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Canadian Journal of Anesthesia 47:819-822 (2000)
© Canadian Anesthesiologists' Society, 2000
Brief Report

Effect of xenon on diaphragmatic contractility in dogs

Takuo Hoshi, MD, Yoshitaka Fujii, MD, Shinji Takahashi, MD and Hidenori Toyooka, MD

From the Department of Anesthesiology, University of Tsukuba Institute of Clinical Medicine, Tsukuba City, Ibaraki, Japan.

Address correspondence to: Dr.Y. Fujii, Department of Anesthesiology, University of Tsukuba Institute of Clinical Medicine, 2-1-1, Amakubo, Tsukuba City, Ibaraki 305, Japan. Phone: 0298-53-3763; Fax: 0298-53-3765; E-mail: yfujii{at}igaku.md.tsukuba.ac.jp


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: This study was undertaken to examine the effect of xenon on diaphragmatic contractility in pentobarbitone-anesthetized, mechanically ventilated dogs.

Methods: Twenty-one dogs were randomly allocated to three groups (n=7 of each): Group I received oxygen 100% ; Group II received xenon 30% in oxygen; Group III received xenon 60% in oxygen. Diaphragmatic contractility was assessed by measuring transdiaphragmatic pressure (Pdi) generated during supramaximal stimulation of phrenic nerves at the neck at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation, after maintaining 60 min of stable condition.

Results: With inhalation of xenon at two different concentration (30% and 60%), no changes were observed in Pdi at either concentration. There was no difference in Pdi among the three groups.

Conclusion: Increasing the concentration of xenon to 60% has no effect on diaphragmatic contractility in dogs. This suggests that xenon may be used safely as an anesthetic with respect to respiratory muscle function.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
XENON is an inert gas with anesthetic properties.1 Volatile anesthetics, including halothane, enflurane, isoflurane, and sevoflurane, depress diaphragmatic contractility in vivo.2–5 The effect of xenon on the diaphragmatic contractility is unknown. This study was undertaken to examine the effect of xenon on the contractile properties of the diaphragm in dogs.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
The protocol was approved by our animal research committee, and care of the animals was in agreement with guidelines for ethical animal research. Twenty-one healthy mongrel dogs (10-15 kg) were anesthetized with pentobarbitone iv to abolish movement spontaneously. Muscle relaxants were not used. The animals' tracheas were intubated and lungs were mechanically ventilated with O2 (FIO2=1.0) to maintain PaO2>100 mmHg, PaCO2 35-45 mmHg, and pHa 7.35-7.45. The right femoral artery was cannulated to monitor arterial blood pressure and to obtain blood gas samples. The right femoral vein was cannulated to administer maintenance fluids, pentobarbitone, and bicarbonate to maintain plasma HCO3- concentration within the normal ranges.

The phrenic nerves were bilaterally exposed at the neck, and the stimulating electrodes placed around them. Transdiaphragmatic pressure (Pdi) was measured by means of two thinwalled latex balloons; one positioned in the stomach, the other in the middle third of the esophagus. The balloons were connected to a differential pressure transducer (TP-604 T, Nihon Koden, Tokyo, Japan) and an amplifier (Type 1257, Nihondenki San-ei, Tokyo, Japan). Supramaximal electrical stimuli (10-15 volts) of 0.1 msec duration were applied for two seconds at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation with an electrical stimulator (SEN-3301, Nihon Kohden). The isometric contractility of the diaphragm was evaluated by measuring the maximal Pdi after airway occlusion at FRC. Transpulmonary pressure, the difference between airway and esophageal pressures, was kept constant by maintaining the same lung volume before each phrenic stimulation. End-expiratory diaphragmatic geometry and muscle fibre length during contraction were kept constant by placing a close-fitting plaster cast around the abdomen and lower one-third of the ribcage. The electrical activity of the crural (Edi-cru) and costal (Edi-cost) parts of the diaphragm was recorded by two pairs of fishhook electrodes placed through a midline laparotomy; electrodes were positioned into the anterior portion of the crural part near the central tendon and the anterior portion of the costal part (away from the zone of apposition) in the left hemi-diaphragm. The abdomen was then sutured in the layers. The signal was rectified and integrated with a leaky integrator (Type 1322, Nihondenki San-ei) with a time constant of 0.1 sec and was regarded as the integrated diaphragmatic electrical activity (Edi-cru, Edi-cost).

The dogs were randomly divided into three groups of seven each. After the baseline measurements of heart rate (HR), mean arterial pressure (MAP), Pdi, Edi-cru, and Edi-cost, Group I received O2 100%; Group II received xenon 30% in oxygen; Group III received xenon 60% in oxygen. The inspired concentration of xenon was continuously monitored using a xenon analyzer (Anzai Medical, Tokyo, Japan) and strictly controlled by using computer controlled functionally-closed anesthesia systems.6 After 60 min of steady state condition, in each group, Pdi and hemodynamic variables were measured. The change of Edi-cru and Edi-cost (%Edi-cru and %Edi-cost, respectively) from baseline values were measured.

All values were expressed as mean ± SD. Statistical analysis was performed by using ANOVA and Student's t test, as appropriate. P < 0.05 was considered significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
With an inhalation of xenon, in Groups II and III, no changes in hemodynamic variables or Pdi at both concentrations were observed. There was no difference in Pdi among the three groups. The PaO2 decreased from baseline values when administered xenon in Groups II and III (P < 0.05). No changes in Edi-cru and Edi-cost were observed throughout the experiment in any of the groups (TableGo). Typical recordings of Pdi, Edi-cru, and Edi-cost are shown in the FigureGo.


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  		TABLE Changes in hemodynamics, blood gas tensions, and Pdi (cmH2O)
 


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  		FIGURE Typical recordings of Pdi, Edi-cru, and Edi-cost.Pdi = transdiaphragmatic pressure, Edi-cru = integrated electrical activity of the crural part of diaphragm, Edi-cost = integrated electrical activity of the costal part of diaphragm.

 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The major finding of this study was that xenon at two different concentrations (30%, 60%) did not affect diaphragmatic contractility (as assessed by Pdi) without any change in Edi. The pressure generated by the diaphragm for a given electrical stimulation depends on its length and geometry.7 A major determinant of length and geometry of the diaphragm is lung volume. The change in Pdi may be secondary to changes in end-expiratory lung volume. However, in this study, the airway was occluded at end-expiratory lung volume during the measurements, and its constancy was monitored by measuring the end-expiratory transpulmonary pressure. Therefore, changes in lung volume during the experimental procedures can reasonably be excluded. The plaster cast around the abdomen and lower third of the ribcage was also placed to prevent the deformation of thoracoabdominal structures.

Volatile anesthetics impair contractile properties of the diaphragm.2–5 Selective loss of force at low-frequency stimulation is closely related to the impairment of excitation-contraction coupling,8 whereas selective loss of force at high-frequency stimulation indicates the failure of neuromuscular transmission.9,10 Halothane reduces both Pdi and electromyographic activity of the diaphragm (as assessed by Edi) at stimulation frequencies ranging 10-Hz to 100-Hz, suggesting that impaired excitation-contraction coupling and/or impaired neuromuscular transmission exist when inhaled halothane.2 Enflurane, isoflurane, and sevoflurane decrease contractility of the diaphragm through the inhibitory effect of these anesthetics on neuromuscular transmission, based on the fact that a decrease in Pdi at high-frequency stimulation is associated a parallel reduction of Edi.3–5 Thus, these volatile anesthetics depress diaphragmatic contractility due to the failure of neuromuscular transmission.

The results of Groups II and III, with inhalation of xenon, showed that Pdi and Edi at both concentrations did not change. These results suggest that xenon, unlike volatile anesthetics, may not impair neuromuscular transmission, and thereby does not affect diaphragmatic contractility.

Xenon has a number of properties of the ideal anesthetic agent. It is an odourless gas with low blood-gas solubility coefficient and without occupational and environmental hazards.1 In addition to these pharmacological properties, based on our results, xenon has no role in diaphragmatic contractility.

In conclusion, increasing the concentration of xenon to 60% does not affect diaphragmatic contractility in dogs. This suggests that xenon may be safely available as an anesthetic regarding the diaphragmatic muscle function.

Accepted for publication April 30, 2000.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Kennedy RR, Stokes JW, Downing P. Anaesthesia and the ‘innert’ gases with special reference of xenon. Anaesth Intensive Care 1992; 20: 66–70.[Medline]

2 Clergue F, Viires N, Lemesle P, Aubier M, Viars P, Pariente R. Effect of halothane on diaphragmatic muscle function in pentobarbital-anesthetized dogs. Anesthesiology 1986; 84: 181–7.

3 Kochi T, Ide T, Isono S, Mizuguchi T, Nishono T. Different effects of halothane and enflurane on diaphragmatic contractility in vivo. Anesth Analg 1990; 70: 362–8.[Abstract/Free Full Text]

4 Veber B, Dureuil B, Viires N, Aubier M, Pariente R, Desmonts JM. Effects of isoffurane on contractile properties of diaphragm. Anesthesiology 1989; 70: 684–8.[Medline]

5 Ide T, Kochi T, Isono S, Mizuguchi T. Diaphragmatic function during sevoflurane anaesthesia in dogs. Can J Anaesth 1991; 38: 116–20.[Abstract/Free Full Text]

6 Luttropp H-H, Rydgren G, Thomasson R, Werner O. A minimal-flow system for xenon anesthesia. Anesthesiology 1991; 75: 896–902.[Medline]

7 Grassino A, Goldman MD, Mead J, Sears TA. Mechanics of the human diaphragm during voluntary contractions: statics. J Appl Physiol 1978; 44: 829–39.[Abstract/Free Full Text]

8 Edwards RHT, Hill DK, Jones DA, Merton PA. Fatigue of long duration in human skeletal muscle after exercise. J Physiol(Lond) 1977; 272: 769–78.[Abstract/Free Full Text]

9 Edwards RHT. Physiological analysis of skeletal muscle weakness and fatigue. Clin Sci Mol Med 1978; 54: 463–70.[Medline]

10 Jones DA, Bigland-Ritchie B, Edwards RHT. Excitation frequency and muscle fatigue: mechanical responses during voluntary and stimulated contraction. Exp Neurol 1979; 64: 401–13.[Medline]





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