Nasal airway response to exercise.
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Adult↗
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Results for “Autonomic Nerve Block”
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Effect of autonomic blockade on digoxin-induced ECG changes at rest and during exercise in healthy subjects.
The effect of pharmacological autonomic blockade on digoxin-induced electrocardiographic changes at rest and during exercise was studied in nine healthy men. The subjects performed bicycle exercise tests on four occasions after: (1) intravenous injection of sodium chloride, (2) intravenous injection of propranolol and atropine, (3) oral ingestion of digoxin 0.5 mg daily for 2 weeks and intravenous injection of sodium chloride, and (4) oral ingestion of digoxin 0.5 mg daily for 2 weeks and intravenous injection of propranolol and atropine. The ST-T segment was significantly depressed after digoxin plus sodium chloride and digoxin plus propranolol and atropine in comparison with sodium chloride only and propranolol and atropine only. The digoxin-induced ST-T changes after sodium chloride and propranolol-atropine injections were not significantly different. Thus, judging from the results of this study, an effect mediated via the autonomic nervous system is an unlikely explanation of digitalis-induced ST-T changes.
Adult↗
Spectral analysis of blood pressure and heart rate in conscious rats: effects of autonomic blockers.
We investigated the fluctuations which underly the spontaneous variability of blood pressure and heart rate in conscious rats. Intrafemoral blood pressure was computed to generate evenly spaced signals (systolic, diastolic, mean blood pressure, heart rate) at 200 ms intervals. This equidistant sampling allowed a direct spectral analysis using a Fast Fourier Transform algorithm. Systolic blood pressure and heart rate exhibited low-frequency oscillations (Mayer waves, 20-605 mHz) and a high- frequency oscillation related to respiration (1855 mHz). The respiratory fluctuations in heart rate were almost abolished by vagal blockade (atropine). Heart rate fluctuations in the low-frequency regime were diminished by vagal blockade or cardiac sympathetic blockade (atenolol). The respiratory frequency fluctuations in systolic blood pressure were markedly increased by alpha-sympathetic blockade (prazosin). In contrast, the low-frequency oscillations in systolic blood pressure were reduced by alpha-sympathetic blockade. These data indicate that in conscious rats: (1) the heart rate oscillation with respiration is vagally mediated; (2) the heart rate fluctuation in the low-frequency range is jointly mediated by beta-sympathetic and parasympathetic activities; (3) the respiratory oscillation in systolic blood pressure depends on fluctuations in cardiac output and is normally counteracted by the sympathetic tone; (4) the low-frequency oscillations in systolic blood pressure reflect the sympathetic activity to the resistance vessels.
Animals↗
The effect of pentobarbital anesthesia on the autonomic nervous system control of heart rate during baroreceptor activation.
This study determined the influence of pentobarbital anesthesia on the autonomic nervous system control of baroreceptor mediated reflex bradycardia in the rat. Reflex bradycardia was elicited by phenylephrine-induced hypertension in conscious and pentobarbital anesthetized (PA) rats before and after sympathetic blockade with the beta-1 receptor antagonist atenolol or parasympathetic blockade with the peripherally acting muscarinic receptor antagonist methyl-atropine. Reflex bradycardia was significantly decreased by pentobarbital anesthesia. Cardiosympathetic blockade produced equivalent relative decreases in baroreflex gain in conscious and PA rats. In contrast, parasympathetic nervous system blockade with methyl-atropine produced relatively less inhibition of baroreflex gain in the PA rat compared with the conscious rat. These results suggest that pentobarbital anesthesia decreases baroreflex gain by inhibiting vagally mediated reflex bradycardia.
Anesthesia, General↗
Power spectral analysis of heart rate variability as a new method for assessing autonomic activity in the rat.
The authors studied power spectral analysis of heart rate variability in the rat, hypothesizing that the quantitative information provided by this analysis reflects the interaction between sympathetic and parasympathetic regulatory activities. For this purpose, an electrocardiogram was recorded from conscious and unrestrained Wistar rats (Nippon, Shizuoka) (12-16 weeks old) by a telemetry system and analyzed by a power spectrum. Because it was thought that the electrocardiogram recorded by the telemetry system could provide more reliable data to assess autonomic nervous activity than the tethering system, the telemetry recording system was used. There were two major spectral components in the power spectrum at low frequency (LF) (0.6 Hz) and high frequency (HF) (approximately 1.4 Hz). On the basis of these data, the authors defined two frequency bands of interest: LF (0.04-1.0 Hz) and HF (1.0-3.0 Hz). The power of LF was higher than that of HF in the normal rat. Atropine (2 mg/kg intraperitoneally) significantly reduced both HF and LF power. Propranolol (4 mg/kg intraperitoneally) also significantly reduced LF power; however, it had no significant effect on HF power. Thus, this study in the rat confirmed earlier observations in the conscious dog and human. Furthermore, the decrease in the parasympathetic mechanism produced by atropine was reflected by a slight increase in the LF/HF ratio. The LF/HF ratio appeared to follow the reductions of sympathetic activity produced by propranolol. From these results, the LF/HF ratio seemed to be a convenient index of parasympathetic and sympathetic interactions in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Latent abnormalities of sinus node function in patients with organic heart disease and normal sinus node on clinical basis.
Sinus node (SN) function was analyzed in 22 patients (mean age: 46.2 +/- 12.9 years) with organic heart disease and normal SN on clinical basis (group I) and in 20 normal subjects (mean age: 43.9 +/- 15.6 years), (control group). Sinus cycle length (SCL), corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After the control study, autonomic blockade (AB) was induced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of SCL, CSRT and SACT were then repeated. The mean SCL values were very similar in the two groups during the control state and after AB. There were no significant differences in SACTs between the two groups during the control state or after AB. On the contrary, the CSRT of group I was significantly longer than that of control group during the control state (344.8 +/- 78.9 versus 262.2 +/- 46.3 msec, P less than 0.001) and after AB (238.9 +/- 72.8 versus 166.8 +/- 39.3 msec, P less than 0.001). The analysis of real depression of SN automaticity (CSRT minus SACT) in the two groups shows that prolongation of CSRT in group I during the control study and after AB is related to an intrinsic abnormality of SN automaticity; on the contrary, no dysfunctions of the autonomic nervous system appear. These data indicate that the intrinsic abnormality of SN automaticity represents the earliest involvement of the SN in subjects with organic heart disease and normal SN on clinical basis, although this conclusion is speculative and requires experimental verification.
Adolescent↗
Effects of autonomic blockade on dual atrioventricular nodal pathways pattern.
Fifteen patients (age: 57.6 +/- 14 years) showing dual A-V nodal pathways pattern during basal electrophysiological testing were studied following pharmacological autonomic blockade (iv propranolol 0.2 mg/Kg and iv atropine 0.04 mg/Kg). After induction of the autonomic blockade, the dual A-V nodal pathways pattern was not present in four patients due to disappearance of the slow pathway; the pattern remained in 11 (73%). The longest A2-H2 interval, the effective and functional refractory periods of the fast pathway did not change significantly following autonomic blockade. Even the electrophysiological measures of the slow pathway, in the 11 patients in whom they were comparable, did not change significantly after autonomic blockade. These data suggest that: the dual A-V nodal pathways pattern is mainly related to the intrinsic structure of the A-V node; the autonomic nervous system only affects in a variable way the refractoriness and the conduction velocity in the two pathways.
Adult↗
Autonomic control of the immediate heart rate response to lying down.
1. The initial heart rate response to lying down was analysed in 18 younger (23-36 years) and 10 older (48-67 years) normal subjects, and consisted of an immediate shortening of the R-R interval reaching a maximum around the third or fourth beat after lying, followed by a lengthening beyond the resting value to reach a steady level around beats 25-30. In six diabetic patients with autonomic neuropathy, no cardiac acceleration occurred and the deceleration was markedly diminished. 2. In eight young normal subjects the pattern of response was altered by atropine, which abolished the initial shortening of the R-R interval over the first 10 beats. Thereafter slow but steady lengthening of the R-R interval occurred. With additional propranolol the later part of the response was further attenuated. Propranolol alone did not affect the normal pattern of response. 3. Six young normal subjects performed short periods of muscular exercise, lying, sitting and standing, and the heart rate patterns were compared with that after lying down. After both manoeuvres R-R interval shortened and then lengthened back to the resting level within 10-15 beats. Thereafter it remained steady after muscular exercise, but continued to lengthen after lying down. 4. In four young normal subjects, no initial R-R interval shortening occurred during fast or slow "passive' tilting from the 80 degrees head-up position to horizontal, whereas shortening was seen both with fast and slow "active' lying down. 5. It is concluded that the immediate part of the heart rate response to lying down (during the first 10 beats) is under vagal control and the later part predominantly under sympathetic control. The first part of the response is probably due to a "muscle-heart' reflex which occurs during the change in posture.
Adult↗
Autonomic nervous control of the heart rate during dynamic exercise in normal man.
The relative contribution of the efferent components of the sympathetic and parasympathetic nervous systems to the heart rate (HR) response to dynamic physical exercise was evaluated in 23 normal males. The dynamic exercise was performed on a bicycle ergometer at work loads of 25, 50 and 100 W, before and after pharmacological blockade with atropine (13 individuals) or propranolol (10 individuals). Parasympathetic blockade significantly depressed the rapid HR response at the beginning of the exercise period at all levels of intensity, whereas sympathetic blockade only affected the slow-response phase (1-4 min), especially at the highest level of effort. The present results suggest that the tachycardia evoked by dynamic exercise is mediated by a biphasic mechanism initially depending on rapid vagal release, which increases progressively with increasing effort. An increased sympathetic activity manifests itself in a more delayed manner, especially at the higher levels of activity. Continuous monitoring of HR during the entire period of activity at different levels of intensity permits the utilization of dynamic exercise as a simple and non-invasive method for the functional evaluation of the two components of the autonomic nervous system of the heart.
Adult↗
Autonomic components of the cardiovascular responses to an acoustic startle stimulus in rats.
1. A loud acoustic stimulus was administered to rats prior to and after treatment with autonomic blockers in order to unravel the autonomic mechanisms of the blood pressure (BP) and heart rate (HR) responses to startle. 2. Six rats, implanted with a BP telemetric system, were used in a randomized crossover saline-controlled (saline vs. autonomic blocker) study with a washout period of 7 days between each active session. A first acoustic stimulus (110 dB, 0.7 s) was administered. An autonomic blocker i.e. atropine methylnitrate (15 mg. kg-1), atenolol (15 mg. kg-1) or prazosin HCl (1 mg. kg-1), or physiological saline was administered i.p. 40 min prior to a second identical acoustic stimulus. 3. The average BP rise following the first stimulus was +25 mmHg and the average HR change was +17 bpm. The responses after autonomic blockades were affected as follows: atropine increased the HR rise (+45.1 +/- 1.7 bpm), atenolol reversed the HR changes to a bradycardic response (-21.4 +/- 9.1 bpm), after prazosin treatment the BP rise was reversed into a BP decrease (-11.3 +/- 3.2 mmHg) and the HR increase was amplified (+76.0 +/- 10.0 bpm). Finally, the delay for obtaining the maximal BP change was increased from 1.9 to 2.6 s following prazosin pretreatment. 4. These results indicate that the BP rise resulting from an acute loud noise depends on a vascular sympathetic activation (prevented with prazosin), which is partly blunted by vasodilation (revealed with prazosin). The evoked HR changes combine a sympathetic activation (fully expressed following atropine) and a vagal activation (unmasked with atenolol). Further experiments are necessary to document the vasodilatory component unmasked with prazosin.
Acoustic Stimulation↗
Autonomic blockade unmasks maturational differences in rate-dependent atrioventricular nodal conduction and facilitation in the mouse.
INTRODUCTION: In large animals, rate-dependent AV nodal (AVN) properties of conduction are modulated by autonomic inputs. In this study, we investigated whether the properties of AVN conduction and facilitation are altered by autonomic blockade in the mouse and whether this effect is age dependent. METHODS AND RESULTS: Young (age 4-6 weeks; n = 11) and adult (age 8-9 months; n = 11) female mice underwent in vivo electrophysiologic testing, before and after autonomic blockade. After autonomic blockade, the adult mice had significantly longer AVN effective refractory period (AVNERP; 67 +/- 14 msec vs 56 +/- 4 msec, P = 0.05) and functional refractory period (AVNFRP; 81 +/- 10 msec vs 72 +/- 4 msec, P = 0.05). With autonomic blockade, the increase from baseline of AVN Wenckebach cycle length (deltaAVW; 1.8 +/- 8.1 msec vs 8.8 +/- 3.3 msec, P = 0.04), as well as of AVNERP (deltaAVNERP; 3.5 +/- 3.5 msec vs 21.4 +/- 12.6 msec, P = 0.002) and AVNFRP (deltaAVNFRP; 2.3 +/- 3.2 msec vs 12.8 +/- 9.0 msec, P = 0.008), was significantly larger in adult than in young mice. Compared with young mice, adult mice were less likely to exhibit AVN facilitation (44% vs 90%, P = 0.03) and had smaller maximal shortening of AVN conduction times after the "test beat" for any coupling of the "facilitating beat" (4 +/- 4 msec vs 7 +/- 3 msec, P = 0.05). CONCLUSION: Complete autonomic blockade significantly increases AVN conduction times and refractory periods in adult but not in young mice. Adult mice also exhibit less AVN facilitation. Our results confirm that, like in larger animals, rate-dependent murine AVN properties of conduction are under autonomic regulation. Adult mice have higher sympathetic AVN inputs at baseline, leading to slower conduction after autonomic blockade.
Adaptation, Physiological↗
Electrophysiological techniques for the study of urethral and vesical innervation.
A new electrophysiological technique for the study of urethral and vesical innervation is reported. The method gives valuable information on the structural integrity and function of two of the reflex arcs involved in micturition. Normal and pathological patterns are described, illustrating the diagnostic value of the method in the assessment of neurogenic disturbances of bladder and urethral function.
Anal Canal↗
Autonomic hyperreflexia: intraoperative control with pentolinium tartrate.
Autonomic hyperreflexia (AH) is a clinical syndrome associated with the development of severe hypertension. It usually occurs in patients with high-level chronic spinal cord injury, and in response to stimuli associated with the distension of a hollow viscus. Protection against AH by the prophylactic use of pentolinium tartrate (Ansolysen) in doses of 10-15 mg was evaluated in a controlled study of unanaesthetized patients who were either quadriplegic or paraplegic and who were undergoing rectal and bladder surgical procedures. When compared with the control group, the systolic and diastolic arterial pressures during operation were significantly less (P less than 0.05) and remained near normal in the pretreated patients. The use of pentolinium to prevent or control AH during surgical procedures in patients with chronic spinal cord damage is a simple alternative to spinal or general anaesthesia.
Adult↗
Left ventricular mechanical consequences of dihydropyridine calcium channel modulation in conscious and anesthetized chronically instrumented dogs.
BACKGROUND: Volatile anesthetics depress left ventricular contractile function by altering voltage-dependent slow calcium (Ca2+) channel activity in the sarcolemmal membrane. This investigation examined the left ventricular systolic and diastolic mechanical effects of the dihydropyridine Ca2+ channel antagonist nifedipine and agonist Bay k 8644 (Bay k) in dogs in the conscious state and during anesthesia. METHODS: Forty-eight experiments were conducted using 16 chronically instrumented dogs during autonomic nervous system blockade. Myocardial contractility was evaluated with the slope (Mw) of the regional preload recruitable stroke work relationship. Diastolic function was assessed using a time constant of isovolumic relaxation (tau), a regional chamber stiffness constant (Kp), and maximum segment lengthening velocity during rapid ventricular filling (dL/dtmax). On 3 separate days (24 experiments), a nifedipine infusion at 0.5, 1.0, 2.0, or 4.0 micrograms.kg-1.min-1 was administered. Hemodynamics and left ventricular pressure-segment length diagrams were recorded after a 10-min equilibration at each dose in the conscious state or during isoflurane or halothane anesthesia (0.8 MAC). In 24 parallel experiments, a Bay k infusion at 0.5, 1.0, 2.0, or 4.0 micrograms.kg-1.min-1 was administered, and hemodynamics and left ventricular function parameters were assessed after a 10-min equilibration in the conscious state or during isoflurane or halothane administration (1.2 MAC). RESULTS: In conscious dogs, nifedipine significantly (P < 0.05) decreased Mw (71 +/- 5 to 42 +/- 4 mmHg during the high dose) and increased tau (35 +/- 1 to 48 +/- 3 ms during the high dose) without changes in dL/dtmax or Kp. In anesthetized dogs, nifedipine decreased Mw and dL/dtmax) (31 +/- 4 during isoflurane to 27 +/- 3 mm/s during the high dose) and increased tau and Kp (0.43 +/- 0.05 during isoflurane to 0.53 +/- 0.04 mm-1 during the high dose). Administration of Bay k increased Mw, decreased tau, and increased dL/dtmax in conscious dogs. In contrast, no changes in tau were observed in dogs anesthetized with isoflurane or halothane during infusions of Bay k despite concomitant increases in Mw. Bay k also enhanced dL/dtmax and decreased Kp during isoflurane but not halothane anesthesia. CONCLUSIONS: Nifedipine caused direct negative inotropic actions in conscious and anesthetized dogs and worsened volatile anesthetic-induced negative lusitropic effects. Bay k improved left ventricular systolic and diastolic function in the conscious state. Bay k also improved contractility during anesthesia; however, Bay k only partially reversed volatile anesthetic-induced abnormalities in indexes of left ventricular diastolic function in dogs during autonomic nervous system blockade.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
A novel mechanism for benign essential blepharospasm.
PURPOSE: The purpose of this study is to test the hypothesis that the photophobia of benign essential blepharospasm (BEB) is caused by sympathetically maintained pain. METHODS: Nineteen patients with photophobia and BEB were enrolled in an unblinded prospective treatment trial. The intervention was blockade of the superior sympathetic ganglion with local anesthetic. Outcome measures included the patient's subjective report of ocular surface dryness, foreign body sensation, and eyelid spasm. We also obtained video recordings of eyelid movements. RESULTS: Of the 19 patients, 13 reported subjective improvement in BEB symptoms after cervical sympathetic blockade (CSB). Thirteen of 19 patients also had objective evidence of decreased light-induced eyelid spasm after CSB. Ocular surface disease was present in 18 of 19 patients. CONCLUSION: These data support the hypothesis that in many patients with BEB there is a sympathetically maintained pain syndrome associated with external ocular disease. We speculate on a neurologic circuit that may explain these findings.
Anesthetics, Local↗
Autonomic control of the diurnal variation in arterial blood pressure and heart rate in spontaneously hypertensive and Wistar-Kyoto rats.
The relative influences of sympathetic and parasympathetic neural modulation on mean arterial pressure (MAP) and heart rate (HR), and their respective variabilities, were studied in young spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). An on-line computerized system was used for continuous intra-arterial measurements of MAP and HR in unrestrained rats. In addition, the autonomic nervous control of MAP and HR was studied in ageing SHR and WKY. Both WKY and SHR showed diurnal rhythms with regard to MAP and HR. The MAP variability was higher in SHR than in WKY during both daytime (inactive) and night-time (active), and did not change in response to either beta 1-adrenoceptor- or cholinergic blockade. Structural vascular changes, with a resultant increase in reactivity, may explain the elevated MAP variability in SHR. HR variability was clearly reduced in SHR; this was not influenced by vagal blockade, whereas HR variability was significantly reduced in WKY. This pattern is suggested to be due to a reduced tonic vagal discharge in SHR, as part of a persistent, mild defence reaction. The initial reduction in vagal activity will in turn eliminate vagally mediated tachycardias. Furthermore, administration beta 1-blockade to SHR of different ages caused a greater fall in MAP and HR than in WKY, indicating an increased dependence upon the sympathetic nervous system in SHR with age.
Animals↗
Time course of cardiovascular neural regulation during programmed 20-sec apnea in rats.
OBJECTIVES: Long-term hypoxia results in hemodynamic breakdown in patients in the intensive care unit; however, intermittent hypoxia causes hypertension in individuals with sleep apnea. The objective of this study was to explore the sequential cardiovascular neural alterations in response to acute hypoxic apnea. DESIGN: The authors conducted a prospective, randomized animal study. SETTING: The study was conducted in a university animal laboratory. METHODS: A programmable apnea model was developed in anesthetized rats, in which a 20-sec period of apnea was produced and subsequently divided into the early (2.0 to 7.9 secs), middle (8.0 to 13.9 secs), and late apneic phases (14.0 to 19.9 secs) and immediate reventilatory phase (20.0 to 25.9 secs). RESULTS: Evident hypoxia developed during 20-sec apnea. Arterial pressure increased in the early apneic phase and returned to control level in the middle phase. Significant hypotension developed in the late apneic phase and deteriorated in the reventilatory phase. Interbeat interval increased mildly along the apneic event. The increase of pressure in the early and middle phases was inhibited by propranolol (1.0 mg/kg intravenously [iv]) but was provoked by phentolamine (2.5 mg/kg iv). The decrease of pressure in the late and reventilatory phases was reversed, at least in part, by phentolamine. Atropine (0.5 mg/kg iv) did not produce discernible effects in the arterial pressure. The increase of interbeat interval was suppressed by propranolol. Power spectral analysis of arterial pressure variability demonstrated significant increases of the low-frequency (sympathetic vasomotor activity) and normalized high-frequency (cardiac sympathetic modulation) power after reventilation. CONCLUSION: Although the sympathetic activity is excited during and after a hypoxic apnea, the immediate pressor effect is related to an inotropic response of cardiac sympathetic regulation, whereas the negative chronotropic and subsequent depressor effect is associated with a failure in the cardiovascular response to sympathetic excitation.
Analysis of Variance↗
Beta-adrenergic receptor responsiveness to isoprenaline in humans: concentration-effect, as compared with dose-effect evaluation and influence of autonomic reflexes.
1. Different techniques of assessing beta-adrenoceptor sensitivity in vivo, by use of i.v. infusions or bolus injections of isoprenaline (ISO), were compared in healthy volunteers. The importance of autonomic reflexes for responses to ISO was evaluated by studying the influence of 'autonomic blockade' by atropine and clonidine, which antagonize muscarinic effects and reduce sympathetic activity, respectively. Estimates of in vivo responsiveness to ISO were compared with parameters reflecting beta 2-adrenoceptor function in vitro in lymphocytes. 2. Heart rate responses to infused ISO were not significantly altered by 'autonomic blockade' when evaluated from concentration-effect curves. When related to the infused dose of ISO, however, sensitivity was artefactually increased (P less than 0.05), as the plasma concentrations of ISO were 40% higher after atropine and clonidine. Heart rate responses to bolus injections of ISO were attenuated (P less than 0.05) by 'autonomic blockade', suggesting that facilitatory reflexes contribute to these non-steady state responses. Intersubject variations in heart rate responsiveness to ISO were greater than the intrasubject variability caused by counterregulatory reflexes. 3. 'Autonomic blockade' lowered venous plasma noradrenaline at rest. The noradrenaline response to ISO infusion was attenuated and the diastolic blood pressure response enhanced, indicating that a counterregulatory vasoconstrictor reflex normally is activated by ISO-induced vasodilatation. The plasma cyclic AMP response to ISO, on the other hand, was unaffected by atropine and clonidine and reflects beta 2-adrenoceptor responsiveness in vivo. 4. In vitro data for beta-adrenoceptor binding sites (Bmax;[125I]-IHYP binding) and cyclic AMP responses to ISO in lymphocytes correlated with DBP and noradrenaline responses to infused ISO. No correlations were found between in vitro data and heart rate, plasma cyclic AMP or plasma glycerol responses to infused ISO in vivo. 5. During prolonged ISO infusions (in six other healthy subjects) physiological responses reached greater than 90% of their steady state level after 8 min, but no definite steady state level could be defined for the plasma concentration of ISO during 40 min of infusion. 6. The ISO infusion test showed a good reproducibility, especially when repeated on the same day. Evaluation of plasma concentration-effect relationships increase the precision of the ISO infusion test as confounding inter- and intra-individual variations in ISO concentrations (as caused by e.g. autonomic blockade) will be taken into account.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗