Phrenic Nerve and vagal nerve activities during differential lung ventilation in cats

The effect of differential lung ventilation (DLV) on afferent vagal and efferent phrenic nerve activities was studied in urethane anesthetized cats. One endotracheal tube was inserted into the left bronchus to ventilate its side lung. Another tube was inserted until its tip reached about 1cm above the carina to ventilate the right lung. Using two respirators, each lung was ventilated independently. Using hooked silver electrodes, the vagal and phrenic nerve activities were recorded.The afferent vagal nerve was activated in concurrence with lung inflation at any ventilation rate. The right and left vagal nerves were activated by right and left lung ventilation, respectively. On the other hand, the right and left efferent phrenic nerves were synchronized, whether the ventilation was disused or ventilation was achieved by right or left one lung ventilation or even by asynchronous DLV.The phrenic nerve activity was surpressed by one-lung, right or left, ventilation independently, so that the rhythm of the phrenic nerve was disturbed by asynchronous DLV. From these results, to reduce the stress of patients during asychronous DLV, it was considered that patients need heavier sedation than a usual mechanical ventilatory support.(Kasaba T, Kosaka Y: Phrenic nerve and vagal nerve activities during differential lung ventilation in cats. J Anesth 2: 170–175, 1988)     

Continuous Positive Airway Pressure Increases Vagal and Phrenic Nerve Activity in Cats

To investigate how continuous positive airway pressure (CPAP) changes the vagal nerve activity and whether CPAP alters the efferent phrenic nerve activity or the breathing pattern similarly before and after vagotomy, a study was made of vagal and phrenic nerve activity in chloralose-anaesthetized cats. In the vagal nerve, CPAP increased the mean impulse frequency during expiratory rest. The breath-related impulse frequency also increased with CPAP. With higher CPAP (greater than or equal to 0.5 kPa), the peak of breath-induced activity in the vagal nerve lasted longer than inspiration. In the phrenic nerve, the impulse frequency in the bursts increased almost linearly with CPAP irrespective of whether the vagal nerves were intact or not. The duration of the phrenic nerve bursts decreased with increasing CPAP when the vagal nerves were intact. When the vagal nerves were cut, the burst duration did not change. The rate of breathing was almost unchanged by CPAP regardless of whether the vagal nerves were cut or not. The inspiration/expiration ratio decreased with increasing CPAP when the vagal nerves were intact, but not when they were cut.     

Effects of high-frequency positive-pressure ventilation (HFPPV) and general anesthesia on intrapulmonary gas distribution in patients undergoing diagnostic bronchoscopy

In nine patients undergoing diagnostic bronchoscopy, intrapulmonary gas distribution was evaluated by means of nitrogen washout. The investigations were performed with the patients in the supine position, first awake during spontaneous breathing and then during general anesthesia with high-frequency positive-pressure ventilation (HFPPV) via a pneumatic valve connector. With HFPPV a ventilatory frequency (f) of 60/min and a relative insufflation time (t%) of 22% of the ventilatory cycle were used. Gas distribution in terms of lung clearance index and nitrogen washout delay improved during HFPPV as compared with spontaneous breathing. Compared with spontaneous breathing and also with apnea during general anesthesia, functional residual capacity was increased during HFPPV. During air breathing arterial PO2 (PaO2) and alveolararterial oxygen tension differences (D(A-a)O2) were the same during spontaneous breathing and HFPPV, but during oxygen breathing PaO2 was lower and D(A-a)O2 higher with HFPPV. Ventilatory volumes set according to a nomogram for the pneumatic valve connector and HFPPV resulted in moderate hyperventilation. PaO2 could be controlled by adjustment of inspired oxygen concentration.     

High-Frequency Positive-Pressure Ventilation (HFPPV) in Neonates and Infants during Neuroleptal Analgesia and Routine Plastic Surgery, and in Postoperative Management

The low pulmonary compliance, the high airway resistance and the "rapid" breathing pattern of neonatal and paediatric patients make it necessary to design special ventilators to match the pulmonary physiology of infants.
A ventilator system which also in small children has a negligible compression volume was evaluated in a lung model and during repair of cleft lip and palate in 16 patients under general anaesthesia and in two other infants during other operations. High-frequency positive-pressure ventilation (HFPPV) was given with an insufflation frequency (f) of 60 per min and a relative insufflation time (t%) of 32%. In addition, two neonates treated postoperatively with HFPPV are reported.
Despite the "open" character of the ventilator system both intra- and postoperative ventilation were uneventful in all patients. The arterial oxygenation was good in all cases, as judged from clinical signs or blood gas analyses. Postoperative ventilation required conventional clinical observation and intermittent analyses of blood.
HFPPV has been shown to depress, or abolish, spontaneous respiration via reflex mechanisms. In all patients in this investigation respiratory movements were absent at normo- or slight hyperventilation during HFPPV.     

Laryngeal pacemaker. Part I. Electronic pacing of reinnervated strap muscles in the dog

The best approach to management of bilateral vocal cord paralysis, with its resultant airway compromise, has not yet been universally agreed upon. Recently proposed methods have included direct stimulation of the laryngeal dilators by the modulation of rhythmic information from the chest wall, diaphragm, phrenic nerve, or accessory muscles of respiration. In such an approach, the information obtained is not necessarily related to inspiration only, and direct implantation of a stimulating electrode into the laryngeal musculature may not be fully efficient and tolerated over time. To obviate such difficulties, the authors propose to broaden the concept of electrical pacing by (1) developing a better source for the triggering of electrical activity during inspiration and (2) devising a reliable means of long-term physiologic stimulation of denervated striated muscle not subject to deterioration over time. Such an experimental unit was constructed in the canine. It is based on afferent information that originates from the mechanical lengthening of the trachea during inspiration and is detected through a linear strain gauge sutured to the tracheal rings. The signal obtained is modulated through an impedance detector and is amplified. An efferent limb consisting of a monopolar cuffed electrode placed around a crossover nerve-muscle pedicle from one sternohyoid muscle to the other was used successfully. Such a preliminary experiment with a strap muscle avoids the extraneous factors related to function of the paralyzed larynx. Successful nerve-muscle pedicle pacing, synchronous with respiration, was verified through electromyographic recordings and direct observation in all animals studied.     

Diaphragmatic pacing in infants: techniques and results

Phrenic nerve pacing was employed in 8 infants with central hypoventilation syndrome. Their ages ranged from 2.5 to 8.5 months. Preoperative diagnosis was established by demonstrating inadequate ventilatory response to hypercapnia and hypoxia. Percutaneous measurements of phrenic nerve conduction time and diaphragmatic action potentials were performed prior to operation to assess the feasibility of diaphragmatic pacing. A single anterolateral thoracotomy incision was used for both electrode placement in the chest and receiver implantation in the flank. The stimulating electrode was inserted around a segment of intrathoracic phrenic nerve isolated with pleura and perineural blood supply. Follow-up is available on all patients six months to 8 years postoperatively. There were no complications or deaths related to the procedure. In all patients, bilateral phrenic nerve stimulation allowed either marked decrease in or discontinuation of positive-pressure ventilation. Phrenic nerve pacing can be performed safely in infants. It provides an effective alternative method for ventilatory support without the drawbacks of positive-pressure ventilation.     

Effects of intravenously administered lidocaine on pulmonary vagal afferents and phrenic nerve activity in cats

The ability of lidocaine to suppress activity of single vagal afferent fiber and that of phrenic nerve was studied in 20 cats anesthetized with pentobarbital. Slowly adapting stretch receptors (SAR, n = 16) and rapidly adapting stretch receptors (RAR, n = 7) were identified by their discharge pattern to pulmonary inflation. Intravenous lidocaine (1mg·kg^–1 or 2mg·kg^–1) produced a suppression of SAR activity but not of RAR activity. Suppression of phrenic nerve activity lasted much longer than that of SAR. These findings indicate that iv lidocaine acts more dominantly on CNS than on peripherals. We conclude that iv lidocaine prevents cough and hemodynamic changes caused by airway manipulation mainly through its action on CNS and not on peripherals (peripheral nerves or their receptor).(Aoki M, Harada Y, Namiki A, et al.: Effects of intravenously administered lidocaine of pulmonary vagal afferents and phrenic nerve activity in cats. J Anesth 6: 395–400, 1992)     

Physiologic Evaluation of the HFPPV Pneumatic Valve Principle and PEEP An Experimental Study

In experiments in dogs the ventilatory and circulatory conditions prevailing with the ventilatory pattern in high-frequency positive-pressure ventilation (HFPPV) were investigated with use of a pneumatic valve principle and a ventilator system of an "open" character. Keeping the gas input constant the importance of insufflation frequency and insufflation time and the reactions to various levels of positive end-expiratory pressure (PEEP) were investigated in terms of changes in arterial pH, P^co2and P^o2.
With the volumes of delivered gas kept constant, an increasing insufflation frequency from 60 to 100 per min gave a parallel decrease in tidal volume accompanied by lower maximum intratracheal pressures and a significant decrease in alveolar ventilation. Also taking into account the possibilities of inducing a suppression of the spontaneous respiration, higher ventilatory frequencies than 60 per min do not seem to introduce any further advantages.
Including the associated effects on cardiac output and venous admixture, the cardiopulmonary and circulatory parameters studied did not show any substantial changes with PEEP levels below 7.5–10 cm H₂O. Thus the level of PEEP, which often is part of the ventilatory pattern in HFPPV, does not seem to have any untoward influence on the circulation (stroke volume, cardiac output, total peripheral vascular resistance) and oxygen transport (arterial oxygen content and oxygen flux) in normovolaemic dogs.     

Respiration: control of ventilation

Control of ventilation involves the basic cycle of inspiration and expiration and the chemoreceptor reflexes. The inspiration-expiration cycle is generated by the medulla, but it is smoothed by the combined actions of the pons and vagi. Inspiration is initiated by neurons that promote lung inflation via the intercostal and phrenic nerves; it is terminated by a combination of fatigue of these neurons and inhibitory actions from the pons, expiratory centre and increasing lung volume (via the vagus). As a result, expiration is initiated; this, in turn, is inhibited by fatigue of the expiratory neurons and by loss of inhibitory influences from the pons and the vagus as the lungs deflate. The physical work during respiration is against lung compliance and airway resistance. Too slow a frequency of very deep breaths would require excessive amounts of work against compliance forces; and rapid shallow breaths would greatly increase the work done against airway resistance. A balance between these extremes is achieved by the vagal afferents that help to terminate inspiration. Whole-body responses to gas changes indicate that rising carbon dioxide levels promote ventilation, a reflex that is increased by the simultaneous presence of acidaemia and, particularly, hypoxia (asphyxia). These reflex changes originate from peripheral chemoreceptors (aortic and carotid bodies) that monitor the oxygen, carbon dioxide and acid levels of the plasma, and from central chemoreceptors (floor of the IVth ventricle) that monitor the pH of the cerebrospinal fluid. Details of the integration between these reflexes and the basic inspiraton-expiration cycle remain to be elucidated.     

Inhibition of phrenic nerve activity during positive-pressure ventilation at high and low frequencies

A study was made to determine whether the ventilatory pattern, in terms of ventilatory frequency, insufflation period and end-expiratory pressure, influences the arterial blood gas level at which central inspiratory activity is inhibited, and whether further expansion of the lung changes this activity. This was accomplished by measuring arterial pH and blood gases, and intratracheal, intrapleural and transpulmonary pressures, at the setting of positive-pressure ventilation causing inhibition of phrenic nerve activity in chloralose-anaesthetized cats. Spontaneous breathing movements were prevented by muscle relaxation. Ventilatory frequencies of 15-120 breaths per minute (b.p.m.) were studied at at least two different insufflation times. A volume-controlled ventilator with a large compressible volume was used in the frequency range 15-45 b.p.m. and a constant flow respirator with a low-compressible volume in the range 45-120 b.p.m. A much lower PCO2 was needed for phrenic nerve activity to be inhibited at a ventilatory frequency of 15 b.p.m. than at higher frequencies. At ventilatory frequencies between 30 and 120 b.p.m. inhibition could be achieved at a higher PCO2, within the normal range. The inhibition of phrenic nerve activity tended to be less stable when PEEP was added during ventilation with a long insufflation period, but PEEP did not influence the arterial blood gas level at which inhibition occurred. In the lower frequency range of 15-30 b.p.m., inspiratory activity was observed with bursts at the same rate as the insufflations given by the ventilator. The intratracheal peak pressures at ventilation causing inhibition of phrenic nerve activity decreased with increasing ventilatory frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ketamine Inhibits Inspiratory-evoked γ-Aminobutyric Acid and Glycine Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus

Background: Ketamine can be used for perioperative pain management as well as a dissociative anesthetic agent in emergency situations. However, ketamine can induce both cardiovascular and respiratory depression, especially in pediatric patients. Although ketamine has usually been regarded as sympathoexcitatory, recent work has demonstrated that ketamine has important actions on parasympathetic cardiac vagal efferent activity. The current study tests the hypothesis that ketamine, at clinical relevant concentrations, alters central cardiorespiratory interactions in the brainstem and, in particular, the inspiration-evoked increase in [gamma]-aminobutyric acid-mediated and glycinergic neurotransmission to parasympathetic cardiac efferent neurons.

Methods: Cardiac vagal neurons were identified by the presence of a retrograde fluorescent tracer. Respiratory evoked [gamma]-aminobutyric acid-mediated and glycinergic synaptic currents were recorded in cardiac vagal neurons using whole cell patch clamp techniques while spontaneous rhythmic respiratory activity was recorded simultaneously.

Results: Ketamine, at concentrations from 0.1 to 10 [mu]m, evoked a concentration-dependent inhibition of inspiratory burst frequency. Inspiration-evoked [gamma]-aminobutyric acid-mediated neurotransmission to cardiac vagal neurons was inhibited at ketamine concentrations of 0.5 and 1 [mu]m. The increase in glycinergic activity to cardiac vagal neurons during inspiration was also inhibited at ketamine concentrations of 0.5 and 1 [mu]m.     

One-lung high-frequency ventilation for tracheoplasty and bronchoplasty: a new technique

Major airway surgery requires the maintenance of adequate ventilation and oxygenation during the period of resection and reconstruction, as well as an unobstructed surgical field and optimal access to the airway's circumference. High-frequency positive-pressure ventilation (HFPPV) at a frequency of 1 Hz (60 breaths/min) or more, along with a small tidal volume (50 to 250 cc), provides adequate ventilation and oxygenation with minimal impairment of pulmonic and systemic circulatory functions. We have used HFPPV of one lung through a 2 mm internal diameter catheter in six patients (three undergoing right sleeve pneumonectomies, two having carinal tumor resections, and one having tracheal resection). High-frequency positive-pressure ventilation of the left lung provided continuous and adequate ventilation and oxygenation during the period of resection and reconstruction of the airways, while the small catheter permitted unimpaired visualization and adequate access to the operative site.     

EFFERENT PHRENIC NERVE ACTIVITY DURING INDUCED CHANGES IN ARTERIAL PRESSURE

Efferent activity in the phrenic nerve was recorded during inducedhypotension and hypertension in anaesthetized, paralysed, artificiallyventilated dogs. Changes in arterial pressure were induced withinfusions of sodium nitroprusside, noradrenaline and angiotensinII, after which ventilation was adjusted to return the Pa_O2near to control values. The Pa_O2 was maintained above chemoreceptorthreshold throughout. When a steady state was achieved quantitativemeasurements of phrenic nerve activity were made. In six dogsan increase in mean arterial pressure from 114 to 167 mm Hgcaused a mean reduction of phrenic nerve activity of 28%. Insix dogs a decrease in mean arterial pressure from 128 to 82mm Hg caused an increase in phrenic nerve activity of 22%. Thisshows that the reduction in arterial pressure induced by vasodilatordrugs causes a major sustained stimulus to respiration, whileincrease in arterial pressure causes marked respiratory depression. ^*Present address: Department of Anaesthetics, The MiddlesexHospital, Mortimer Street, London W1     

Combined high-frequency ventilation for management of terminal respiratory failure: a new technique

Seven patients with severe adult respiratory distress syndrome (ARDS) developed terminal respiratory failure and severe hypoxemia (PaO2 below 50 mm Hg) with death imminent despite maximal ventilatory support with intermittent positive-pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). High-frequency positive-pressure ventilation (HFPPV) was used in these patients for one day at a rate of 250 breaths/min, with slight improvement of PaO2 to a mean of 80 mm Hg. High-frequency oscillatory (HFO) ventilation was used during the second day at a rate of 2000 breaths/min; this provided adequate oxygenation with a mean PaO2 of 244 mm Hg. Nonetheless, during HFO there was progressive CO2 retention and respiratory acidosis (mean PCO2 67 mm Hg). On the third study day, all seven patients were ventilated with combined high-frequency ventilation (CHFV) for a period from 5-21 days. CHFV is based on the administration of HFPPV simultaneously with HFO and provided adequate oxygenation by accelerated gas diffusion and CO2 elimination by convection. PaO2 was maintained during CHFV at a mean of 280 mm Hg. CO2 elimination was adequate with a mean PaCO2 of 32 mm Hg. Cardiac output also was adequately maintained during CHFV. Moreover, CHFV was well tolerated in our patients, allowing them to communicate with their families and nurses. CHFV successfully treated the hypoxemia of respiratory failure in all the patients. However, five patients (71%) died of cardiac arrest as a result of multisystem failure despite adequate oxygenation (PaO2 above 80 mm Hg).     

The renal nerve and cardiovascular responses to renal receptor stimulation with veratrine in dogs]

Renal nerve and cardiovascular effects of intrarenal veratrine (Ver) were investigated using the cross-perfused kidney preparations of anesthetized dogs. Ver (1 and 3 micrograms/kg), injected as a bolus, elicited increases in arterial blood pressure (ABP), heart rate (HR) and renal efferent nerve activity (RENA). Ganglion blockade, hexametonium (2 mg/kg) markedly diminished increases in ABP, HR and RENA induced by Ver. In a separate group of animals, significant increases in renal afferent nerve activity (RANA) occurred after Ver administration. It is concluded that selective intrarenal Ver activates renal nerve afferents, and these results in cardiovascular changes are consistent with efferent sympathetic activation.     

Effects of sevoflurane on respiratory activities in the phrenic nerve of decerebrate cats

Although the depressive effect of sevoflurane on ventilation has been reported, its potency and mode of action on the neural respiratory activity is still unclear. Therefore, the effects of sevoflurane on the phrenic nerve discharge and the respiratory timing were compared with those of halothane.
The efferent activity of the phrenic nerve was recorded from decerebrate, un-anesthetized and artificially ventilated cats, and its power spectrum was calculated. The inspiratory and expiratory periods were measured. Sevoflurane and halothane of the doses of 0.5–1.5 MAC were inhaled for 15 min.
With 0.5 MAC, sevoflurane decreased the total power and two dominant spectral components of the high-frequency oscillation and medium-frequency oscillation in the power spectrum. With the same MAC dose, halothane had a greater depressive effect in a normocapnic condition with the vagus nerves being intact. In a state of hypercapnia or after vagotomy, the effect of halothane was considerably attenuated whereas that of sevoflurane remained unaltered. Halothane increased the neural respiratory rate much more than sevoflurane in both normocapme and hypercapnic states. Vagotomy significantly weakened the effect of halothane to increase the respiratory rate but did not modify the effect of sevoflurane. With 1.0–1.5 MAC, both anesthetics severely decreased the phrenic power spectra and the potency difference became indistinct.
The present findings demonstrate that sevoflurane has a weaker depressive effect on the respiratory nerve discharge and a smaller effect on the neural respiratory rate than halothane when the effects of 0.5 MAC were compared. This may be due to the lesser effect of sevoflurane on the vagal mediated and CO₂-related mechanisms which modulate the global outputs of the central respiratory control system.     

Vagal involvement in the action of exogenous adenosine triphosphate on reflex renal sympathetic nerve activity

The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.     

A cardiogenic hypertensive chemoreflex

A cardiogenic hypertensive chemoreflex is elicited by serotonin administered experimentally in the dog. The reflex nearly doubles aortic pressure within 4-6 sec and is associated with powerful inotropic, chronotropic, and dromotropic responses. The afferent pathway is via intrathoracic vagal branches, whereas the efferent paths engage not only the vagal and sympathetic routes but also the phrenic nerve. The reflex can be abolished by vagotomy or with cyproheptadine, and can be attenuated by local anesthesia of the intertruncal space. Small chemoreceptors lying between the aorta and pulmonary artery are the source of the reflex, and they receive their blood supply from the proximal left coronary artery. Human counterparts of the reflex may include new hypertension during angina pectoris or acute myocardial infarction, new postoperative hypertension after coronary bypass grafting, and hypertensive patients with carcinoid syndrome. Many unresolved problems include the precise mechanism of chemoreception, whether the chemoreflex has any tonic influence, and mechanisms of integration of the reflex with other events peripherally and centrally. Answers to these questions could be of great clinical value.     

Effect of stimulation of the tooth pulp on gastrointestinal motility in rabbits

Effects of electrical stimulation of the inciser tooth pulp on the gastrointestinal motility were investigated in the rabbit anesthetized with urethane and chloralose. Pulpal Stimulation caused an excitatory or an inhibitory effect in the gastric body and antrum and the ducodenum. After bilateral splanchnicotomy the excitatory response to the pulpal stimulation was reinforced or the inhibitory response converted to the excitatory response. An additional cervical vagotomy abolished the excitatory and inhibitory response. Atropine diminished the spontaneous efferent discharges of vagal gastric branch (VGB) and abolished the excitatory and inhibitory response to stimulation of the pulp and the inferior alveolar nerve. This agent also blocked the potentials of the VGB evoked by afferent stimulation of the inferior aveolar nerve. Hexamethonium bromide abolished the excitatory and inhibitory responses to the pulpal stimulation but did not affect spontaneous discharges and increased discharges of the VGB to pulpal stimulation. Morphine produced decreased rate of the spontaneous discharge of the VGB and abolished increased rate of discharges of the VGB as well as the gastrointestinal responses to pulpal stimulation. It is concluded from these results that the afferent impulses caused by pulpal stimulation and the inferior alveolar nerve 'reflex'ly activate the vagal motor nuclei in the medulla oblongata and the sympathetic splanchnic nuclei in the thoracic segments through the trigeminal nerve: The vagus nerves produced the excitatory response in the gastrointestinal motility, while the splanchnic nerves caused the inhibitory response. It was supposed that sites of action of atropine and morphine is not in peripheral site, but in the central nerves site.     

严重烧伤早期大鼠心脏交感神经电生理活动的变化

目的 研究严重烧伤早期大鼠心脏交感神经电生理活动的变化规律及其机制,探讨心脏交感神经活动的变化与严重烧伤后心脏损伤的关系。方法 SD大鼠随机分为正常组（6只）、假伤组（18只）和烧伤组（20只）,在烧伤组大鼠背部制成30％TBSA的Ⅲ度烫伤。应用神经电生理方法记录心脏交感神经的放电活动,同时观察心电图和心肌力学指标的变化。结果 严重烧伤后大鼠心脏交感神经传出活动即刻增强,而传入活动经一潜伏期（约90s)后也显增强,且传入活动增强后传出活动进一步增强。交感神经传出、传入活动增强约持续3h左右,而后显降低,传入活动的变化早于传出活动的变化。部分大鼠在烧伤后1h左右,心脏交感神经放电活动除平均值增加外,波动性增大,呈间歇性“爆发”现象,其中4只大鼠在放电爆发性增加的同时频发室性早搏。烧伤后左心室收缩压峰值和左室内压最大上升／下降速率显降低。结论 严重烧伤后早期心脏交感神经传入和传出活动均增强,且传入活动的变化对传出活动的变化有一定的影响。心脏交感神经电生理活动增强可能是严重烧伤后早期心脏损伤的原因之一。