Halothane, enflurane, and isoflurane depress the peripheral vagal motor pathway in isolated canine tracheal smooth muscle.

in Anesthesiology (1991), 74(2), 325-32

Volatile anesthetics are potent bronchodilators, but the site of action for the dilation is unclear. To determine the site of action of halothane, enflurane, and isoflurane on the peripheral vagal motor ... [more ▼]

Volatile anesthetics are potent bronchodilators, but the site of action for the dilation is unclear. To determine the site of action of halothane, enflurane, and isoflurane on the peripheral vagal motor pathway, isolated strips of canine trachealis muscle were stimulated before and during exposure to halothane at 0.3, 1.0, 1.7, or 2.4 MAC, enflurane at 1 MAC, or isoflurane at 1 MAC. The sites and methods of stimulation were: 1) postsynaptic nicotinic cholinergic receptors in the intramural parasympathetic ganglia, with 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP); 2) postganglionic cholinergic nerve fibers, with electrical field stimulation (EFS); and 3) muscarinic cholinergic receptors of the smooth muscle, with acetylcholine (ACh). The concentration-response curve to DMPP was significantly shifted to the right by 0.3 MAC halothane, whereas 0.3 MAC halothane had no significant effect on the concentration-response curves to ACh and EFS. At concentrations greater than 1 MAC of halothane, enflurane, or isoflurane, concentration-response curves to all three stimuli were shifted significantly to the right; i.e., the contractile responses to ACh, EFS, and DMPP were reduced. At all concentrations of halothane the force of contraction was significantly more reduced during stimulation with DMPP than during stimulation with ACh, and at halothane concentrations greater than or equal to 1.7 MAC the response to EFS was significantly more reduced than that to ACh. We conclude that halothane, enflurane, and isoflurane attenuated airway constriction by several mechanisms, including 1) reduced excitability of the postsynaptic nicotinic receptors of the intramural parasympathetic ganglia and 2) an effect on the smooth muscle and/or on the muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

Direct and neurally mediated effects of halothane on pulmonary resistance in vivo.

in Anesthesiology (1990), 72(6), 1057-63

It has been suggested that halothane inhibits contraction of airway smooth muscle in vivo mainly by reducing reflex activity in nerves innervating the muscle with only minimal direct effects on the muscle ... [more ▼]

It has been suggested that halothane inhibits contraction of airway smooth muscle in vivo mainly by reducing reflex activity in nerves innervating the muscle with only minimal direct effects on the muscle itself. To examine possible mechanisms of action of halothane at clinically relevant concentrations the authors studied the effect of halothane on increases in pulmonary resistance (RL) produced by either vagus nerve stimulation (VNS, which caused neurally mediated constriction) or the inhalation of nebulized acetylcholine (ACh, which directly stimulated the smooth muscle cell) in nine mongrel dogs. The frequency of bilateral VNS and the dose of nebulized ACh were adjusted to produce approximately equal increases in RL. Halothane reduced the response to both types of stimulation in a dose-dependent fashion. At halothane concentrations greater than or equal to 0.4 MAC, the VNS response was significantly less than the ACh response. When tetrodotoxin was given to block neural activity, the ACh response was unchanged, confirming that neural activation did not contribute significantly to smooth muscle contraction in response to ACh. The authors conclude that in addition to neurally mediated effects, halothane at clinically used concentrations has significant direct effects on airway smooth muscle stimulated by ACh. The relative importance of each factor in vivo should depend on the stimulus that causes contraction of airway smooth muscle. [less ▲]

Halothane decreases both tissue and airway resistances in excised canine lungs.

in Journal of Applied Physiology (Bethesda, Md. : 1985) (1989), 66(6), 2698-703

Studies of the anesthetic effects on the airway often use pulmonary resistance (RL) as an index of airway caliber. To determine the effects of the volatile anesthetic, halothane, on tissue and airway ... [more ▼]

Studies of the anesthetic effects on the airway often use pulmonary resistance (RL) as an index of airway caliber. To determine the effects of the volatile anesthetic, halothane, on tissue and airway components of RL, we measured both components in excised canine lungs before and during halothane administration. Tissue resistance (Rti), airway resistance (Raw), and dynamic lung compliance (CL, dyn) were determined at constant tidal volume and at ventilatory frequencies ranging from 5 to 45 min-1 by an alveolar capsule technique. Halothane decreased RL at each breathing frequency by causing significant decreases in both Raw and Rti but did not change the relative contribution of Rti to RL at any frequency. Halothane increased CL,dyn at each breathing frequency, although there was little change in the static pressure-volume relationship. The administration of isoproterenol both airway and tissue components of RL; it may act by relaxing the contractile elements in the lung. Both components must be considered when the effects of volatile anesthetics on RL are interpreted. [less ▲]

Actions of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance in dogs.

in Anesthesiology (1988), 69(5), 688-95

The effects of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance and heart rate were studied in 30 vagotomized dogs lying supine and anesthetized with chloralose ... [more ▼]

The effects of enflurane, isoflurane, vecuronium, atracurium, and pancuronium on pulmonary resistance and heart rate were studied in 30 vagotomized dogs lying supine and anesthetized with chloralose-urethane. None of the five drugs affected pulmonary resistance when the airway was unstimulated. Enflurane and isoflurane significantly attenuated the increase in pulmonary resistance induced by electrical stimulation of the vagus nerves. This effect was dose-dependent and similar for both anesthetics at equivalent multiples of their minimum alveolar concentration. Atracurium significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; vecuronium had no significant effect. Pancuronium, up to a cumulative dose of 0.14 mg/kg, also significantly (P less than 0.05) enhanced the increase in pulmonary resistance induced by vagus nerve stimulation; but this effect was reversed by further increasing the dose. Pancuronium also attenuated the cardiodecelerator response to vagus nerve stimulation in a dose-dependent fashion. The underlying mechanisms for the attenuation of responses to vagus nerve stimulation by enflurane or isoflurane or for the increase in response with atracurium are unknown. Pancuronium at lower doses increases the response most likely by blocking prejunctional muscarinic receptors (M2) that physiologically inhibit vagally mediated increases in pulmonary resistance. [less ▲]

Monitorage des fractions inspirées et alvéolaires

in Anesthésie par inhalation (1987)

Monitorage de la ventilation assistée

in La ventilation artificielle (1987)

Effects of high-frequency jet ventilation on arterial baroreflex regulation of heart rate.

in Journal of Applied Physiology (Bethesda, Md. : 1985) (1987), 63(6), 2216-22

Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ... [more ▼]

Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ventilation (CPPV) on arterial baroreflex regulation of heart rate. Systolic arterial pressure and right atrial pressure were measured using indwelling catheters. Electrocardiogram (ECG) and mean airway pressure were continuously monitored. Lung volumes were measured using two linear differential transformers mounted on thoracic and abdominal belts. Baroreflex testing was performed by sequential intravenous bolus injections of phenylephrine (200 micrograms) and nitroglycerin (200 micrograms) to raise or lower systolic arterial pressure by 20-30 Torr. Baroreflex regulation of heart rate was expressed as the slope of the regression line between R-R interval of the ECG and systolic arterial pressure. In each mode of ventilation the ventilatory settings were chosen to control mean airway pressure and arterial PCO2 (PaCO2). In HFJV a tidal volume of 159 +/- 61 ml was administered at a frequency of 320 +/- 104 breaths/min, whereas in CPPV a tidal volume of 702 +/- 201 ml was administered at a frequency of 13 +/- 2 breaths/min. Control values of systolic arterial pressure, R-R interval, mean pulmonary volume above apneic functional residual capacity, end-expiratory pulmonary volume, right atrial pressure, mean airway pressure, PaCO2, pH, PaO2, and temperature before injection of phenylephrine or nitroglycerin were comparable in HFJV and CPPV. Baroreflex regulation of heart rate after nitroglycerin injection was significantly higher in HFJV (4.1 +/- 2.8 ms/Torr) than in CPPV (1.96 +/- 1.23 ms/Torr).(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

Mesure de la pression artérielle par voie non sanglante

in La sécurité en anesthésie (1987)

Effects respiratoires de l'anesthésie et de l'analgésie par voie spinale

in Anesthésie loco-régionale (1986)

A.L.R. et anticoagulant: choisir le risque

in Mise au point en anesthésie-réanimation (1985)