Randomized, prospective comparison of halothane, isoflurane, and enflurane on baroreflex control of heart rate in humans.
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Adult↗
Biomedical subjects
T J Ebert
Publications and source records attributed to T J Ebert.
Effect of aerobic training on baroreflex regulation of cardiac and sympathetic function.
To investigate the effect of aerobic exercise training on baroreflex regulation of muscle sympathetic nerve activity (MSNA) and cardiac R-R intervals in a middle-aged to older population, 10 healthy men > 40 yr of age underwent tests of autonomic function before and after 12 wk of high-intensity training. Cardiac and peripheral baroslopes were determined from the R-R interval vs. mean arterial pressure (MAP) and peroneal MSNA vs. diastolic pressure relationships, respectively, during sequential bolus injections of nitroprusside and phenylephrine. Maximal oxygen uptake increased (P < 0.05) 17% with training. Resting R-R interval increased (881 +/- 23 to 956 +/- 38 ms, P < 0.05), MAP decreased (96 +/- 2 to 91 +/- 3 mmHg, P < 0.05), and MSNA was unaltered (23.1 +/- 2.3 to 23.6 +/- 1.9 bursts/min) with training. Before and after training, respectively, cardiac baroslopes determined with decreasing (8.7 +/- 0.9 to 9.9 +/- 5.5 ms/mmHg) and increasing MAP (9.6 +/- 2.1 to 9.9 +/- 2.2 ms/mmHg) and the peripheral sympathetic baroslope (-3.3 +/- 0.4 to -3.5 +/- 0.6 bursts.min-1 x mmHg-1) did not differ. The results suggest that short-term aerobic training does not alter resting MSNA or neurocirculatory responses to baroreceptor challenges in middle-aged and older men.
Adult↗
Propofol and autonomic reflex function in humans.
The effects of continuous infusions of propofol on baroreceptor reflex regulation of cardiac rate and peripheral sympathetic nerve activity were evaluated in seven healthy, normotensive, young (19-26 yr), male volunteers. Heart rate, radial artery pressure, and continuous recordings of efferent sympathetic vasoconstrictor outflow (from the peroneal nerve) were monitored. Baroreceptor perturbations were produced by bolus intravenous injections of nitroprusside (100 micrograms) followed 60 s later by phenylephrine (150 micrograms). These stimuli were delivered to subjects while conscious and during propofol anesthesia (200 micrograms.kg-1 x min-1) at least 25 min after subjects were paralyzed (vecuronium), had tracheas intubated, and were ventilated (30% O2:70% N2) to maintain normocarbia. Additional data were collected during hypercarbic conditions and during a lower infusion rate of propofol (100 micrograms.kg-1 x min-1) combined with 70% nitrous oxide. Propofol infusions significantly lowered sympathetic nerve activity (SNA) and blood pressure (BP) and increased heart rate (HR). Cardiac baroreceptor sensitivity determined during nitroprusside was reduced 60% during propofol infusions and was only subtly improved during simultaneous N2O administration. In contrast, reflex sensitivity during phenylephrine was not changed from awake values during each of the three experimental conditions. Reflex regulation of SNA was nearly abolished during normocarbic conditions under propofol anesthesia but restored to conscious levels during hypercarbia and during N2O administration. These data indicate that propofol markedly attenuates reflex responses to hypotension, but that reflex sympathetic responses are better maintained in hypercarbic conditions and when lower doses of propofol are used in conjunction with N2O.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Sympathetic hyperactivity during desflurane anesthesia in healthy volunteers. A comparison with isoflurane.
BACKGROUND: Desflurane has been reported to produce more tachycardia and hypertension on induction than isoflurane. The present study employed microneurography to determine whether these cardiovascular effects were related to sympathetic outflow. METHODS: In 14 healthy, young (age 20-31 yr) volunteers, arterial pressure was measured from the radial artery, forearm blood flow was derived by strain gauge plethysmography, and sympathetic nerve activity (SNA) directed to skeletal muscle blood vessels was recorded from a tungsten needle placed percutaneously into the peroneal nerve. Heart rate, blood pressure, muscle SNA, respiration, tidal volume, end-tidal carbon dioxide, and desflurane or isoflurane concentrations (infrared spectroscopy) were continuously monitored before and during anesthesia. Two minutes after administering thiopental (5 mg/kg) and vecuronium (0.2 mg/kg), desflurane (n = 7) or isoflurane (n = 7) was titrated gradually to the inspired gas over several minutes to 1.5 MAC. RESULTS: The initiation of desflurane anesthesia resulted in significant changes that included a 2.5-fold increase in SNA, hypertension (peak mean arterial pressure 114 +/- 3 mmHg), tachycardia (peak heart rate 102 +/- 6 beats/min), facial flushing, and tearing. Moderate upper airway obstruction developed in three subjects approximately 4 min after initiating desflurane, despite neuromuscular blockade. These responses were not observed in subjects receiving isoflurane. After tracheal intubation, the anesthetic concentration was maintained at 0.5 MAC for 30 min. Steady-state measurements of hemodynamics and SNA were obtained. Similar steady-state measurements were obtained 15 min after establishing 1.0 and 1.5 MAC. Both anesthetics produced a progressive reduction in blood pressure and forearm vascular resistance, and muscle SNA gradually increased. In subjects receiving desflurane, heart rate remained unchanged until the 1.5-MAC level was reached, at which time tachycardia (a 10-beat/min increase) was noted. The transition from 1.0 to 1.5 MAC desflurane resulted in significant heart rate increases (> 30 beats/min), hypertension (> 30 mmHg), and a doubling of SNA that persisted for several minutes. These responses did not occur in the isoflurane group. CONCLUSIONS: Titration of desflurane following thiopental induction and increasing the concentration of desflurane from 1.0 to 1.5 MAC result in sympatho-excitation, hypertension and tachycardia in healthy, young volunteers. Until methods are determined to attenuate these responses, desflurane should be administered with great caution to patients who may be placed at risk by these responses.
Adult↗
Improved baroreflex sensitivity in elderly hypertensives on lisinopril is not explained by blood pressure reduction alone.
OBJECTIVE: The major goals of this study were to determine whether lisinopril and nifedipine lowered blood pressure and improved carotid baroreflexes in older hypertensives. DESIGN: The effects of lisinopril at 10-40 mg/day versus nifedipine gastrointestinal therapeutic system (GITS) at 30-90 mg/day on blood pressure and baroreflex sensitivity were studied after 3 weeks each on (1) single-blind placebo, (2) double-blind assignment to either lisinopril or nifedipine, (3) single-blind placebo, and (4) crossover to double-blind lisinopril or nifedipine. Measurements at the end of the four phases included 24-h blood pressure using the Accutracker, laboratory hemodynamics with the Dinamap and impedance cardiography, baroreflex sensitivity with the pneumatic neck chamber, and plasma samples for neurohumoral and metabolic activity. PATIENTS: Thirteen patients aged 55 years or older (mean +/- SEM 65 +/- 1 years) with mild-to-moderate hypertension completed the study. MAIN OUTCOME MEASURES: The primary data for analysis across the four study phases included ambulatory blood pressure values, laboratory hemodynamics, and baroreflex sensitivity. RESULTS: Compared with the preceding placebo, lisinopril and nifedipine lowered 24-h blood pressure significantly. In the laboratory, the effects of both compounds on blood pressure, cardiac output, calculated total systemic resistance, and the stroke volume-pulse pressure relationship, an index of arterial compliance, were similar. Lisinopril was associated with a relative increase in the standing systolic blood pressure compared with nifedipine (P < 0.05). This coincided with an enhanced heart-rate (R-R interval) response to neck pressure, which also decreased carotid transmural pressure, with lisinopril versus nifedipine (P < 0.05). CONCLUSIONS: Lisinopril and nifedipine were both effective as monotherapy for controlling blood pressure in these elderly patients. Despite similar effects on blood pressure and systemic hemodynamics, baroreflex sensitivity in response to a reduction in carotid transmural pressure was greater with lisinopril than with nifedipine.
Aged↗
Neurocirculatory consequences of negative intrathoracic pressure vs. asphyxia during voluntary apnea.
To investigate the mechanisms responsible for fluctuations in arterial pressure and sympathetic nerve activity that occur during obstructive sleep apnea, we studied neurocirculatory responses to Mueller maneuvers and breath holds in conscious humans. During 20-s Mueller maneuvers at -40 mmHg, mean arterial pressure fell initially (-11 +/- 3 mmHg) and then rose above baseline (+8 +/- 3 mmHg) on release of the inspiratory strain. Sympathetic outflow to skeletal muscle was almost completely suppressed during the initial moments of the maneuver and rose to more than three times the baseline level at the termination of the maneuver. Simple 20-s breath holds were accompanied by time-dependent increases in both arterial pressure (+11 +/- 3 mmHg) and sympathetic nerve activity (> 3 times baseline). The administration of supplemental O2 greatly attenuated the increases in arterial pressure and sympathetic nerve activity during Mueller maneuvers and breath holds. We conclude that carotid chemoreflex stimulation is the primary mechanism responsible for apnea-induced sympathetic activation during wakefulness and that it may contribute importantly to the sympathetic activation that accompanies sleep-disordered breathing.
Adult↗
Sympathetic responses to induction of anesthesia in humans with propofol or etomidate.
Anesthetic induction with propofol commonly results in hypotension. This study explored potential mechanisms contributing to hypotension by recording cardiovascular responses including sympathetic neural activity from patients during induction of anesthesia with propofol (2.5 mg.kg-1 plus 200 micrograms.kg-1.min-1) or, for comparison, etomidate (0.3 mg.kg-1 plus 15 micrograms.kg-1.min-1). Twenty-five consenting, nonpremedicated, ASA physical status 1 and 2, surgical patients were evaluated. Measurements of R-R intervals (ECG), blood pressure (radial artery), forearm vascular resistance (plethysmography), and efferent muscle sympathetic nerve activity ([MSNA] microneurography: peroneal nerve) were obtained at rest and during induction of anesthesia. In addition, a sequential bolus of nitroprusside (100 micrograms) followed by phenylephrine (150 micrograms) was used to obtain data to quantitate the baroreflex regulation of cardiac function (R-R interval) and sympathetic outflow (MSNA) in the awake and anesthetized states. Etomidate induction preserved MSNA, forearm vascular resistance, and blood pressure, whereas propofol reduced MSNA by 76 +/- 5% (mean +/- SEM), leading to a reduction in forearm vascular resistance and a significant hypotension. Both cardiac and sympathetic baroslopes were maintained with etomidate but were significantly reduced with propofol, especially in response to hypotension. These findings suggest that propofol-induced hypotension is mediated by an inhibition of the sympathetic nervous system and impairment of baroreflex regulatory mechanisms. Etomidate, conversely, maintains hemodynamic stability through preservation of both sympathetic outflow and autonomic reflexes.
Adult↗
Clonidine reduces sympathetic activity but maintains baroreflex responses in normotensive humans.
Clonidine, an alpha 2-adrenergic agonist, has been shown to modify the hemodynamic responses to surgery. To examine further the mechanism underlying this action, we evaluated the neurocirculatory effects of oral clonidine and the ability of clonidine to alter the hemodynamic and sympathetic responses to a noxious stimulus (cold pressor test) and to baroreceptor perturbations in nine healthy men (ages 20-29 yr). Heart rate (ECG), blood pressure (radial artery catheter), central venous pressure (jugular vein), and cardiac output (impedance cardiography) were monitored before and after oral clonidine (0.3 mg) or placebo. Plasma norepinephrine was measured with high-performance liquid chromatography. Sympathetic nerve activity (SNA) to skeletal muscle blood vessels was recorded from a Tungsten needle positioned within the peroneal nerve. Baroreceptor testing was carried out by intravenous bolus injections of nitroprusside (100 micrograms) followed 60 s later by intravenous phenylephrine (150 micrograms). The slope of the linear relationship between the change in R-R interval versus the change in mean pressure (cardiac baroslope) or change in SNA versus change in diastolic pressure (sympathetic baroslope) was determined at baseline and 75 min after clonidine or placebo. In addition, peak responses to the cold pressor test (60-s hand immersion in ice water) were determined at the same intervals. Clonidine progressively decreased blood pressure and muscle SNA over the 75-min session. Clonidine subtly reduced the sympathoexcitation produced by the cold pressor test but did not alter the gain of the baroreceptor reflex regulating cardiac interval or peripheral SNA; baroslope relationships were simply shifted leftward (to operate at lower pressures).(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Baroreflex modulation of sympathetic outflow during physiological increases of vasopressin in humans.
Two studies were carried out to determine whether vasopressin influences the baroreceptor reflex of humans. In protocol 1, eight healthy subjects received sequential infusions of nitroprusside and phenylephrine to alter baroreceptor input. Muscle sympathetic nerve activity (SNA) was recorded to assess baroreceptor reflex modulation of efferent vasoconstrictor drive. Baroreceptor sensitivity (slopes) of the relationship between systolic pressure and R-R interval (cardiac baroslopes) and slopes relating muscle SNA to diastolic pressure were not altered during subpressor infusions of vasopressin, which raised basal plasma levels to 19 +/- 6 and 26 +/- 6 (mean +/- SE) pg/ml. A second protocol (n = 10 subjects) compared the reflex inhibition of SNA and heart rate produced by incremental pressor doses of phenylephrine and vasopressin. The calculated cardiac and sympathetic baroreflex gains did not differ between pressor agents. However, immediately following the peak dose of vasopressin (which elevated plasma levels to 35 +/- 3.6 pg/ml), reflex sympathoexcitation produced by unloading baroreceptors (with a bolus of nitroprusside) was significantly enhanced compared with an identical stress initiated at peak phenylephrine infusion. Thus increased levels of vasopressin ranging from 19 to 26 pg/ml did not alter cardiac or sympathetic baroreflex responses in humans. Higher levels of vasopressin may enhance the sympathetic response to unloading of baroreceptors.
Adult↗
Effects of aging on baroreflex regulation of sympathetic activity in humans.
Arterial baroreflexes contribute importantly to blood pressure regulation through their influence on parasympathetic outflow to the sinus node and sympathetic outflow to the peripheral circulation. Baroreflex control of heart rate is known to be diminished in older individuals. Whether advancing age is associated with a parallel attenuation in baroreflex control of sympathetic outflow to the peripheral circulation has not been studied in humans. To provide such information, we made direct measurements of muscle sympathetic nerve activity (MSNA) in healthy males who ranged in age from 18 to 71 yr. The subjects were arbitrarily divided into three groups: younger (18-34 yr; n = 35), middle aged (35-50 yr; n = 15), and older (51-71 yr; n = 16). Although basal levels of MSNA were higher in older subjects than in younger and middle-aged subjects, the gains of baroreflex control of MSNA were the same in the older, middle-aged, and younger subjects (-4.6 +/- 0.6, -4.8 +/- 0.9, -5.1 +/- 0.5 U/mmHg, P greater than 0.10). In contrast, the gains of baroreflex control of cardiac intervals were attenuated in the older and middle-aged subjects compared with the younger subjects (9.8 +/- 1.2, 13.6 +/- 1.4, 21.7 +/- 1.3 ms/mmHg, P less than 0.05). Our data indicate that although the parasympathetic component of the arterial baroreflex becomes impaired with advancing age, the sympathetic component can be well maintained in healthy individuals even into the seventh decade.
Adolescent↗
ANP-mediated volume depletion attenuates renal responses in humans.
Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Venodilation contributes to propofol-mediated hypotension in humans.
The present investigation explored the possibility that the commonly observed hypotension that occurs during induction of anesthesia with propofol might be related to its ability to produce venodilation. Thirty-six ASA I and II patients who received no premedication were studied. The first 20 patients were divided into two equal groups. Hemodynamic measurements consisted of heart rate, arterial blood pressure, and forearm venous compliance by occlusive plethysmography. Baseline measurements were made in awake patients while resting in a supine position. Repeat measurements were made during steady-state infusions of propofol (2.5 mg/kg bolus injection, followed by a continuous infusion at 200 micrograms.kg-1.min-1) or thiopental (4 mg/kg bolus injection, followed by continuous infusion at 200 micrograms.kg-1.min-1), 10 min after tracheal intubation while patients were artificially ventilated. Both anesthetics resulted in a significant (P less than 0.05) and similar tachycardia; however, propofol produced significant decreases in systolic (-30 +/- 9 mm Hg) and diastolic (-11 +/- 4 mm Hg) arterial blood pressure. Forearm venous compliance was significantly increased during propofol administration but unchanged in patients receiving thiopental. In four additional patients receiving smaller consecutive infusions of propofol (50 and 100 micrograms.kg-1.min-1), significant subtle increases in forearm compliance were also recorded. These increases were not observed in four patients who received placebo infusions. Thus, one mechanism promoting hypotension during propofol anesthesia in humans seems to be related to its direct effects on venous smooth muscle tone and presumably venous return.
Adult↗
Lidocaine attenuates efferent sympathetic responses to stress in humans.
The effects of antiarrhythmic doses of lidocaine on efferent sympathetic outflow or sympathetic responses to autonomic stimuli in humans are unknown. In the present study, direct recordings of postganglionic muscle sympathetic nerve activity (MSNA), which modulates vascular tone, were obtained from the peroneal nerve of 22 healthy volunteers (aged 20 to 27 years). Baseline cardiac intervals (ECG), arterial pressure (radial artery), central venous pressure (CVP, jugular vein), forearm vascular resistance (FVR, Hg-in-Silastic plethysmography), and MSNA were identical in two randomized study groups (lidocaine [L], 1.5 mg/kg bolus, followed by 2 mg/min infusion, n = 12; and placebo [P] saline bolus and infusion, n = 10). Each underwent a cold pressor test (CPT, ice packs to foot for 90 seconds) and baroreceptor test (sequential boluses of 100 micrograms of sodium nitroprusside and 100 micrograms of phenylephrine). Five minutes after the bolus administration of L, plasma L levels were 3 micrograms/mL, which was associated with significant (P less than 0.05) increases in systolic and diastolic pressures (6.6 +/- 2.4 and 5.5 +/- 1.1 mm Hg). This elicited significant reflex decreases in MSNA (-3 +/- 1.1 bursts/100 cardiac cycles) and RR interval (-63 +/- 14 ms). The hypertension, tachycardia, forearm vasoconstriction, and MSNA increase in response to the CPT were significantly attenuated and the sympathoexcitatory response to baroreceptor unloading was blunted by L. These responses were not altered during the administration of P. In the steady-state L infusion period, plasma levels were subtherapeutic (1 microgram/mL) and were insufficient to consistently alter autonomic stress responses.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Naloxone augments muscle sympathetic nerve activity during isometric exercise in humans.
The influence of an endogenous opioid peptide (EOP) antagonist (naloxone, 1.2 mg iv bolus) on muscle sympathetic nerve activity (MSNA, microneurography) was studied on 19 young male and female volunteers. Isometric handgrip, cold pressor test, and acute baroreceptor unloading with sodium nitroprusside (autonomic stresses) were carried out under two conditions, one group (n = 11) before (control responses) and after naloxone and another group (n = 8) before and after placebo saline. Monitored cardiovascular variables included heart rate, central venous pressure (jugular vein catheter), arterial blood pressure (radial artery catheter), circulating catecholamines, and forearm blood flow. At rest, cardiovascular variables and MSNA were not affected by either naloxone or saline. MSNA (total activity = burst frequency x burst amplitude/100 cardiac cycles) increased during isometric handgrip to a greater extent (30 +/- 6 vs. 16 +/- 5 arbitrary units) after naloxone compared with control trials (P less than 0.05). After naloxone, arterial systolic and diastolic blood pressures were higher during handgrip exercise. These augmented arterial pressures and MSNA responses were not evident during either the cold pressor test or the sodium nitroprusside stress. These data suggest that isometric muscle contraction elicits a sympathetic neural response that may be modified by EOP. This interaction is not evident during two other stresses, when sympathetic responses are equal to or greater than those provoked by isometric handgrip exercise.
Adult↗
Pathophysiologic levels of atrial natriuretic factor do not alter reflex sympathetic control: direct evidence from microneurographic studies in humans.
To determine if circulating levels of atrial natriuretic factor comparable with those seen in pathophysiologic states alter autonomic control of the circulation, direct recordings of hemodynamic variables and efferent sympathetic nerve activity to muscle (microneurography) were obtained during two separate protocols in a total of 21 normal men (age 25 +/- 1 years). In protocol 1, the responses of 10 men were compared during incremental mechanical unloading of cardiopulmonary baroreceptors with lower body negative pressure versus responses to comparable unloading during infusion of alpha-human atrial natriuretic factor. Lower body negative pressure decreased pulmonary artery diastolic and right atrial pressures, did not alter arterial pressure or heart rate and increased muscle sympathetic nerve activity from 205.2 +/- 36.3 to 438.7 +/- 100.2 units/min (p less than 0.01). Intravenous infusion of atrial natriuretic factor (25 ng/kg per min) increased plasma levels of the hormone from 24 +/- 4 to 322 +/- 34 pg/ml (p less than 0.01, n = 6), produced similar decreases in pulmonary artery diastolic and right atrial pressures, did not alter arterial pressure, increased heart rate and increased sympathetic nerve activity from 233.1 +/- 35.6 to 387.2 +/- 64.9 units/min (p less than 0.05). Thus, during similar hemodynamic perturbations produced by lower body negative pressure or infusion of atrial natriuretic factor at the dose used in this study, these subjects exhibited comparable sympathoexcitatory responses, with a 109 +/- 23% increase in sympathetic activity during lower body negative pressure and a 76 +/- 19% increase during atrial natriuretic factor infusion (p = NS). In protocol 2, the responses of 11 additional men were examined during lower body negative pressure performed before and again during infusion of atrial natriuretic factor (12.5 ng/kg per min). During baseline (prehormone) trials, lower body negative pressure (-14.5 +/- 1.6 mm Hg) decreased central venous pressure, did not change arterial pressure or heart rate and increased sympathetic nerve activity from 215 +/- 47.7 to 372.3 +/- 64.3 units/min (p less than 0.001). Infusion of atrial natriuretic factor increased plasma levels of the hormone from 39 +/- 8 to 313 +/- 18 pg/ml (p less than 0.01, n = 7); central venous pressure was held constant during hormone infusion by intravenous infusion of saline solution.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Differential effects of nitrous oxide on baroreflex control of heart rate and peripheral sympathetic nerve activity in humans.
Acute regulation of blood pressure in humans is mediated by arterial baroreflex regulation of heart rate, cardiac contractility, and peripheral sympathetic outflow. Brief pharmacologic reductions of blood pressure were employed in 11 healthy volunteers to determine the effects of N2O on baroreflex-mediated increases in heart rate and efferent muscle sympathetic nerve activity. R-R intervals (ECG), blood pressure (radial artery), central venous pressure, respiratory rate (abdominal bellows), and end-tidal gas concentrations (mass spectrometer) were monitored. Efferent sympathetic nerve activity directed to skeletal muscle blood vessels (MSNA) was recorded from an epoxy-coated tungsten needle placed into the peroneal nerve. Data were obtained from six subjects before and during iv bolus administration of sodium nitroprusside (100 micrograms), during control while breathing 40% N2/60% O2, during administration of N2O (40% N2O/60% O2), and during recovery (40% N2/60% O2). Five subjects served as time controls and breathed 40% N2 in O2 throughout the protocol. Nitrous oxide produced a 59 +/- 18% (P less than 0.05) increase in baseline MSNA but did not alter the reflex augmentations in MSNA produced by nitroprusside. In contrast, there was a 39 +/- 14% decrease in the slope of the relationship between systolic pressure and R-R interval (P less than 0.05) in subjects breathing N2O. N2O thus produces activation of the sympathetic nerves directed to skeletal muscle blood vessels, and it decreases baroreflex-mediated tachycardia without diminishing baroreflex-mediated augmentations in sympathetic outflow.
Adult↗
Atrial natriuretic peptide augments forearm capillary filtration in humans.
Low-dose infusions of atrial natriuretic peptide (ANP) into humans reduce cardiac filling pressures without enhancing renal excretion or producing vasodilation. The present human study was undertaken to seek an effect of ANP on capillary filtration in humans and to determine its relationship to reductions in cardiac filling pressures. Heart rate (electrocardiogram), blood pressure (cuff method), and renal excretion of salt and water were determined, and central venous pressure (jugular vein cannulation, strain-gauge transducer) and forearm venous compliance and capillary filtration coefficient (strain-gauge plethysmography) were derived by computer. Forearm girth and venous pressure (peripheral vein catheter) measurements were obtained while the arm was elevated above heart level, and an upper arm blood pressure cuff was intermittently inflated to venous occluding pressures of 20, 30, and 40 mmHg. Forearm measurements, hematocrit, plasma proteins, albumin and plasma levels of ANP were determined from euvolemic volunteers before and during 60 min intravenous infusions of ANP (5 ng.kg-1.min-1, n = 9) or placebo (isotonic saline, n = 7). ANP infusions produced physiological increases (4- to 5-fold) in plasma ANP (from a base line 35 +/- 6 pg/ml) (P less than 0.05). Hemodynamic responses to ANP consisted of a reduction in central venous pressure (P less than 0.05) and no change in heart rate, mean arterial pressure, or renal excretory parameters. ANP increased forearm capillary filtration between 37 and 63% (P less than 0.05) from base line but did not significantly alter forearm compliance measurements.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Inhibition of sympathetic neural outflow during thiopental anesthesia in humans.
The effects of sodium thiopental on postganglionic muscle sympathetic nerve activity (MSNA) and the reflex augmentation in MSNA produced by hypotension were examined in seven ASA physical status I and II patients, 34-65 yr old. Direct recordings of MSNA were obtained from a 5-micron-tipped, epoxy-coated needle percutaneously placed into the common peroneal nerve. Induction of anesthesia with sodium thiopental (4 mg/kg) significantly decreased R-R interval duration an average of 157 +/- 44 ms (mean +/- SEM) decreased systolic pressure (radial artery) an average of 11 +/- 4 mm Hg, and reduced tonic MSNA from 38 +/- 11 to 18 +/- 5 bursts/100 cardiac cycles (P less than 0.01). Baroreceptor reflex regulation of cardiac intervals and MSNA were determined by sequential boluses of nipride (100 micrograms) and phenylephrine (150 micrograms). Awake baroreceptor slopes relating R-R interval to systolic pressure were 9.5 +/- 2.9 ms/mm Hg and decreased 61% to 2.4 +/- 0.5 ms/mm Hg (P less than 0.01) during sodium thiopental infusions (0.25 mg.kg-1.min-1). Moreover baroreceptor slopes relating MSNA to diastolic pressure in awake patients were -4.0 +/- 0.9 bursts/mm Hg and were reduced by 95% to -0.3 +/- 0.18 bursts/mm Hg (P less than 0.01). Despite the fact that hypotension did not elicit increases in MSNA in anesthetized patients, laryngoscopy and tracheal intubation produced profound augmentations in MSNA. Thus, sodium thiopental reduces tonic levels of MSNA and markedly attenuates baroreceptor reflex control mechanisms. However, profound augmentations in sympathetic activity occurred in response to laryngoscopy and tracheal intubation during thiopental anesthesia.
Adult↗