[Effect of a peridural block on the function of the external respiratory apparatus and on the autonomic nervous system in bronchial asthma].
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Anesthesia, Epidural↗
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Results for “Autonomic Nerve Block”
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The action of substances which block sympathetic postganglionic nervous transmission.
The substances which block sympathetic postganglionic transmission, xylocholine, bretylium and guanethidine, also block neuromuscular and sympathetic ganglionic transmission. To see if these last properties were related to the sympathetic blocking property, phenyltrimethylammonium, which blocks the neuromuscular junction (Riker, 1953), was used. It blocked the inhibition of the rabbit ileum produced by stimulating the periarterial nerves in the mesentery, though with higher concentrations the effect of stimulation was initially increased. The action was not modified by the presence of hyoscine. The blocking action was exerted on the response to stimulation of the highest frequency first, and on the response to stimulation of the lowest frequency last. This relation of block to stimulus frequency is similar to that at the neuromuscular junction when tubocurarine is used. Nine compounds have now been shown to block responses to sympathetic postganglionic stimulation, and seven of these are onium compounds. They are, however, mon-onium compounds, and not bis-onium compounds like hexamethonium and decamethonium, so that they can probably enter the postganglionic fibre, which bis-onium compounds (having a charged group at each end of the molecule) may not be able to do. Since these mon-onium compounds have some blocking action at neuromuscular junctions and at sympathetic ganglia, their block of postganglionic transmission may be essentially similar to that by hexamethonium at ganglia and to that by decamethonium at neuromuscular junctions. It is known that acetylcholine releases noradrenaline from sympathetic postganglionic terminations, and xylocholine and bretylium block this release in the vessels of the rabbit ear and in the rabbit isolated atria.
Acetylcholine↗
The autonomic margins of safety of metocurine and d-tubocurarine in the cat.
The potencies of metocurine and d-tubocurarine for neuromuscular and autonomic blockade and histamine release were determined in cats anesthetized with chloralose and pentobarbital. The autonomic margins of safety of these drugs were determined by measuring the ratios of ED50 for sympathetic block to ED95 for neuromuscular block; ED50 for vagal block to ED95 for neuromuscular block; ED50 for histamine release to ED95 for neuromuscular block. Metocurine is 14 times more potent than d-tubocurarine as a neuromuscular blocking agent in the cat, but its autonomic blocking action is three times weaker than the of d-tubocurarine and its histamine-releasing action is less than half that of d-tubocurarine. The combination of higher neuromuscular blocking potency and weaker autonomic effect gives metocurine a much higher autonomic margin of safety than d-tubocurarine in the cat.
Animals↗
Heart rate changes accompanying jaw movement Pavlovian conditioning in rabbits: concomitant blood pressure adjustments and effects of peripheral autonomic blockade.
Two experiments were conducted to ascertain the cardiovascular accompaniments of differential Pavlovian jaw movement (JM) conditioning. The first examined the blood pressure (BP) changes that accompany the tachycardiac conditioned responses (CRs) associated with JM conditioning. The BP response in all instances consisted of a depressor response that was greater to the reinforced CS+ than CS-, although the magnitude of the CR was quite small. The second experiment determined the effects of peripheral autonomic antagonists on the cardiac accelerations associated with JM conditioning. It was found that the peripheral vagal antagonist methyl scopolamine completely abolished responses to both CS+ and CS-, whereas atenolol, a beta adrenergic antagonist, augmented the response, compared to saline control injections. The JM responses were also affected by the autonomic blockades, with minimal responding occurring in the scopolamine group but slightly more JM CRs in the atenolol group, compared to saline control animals. These results suggest that the major cardiovascular response to an appetitive stimulus, which evokes JM conditioning, consists of cardiac accelerations with the BP depressor responses playing a minimal, if any, role. Moreover, these conditioned cardiac increases appear to be due solely to the release of vagal inhibition.
Animals↗
Comparative haemodynamic effects of verapamil, flecainide, amiodarone and sotalol in the conscious rabbit.
1. The effect of intravenous boluses of verapamil (0.15 mg/kg), flecainide (2 mg/kg), amiodarone (5 mg/kg), and sotalol (1.5 mg/kg) on mean arterial pressure, heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and peak rate of change of left ventricular pressure (LV dP/dt) were assessed in the conscious rabbit. 2. All four drugs had negative inotropic effects: verapamil reduced peak LV dP/dt by 19 +/- 4% (mean +/- s.e.m.; P < 0.01), flecainide by 27 +/- 9% (P < 0.001), amiodarone by 11 +/- 2% (P < 0.01) and sotalol by 13 +/- 3% (P < 0.01). 3. The drugs had different effects on CO as a result of differences in their actions on peripheral blood vessels: verapamil and amiodarone produced, respectively, a 12 +/- 4% (P < 0.03) and 16 +/- 6% (P < 0.01) increase in CO associated with a substantial vasodilatory effect (TPR reduced 15 +/- 7% [P < 0.05] and 20 +/- 5% [P < 0.01], respectively). Flecainide caused only a small (6 +/- 1%; P < 0.01) increase in CO and sotalol had no effect on either CO or TPR. 4. Bolus intravenous injections of verapamil, flecainide and amiodarone produced an increase in HR, while sotalol reduced HR by 10 +/- 2% (P < 0.01). The increase in HR and cardiac output seen with verapamil, flecainide and amiodarone was in part secondary to reflex increase in sympathetic tone and these changes were abolished after total cardiac autonomic blockade. 5. The modest reduction in cardiac performance associated with sotalol was abolished by cardiac autonomic blockade, suggesting that the predominant effect of sotalol on contractility was mediated through its beta-adrenoceptor blocking effect.
Amiodarone↗
Electrophysiology of normal anterograde atrio-ventricular conduction with and without autonomic blockade.
The electrophysiological measures of atrio-ventricular (A-V) conduction were investigated in 20 normal subjects (mean age: 43.9 +/- 15.7 years) both during basal state and after pharmacological autonomic blockade. In the basal state A-H and H-V intervals and H wave duration ranged from 55-110 ms (mean 83 +/- 15.9), 35-45 ms (mean 39.5 +/- 3.9) and 10-20 ms (mean 17 +/- 4.1), respectively. The lowest atrial rate inducing Wenckebach periods ranged from 150-200 beats min-1 (mean 176.5 +/- 13.8). The effective refractory period (ERP) and the functional refractory period from FRP) of the atrium ranged from 160-260 ms (mean 211 +/- 26.7) and 210-280 ms (mean 252.5 +/- 21.2), respectively. The ERP and the FRP of the A-V node were in the ranges 230-310 ms (mean 269.3 +/- 27.2) and 330-450 ms (mean 395 +/- 41.2), respectively. After autonomic blockade the H-V interval and the H wave duration did not change in any subject. The A-H interval was in the range 55-105 ms (mean 82.5 +/- 15) and the lowest atrial rate inducing Wenckebach periods 150-220 beats min-1 (mean 179.5 +/- 13.5). The ERP and the FRP of the atrium ranged from 170-270 ms (mean 215.5 +/- 28.3) and 210-300 ms (mean 254 +/- 27.2), respectively. The ERP and the FRP of the A-V node were in the ranges 220-320 ms (mean 260.8 +/- 32) and 330-440 ms (mean 383.3 +/- 43.7), respectively. The A-V node variables did not change significantly following autonomic blockade. These data indicate that: the definition of normal values of A-V node measurements after autonomic blockade allow us to evaluate the role of the autonomic nervous system in the patients with A-V node conduction disturbances; in the basal state the normal values of A-V conduction variables we obtained, of refractory periods in particular, are shorter than those previously reported; this appears to be related to the strict criteria we used in subject selection.
Adolescent↗
Colonic motility in the cat. V. Influence of telencephalic stimulation and the peripheral pathways mediating the effects.
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Amygdala↗
Effects of unilateral stellate ganglion block on the spectral characteristics of heart rate variability.
The effect of unilateral stellate ganglion block on cardiovascular regulation remains controversial, so the present study used power spectral analysis of heart rate variability to investigate its effect on the autonomic neural control of the heart. In 20 young healthy volunteers (mean age: 25 years), heart rate variability was determined before and after unilateral stellate ganglion block (right side 11, left side 9) using 8 ml of 1% mepivacaine during supine rest. Using autoregressive spectrum analysis, power spectra were quantified by measuring the area in 3 frequency bands: high-frequency power (lnHF, parasympathetic influence) from 0.15 to 0.40 Hz, low-frequency power (lnLF, predominantly sympathetic influence) from 0.04 to 0.15 Hz, and total-frequency power (lnTF) less than 0.40 Hz. Right stellate ganglion block decreased not only the lnLF component from 6.55+/-0.84 to 5.77+/-0.47 but also the lnHF component from 4.40+/-0.95 to 3.42+/-1.12 (p<0.05). In contrast, left stellate ganglion block changed neither the lnLF nor the lnHF component. The lnTF component was also decreased significantly by right stellate ganglion block from 7.80+/-0.95 to 7.01+/-0.36 (p<0.05), but was unchanged following left stellate ganglion block. Neither right nor left stellate ganglion block induced any significant change in both the RR and corrected QT intervals. However, changes in the RR interval induced by right stellate ganglion block showed significant positive correlation with changes in lnHF (p<0.005) and lnTF (p<0.05). These results suggest that (1) autonomic innervation to the sinus node is mainly through the right-sided stellate ganglion, (2) pharmacological right-sided stellate ganglion block may attenuate not only sympathetic but also parasympathetic activity and (3) following right stellate ganglion block the decrease in both the sympathetic and parasympathetic influence on the sinus node may inconsistently counterbalance and change the RR interval.
Adult↗
[Discussion on so-called cryptogenic digestive hemorrhages. Role of autonomic and neuro-psychic factors].
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Adult↗
Pressure diuresis and autonomic function in conscious dogs.
Pressure diuresis is thought to be a major long-term regulator of arterial blood pressure (AP). Previously, pressure diuresis has been characterized using pharmacological or surgical blockade of other mechanisms known to affect renal function. This study evaluated pressure diuresis in conscious dogs with minimal experimental interference. Dogs were chronically instrumented under pentobarbital anesthesia with aortic and urinary bladder catheters. AP was increased by 10% in resting dogs by exposure to increased light and sound intensity (arousal) for 90 min. During arousal, urine flow (UV) and Na+ excretion (UNa+ V) correlated with AP (UV vs. AP, r = 0.12, P less than 0.05; UNa+ V vs. AP, r = 0.19, P less than 0.005; 17 trials in 7 dogs). Arousal did not affect the plasma concentration of atrial natriuretic factor, suggesting that this hormone did not contribute to the correlations between UV or UNa+ V and AP. Because arousal may induce an autonomically mediated antidiuresis, studies were repeated during autonomic ganglionic blockade with hexamethonium. During autonomic blockade, the correlations between UV or UNa+ V and AP were increased (UV vs. AP, r = 0.72; UNa+ V vs. AP, r = 0.72, P less than 0.001; 6 trials in 4 dogs). We conclude that the effect of pressure diuresis on UV and UNa+ V can be detected in the intact animal, during normal operation of all the mechanisms that control renal function. Furthermore, when autonomic reflexes are blocked, the pressure-diuresis mechanism is a major determinant of UV and UNa+ V.
Animals↗
[CLINICAL CONSIDERATIONS ON THE TREATMENT OF PERIPHERAL VASCULAR DISEASES BY MEANS OF ANTALGIC NERVE BLOCKS].
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Autonomic Nerve Block↗
Direct negative inotropic and lusitropic effects of sevoflurane.
BACKGROUND: Volatile anesthetics depress left ventricular mechanical performance during multiple phases of the cardiac cycle. The effects of sevoflurane on systolic and diastolic function have yet to be fully evaluated. This investigation characterized the systemic and coronary hemodynamic, inotropic, and lusitropic actions of sevoflurane in chronically instrumented dogs in the presence and absence of autonomic nervous system (ANS) reflexes. METHODS: Because ANS activity may influence the actions of volatile anesthetics in vivo, experiments were conducted in both ANS-intact and ANS-blocked animals. Eighteen experiments were performed in nine dogs chronically instrumented for measurement of aortic and left ventricular pressure, rate of change of left ventricular pressure, subendocardial segment length, diastolic coronary blood flow velocity, and cardiac output. The preload recruitable stroke work slope was used to assess myocardial contractility. Diastolic function was evaluated by a time constant of isovolumic relaxation, maximum segment lengthening velocity during rapid ventricular filling, and a regional chamber stiffness constant. Dogs were assigned to receive sevoflurane with or without pharmacologic blockade of the ANS in a random fashion. On separate experimental days, systemic and coronary hemodynamics and left ventricular pressure--segment length diagrams and waveforms were recorded in the conscious state and during sevoflurane anesthesia (1.0, 1.25, 1.5, and 1.75 MAC). RESULTS: In dogs with intact ANS reflexes, sevoflurane caused significant (P < 0.05) increases in heart rate and dose-related decreases in mean arterial pressure, left ventricular systolic pressure, cardiac output, and diastolic coronary vascular resistance. Sevoflurane also decreased myocardial contractility (preload recruitable stroke work slope 96 +/- 4 in the conscious state to 42 +/- 3 mmHg at 1.75 MAC). Sevoflurane prolonged isovolumic relaxation (time constant of isovolumic relaxation 35 +/- 1 in the conscious state to 51 +/- 3 ms at 1.75 MAC) and decreased rapid ventricular filling (maximum segment lengthening velocity 40.2 +/- 6.0 in the conscious state to 21.8 +/- 3.8 mm.s-1 at 1.75 MAC) without affecting regional chamber stiffness. Sevoflurane caused similar alterations in functional indices of left ventricular systolic and diastolic performance in autonomically blocked dogs. CONCLUSIONS: Sevoflurane caused direct negative inotropic and lusitropic effects in chronically instrumented dogs with and without ANS blockade.
Anesthetics↗
Circulatory responses to airway stimulation and cervical epidural blockade.
In order to investigate the effects of acute cardiac sympathectomy, the circulatory responses due to tracheal intubation and broncho-carinal stimulation were compared in lightly anesthetized, paralyzed patients who had either cervical (n = 18) or lumbar epidural blockade (n = 18), or neither (n = 12). The mean analgesic levels obtained using 2% mepivacaine with epinephrine were C4-T8 in the cervical group, and T7-S1 in the lumbar group. Increases in arterial blood pressure (AP) and heart rate (HR) due to laryngoscopy were significant (P less than 0.01) but similar in the three groups of patients. Broncho-carinal stimulation by a suction catheter did not produce noticeable changes in AP and HR in the cervical group; significant increases were observed in the other two groups (P less than 0.01). It was concluded from this study that acute sympathectomy induced in part by cervical or lumbar epidural block does not attentuate circulatory responses due to laryngoscopy and tracheal intubation. The cervical blockade, however, can prevent such responses due to broncho-carinal stimulation without predominant vagotonic reflexes; this may be attributed to the interruption of sympathetic afferents to the spinal cord at the epidural level.
Adult↗
Ablation of Ca(v)2.3 / E-type voltage-gated calcium channel results in cardiac arrhythmia and altered autonomic control within the murine cardiovascular system.
Voltage-gated calcium channels are key components in cardiac electrophysiology. We demonstrate that Ca(v)2.3 is expressed in mouse and human heart and that mice lacking the Ca(v)2.3 voltage-gated calcium channel exhibit severe alterations in cardiac function. Amplified cDNA fragments from murine heart and single cardiomyocytes reveal the expression of three different Ca(v)2.3 splice variants. The ablation of Ca(v)2.3 was found to be accompanied by a compensatory upregulation of the Ca(v)3.1 T-type calcium channel, while other voltage-gated calcium channels remained unaffected. Telemetric ECG recordings from Ca(v)2.3 deficient mice displayed subsidiary escape rhythm, altered atrial activation patterns, atrioventricular conduction disturbances and alteration in QRS-morphology. Furthermore, time domain analysis of heart rate variability (HRV) in Ca(v)2.3(-/-) mice exhibited a significant increase in heart rate as well as in the coefficient of variance (CV) compared to control mice. Administration of atropin/propranolol revealed that increased heart rate was due to enhanced sympathetic tonus and that partial decrease of CV in Ca(v)2.3(-/-) mice after autonomic block was in accordance with a complete abolishment of 2(nd) degree atrioventricular block. However, escape rhythms, atrial activation disturbances and QRS-dysmorphology remained unaffected, indicating that these are intrinsic cardiac features in Ca(v)2.3(-/-) mice. We conclude that the expression of Ca(v)2.3 is essential for normal impulse generation and conduction in murine heart.
Animals↗
Estimation of non-autonomic and autonomic components of iliac bed vascular resistance in renal hypertensive rabbits.
Iliac bed vascular resistance (IVR) was measured before and after pharmacological block of the autonomic effectors in unanaesthetized renal hypertensive and normotensive rabbits with previously implanted Doppler flowmeters. This permitted partitioning the resting IVR into a non-autonomic component (ie, steady-state IVR after block) and an autonomic component (ie, resting IVR minus non-autonomic IVR). When IVR was measured at the same mean arterial pressure (MAP) before and after block in each animal, the increase in estimated non-autonomic IVR accounted entirely for the rise in resting IVR in renal hypertensive rabbits. However, if IVR measurements after block were made at a lower MAP than before block, the estimated non-autonomic and autonomic components were both significantly increased in renal hypertensive rabbits. It is concluded that in the latter experiment non-autonomic IVR in renal hypertension was underestimated, whilst the autonomic component was overestimated. The rise in non-autonomic IVR in renal hypertension was partly due to structural changes in the iliac bed, since IVR remained higher in hypertensive than in normotensive rabbits after abolishing smooth muscle tone with vasodilator drugs.
Animals↗
Autonomic modulation of ovine fetal responses to atrial natriuretic factor infusion.
The aim of this study was to determine whether the autonomic nervous system modulates the cardiovascular, endocrine, and/or urinary responses to atrial natriuretic factor (ANF) infusion in the fetus. We infused ANF intravenously for 30 min into chronically catheterized, late-gestation sheep fetuses with autonomic blockade and compared the responses to those in autonomically intact fetuses. During the infusions, plasma ANF concentration increased similarly in the blocked and intact fetuses. Arterial pressure decreased by 2 mmHg in both groups, but the decrease occurred earlier in the blocked fetuses. Heart rate was significantly decreased by an average of 15 beats/min in the blocked compared with the intact fetuses. Plasma protein concentration decreased in the blocked fetuses compared with a rise in the intact fetuses. In the blocked fetuses, the restoration of blood volume to normal during the postinfusion period occurred earlier. In the blocked animals, low doses of ANF produced a diuresis, whereas high doses did not increase urine flow; the opposite responses occurred in the intact group. Plasma arginine vasopressin (AVP) concentration increased during the infusion only in the blocked animals. The fetal venous pressure, plasma renin activity, and norepinephrine responses were similar in both groups. These data suggest that the autonomic nervous system may play a role in modulating the fetal arterial pressure, heart rate, blood volume, plasma protein concentration, AVP, and urine flow responses to ANF. Thus the autonomic nervous system appears to significantly modulate multiple responses to ANF in the late-gestation ovine fetus.
Animals↗
Importance of the autonomic nervous system in an experimental model of commotio cordis.
BACKGROUND: Young athletes may die suddenly when they are struck in the chest (commotio cordis). Proposed mechanisms of sudden death in commotio cordis include hypervagatonia and activation of the sympathetic nervous system. In an experimental model of commotio cordis, the importance of the sympathetic and parasympathetic nervous system in the initiation of ventricular fibrillation was evaluated. MATERIAL/METHODS: Juvenile swine weighing between 8 and 12 kg were anesthetized with ketamine and isoflurane and placed prone in a sling. Twenty animals were randomized to pretreatment with placebo or sympathetic and parasympathetic blockade. Chest blows were guided by echocardiography to the center of the left ventricle and animals received 1-3 strikes with a regulation baseball propelled at 30 mph and timed to impact 10-30 ms prior to the peak of the T-wave. RESULTS: With 17 impacts in 10 autonomically blocked animals, 6 episodes of ventricular fibrillation were seen; with 15 impacts in 10 control animals, ventricular fibrillation occurred 6 times. There was also no significant difference between the groups in occurrence of nonsustained polymorphic ventricular tachycardia or ST elevation. Transient complete heart block was less commonly seen in animals treated with autonomic blockade, although this did not achieve statistical significance. CONCLUSIONS: In this experimental model of commotio cordis, autonomic blockade did not affect the frequency of sudden cardiac death, polymorphic ventricular tachycardia or ST segment elevation. Thus, vagotonic and sympathetic surges likely do not contribute to the syndrome of sudden death due to chest blows in young people and athletes.
Animals↗