipine sensitized baroreceptor-mediated control of peripheral vascular resistance in normal human subjects. However, baroreflex control of vascular tone does not necessarily imply parallel control of heart rate. A series of experiments was therefore performed to test the hypothesis that therapeutic doses of nifedipine would potentiate arterial baroreflex modulation of heart rate during ramp increases of arterial pressure in normal volunteers. Arterial baroreflex control was assessed by measuring heart interval (HI) responses to dynamic ramp elevation of systolic arterial pressure (SAP) with bolus administration of phenylephrine (PE) before and after nifedipine or placebo in 19 normal subjects. Arterial baroreflex control was calculated from the slope of the regression of SAP on succeeding HI during the first 18 cardiac cycles following onset of rise of SAP after PE bolus. In 13 subjects, bolus PE produced an increase in SAP from 125 ± 3 mm Hg to 152 ± 5 mm Hg ( p < 0.01), with a resultant increase in HI from 1110 ± 57 msec to 1541 ± 87 msec ( p < 0.01). The baroreflex response was linear ( r > 0.80, p < 0.025) and = 17.8 ± 3.3 msec/mm Hg. After nifedipine (20 mg sublingual), there was no change in central venous pressure and the same dose of PE increased SAP from a similar baseline value of 119 ± 3 mm Hg ( p = NS vs pre nifedipine) to 133 ± 3 mm Hg ( p < 0.01), with a consequent increase in HI from 957 ± 41 msec to 1254 ± 64 msec ( p < 0.01). The baroreflex slope of this response post nifedipine was augmented to 22.5 ± 2.8 msec/mm Hg ( p < 0.05 pre vs post nifedipine). In six additional subjects, administration of placebo had no effect on arterial baroreflex responses to PE-induced increase in SAP. Thus, in addition to augmenting baroreceptor modulation of vascular resistance in normal man, nifedipine also augments arterial baroreceptor modulation of heart rate during dynamic elevations of arterial pressure.