RETRACTED ARTICLE: Effect of xenon on diaphragmatic contractility in dogs

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.     

Dobutamine increases diaphragmatic contractility in dogs

The effects of dobutamine on diaphragmatic contractility were studied in 24 dogs anaesthetized with secobarbital and receiving mechanical lung ventilation. The phrenic nerves were stimulated supramaximally for two seconds with electrodes placed around the fifth and sixth cervical roots when the airway was closed at the level of FRC. The stimulating frequency ranged from 10 to 100 Hz. Transdiaphragmatic pressure gradient (Pdi) generated by the electrophrenic stimulation was used as an index of diaphragmatic contractility. The electrical activity of the diaphragm during the stimulation (Edi) was also measured with needle electrodes inserted in the right hemidiaphragm percutaneously. During an infusion of dobutamine (10 micrograms.kg-1.min-1 for 20 min), Pdi increased by 15 +/- 2.1% of control value at 20 Hz stimulation (P less than 0.01), and by 13 +/- 1.2% at 100 Hz stimulation (P less than 0.01). The Edi was not altered by dobutamine infusion. This enhancement of Pdi by dobutamine was abolished by simultaneous infusion of nicardipine, a Ca-channel blocker, but was not affected by prostaglandin E1. These results suggest that dobutamine has a stimulating effect on canine diaphragmatic contraction, and this action may be related to the increased inward movement of extracellular calcium.     

Propofol decreases diaphragmatic contractility in dogs

Volatile anesthetics depress diaphragmatic muscle function; however, no data are available regarding the effect of propofol on diaphragmatic contractility. We therefore studied this effect in dogs. Pentobarbital-anesthetized animals were divided into three groups of 10 each. Group I received only maintenance fluid; Group II was infused with a subhypnotic dose of propofol (0.1-mg/kg initial dose plus 1.5-mg x kg(-1) x h(-1) maintenance dose); Group III was infused with an anesthetic dose of propofol (0.1-mg/kg initial dose plus 6.0-mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of propofol in Groups II and III, Pdi at low-frequency (20-Hz) stimulation decreased from the baseline values (P < 0.05), whereas Pdi at high-frequency (100-Hz) stimulation did not change. Compared with Group I, Pdi at 20-Hz stimulation decreased during propofol administration in Groups II and III (P < 0.05). The decrease in Pdi was more in Group III than in Group II (P < 0.05). We conclude that propofol is associated with a dose-related inhibitory effect on diaphragmatic contractility in dogs. IMPLICATIONS: Propofol is an effective IV anesthetic for the induction and maintenance of anesthesia. Subhypnotic and anesthetic doses of propofol decrease diaphragmatic contractility in dogs.     

High-dose colforsin daropate increases diaphragmatic contractility in dogs

PURPOSE: To evaluate the effects of colforsin daropate, a water-soluble derivate known to improve contractility in fatigued canine diaphragm, at two different doses (low-dose and high-dose) on contractility of the non-fatigued diaphragm of dogs. METHODS: Twenty-four pentobarbitone-anesthetized dogs were divided into three groups of eight each: Group I received no study drug; Group II received low-dose (0.2 microg x kg-1 x min-1) colforsin daropate; Group III received high-dose (0.5 microg x kg-1 x min-1) colforsin daropate. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). RESULTS: In Group III, with an infusion of high-dose colforsin daropate, Pdi at low-frequency (20 Hz) and high-frequency (100 Hz) stimulation increased from baseline values (P < 0.05). Compared with Group I, Pdi at both stimuli increased during colforsin daropate administration in Group III (P < 0.05). In Group II, with an infusion of low- dose colforsin daropate, Pdi to each stimulus did not change. CONCLUSION: Colforsin daropate, only when administered at high-dose, increases contractility of non-fatigued diaphragm in dogs.     

Comparative effects of xenon and nitrous oxide on diaphragmatic contractility in dogs

BACKGROUND: Xenon at two different concentrations (30%, 60%) has no effect on diaphragmatic contractility. This study was undertaken to compare the effects of xenon and nitrous oxide (N2O), a commonly used and well-established gas anesthetic, on diaphragmatic contractility in dogs. METHODS: Twenty-one pentobarbitone-anesthetized dogs were randomly divided into three groups of seven each: group 1 received xenon 30% (0.25 MAC) in oxygen; group 2 received N2O 47% (0.25 MAC) in oxygen; and group 3 received N2O 60% (0.32 MAC) in oxygen. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at low- (20-Hz) and high-frequency (100-Hz) stimulation, after maintaining 60 min of stable condition. The integrated electrical activity of diaphragm (Edi) to each stimulus was measured. RESULTS: With an inhalation of xenon 30%, N2O 47%, or N2O 60%, Pdi and Edi at both stimuli did not change. No difference in Pdi or Edi was observed among the groups. CONCLUSION: When used at clinical concentration, xenon or N2O does not affect contractility and electrical activity of the diaphragm in dogs.     

The recovery profile of reduced diaphragmatic contractility induced by propofol in dogs

Propofol decreases contractility of the diaphragm, but no data are available for its effects on recovery. We studied the recovery profile of reduced diaphragmatic contractility induced by propofol in dogs. Animals were divided into 4 groups of 7 each. Group I, without fatigue, received only maintenance fluid; Group II, without fatigue, was infused with propofol; Group III, with fatigue, received no study drug; Group IV, with fatigue, was infused propofol. Propofol at an anesthetic dose (0.1 mg/kg initial dose plus 6.0 mg x kg(-1) x h(-1)) was administered for 60 min. In Groups III and IV, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at 20-Hz for 30 min. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). In group II, Pdi at low-frequency (20-Hz) stimulation decreased to less than baseline (P < 0.05), whereas there was no change in Pdi at high-frequency (100-Hz) stimulation. At 10 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to baseline. When fatigue was established, in Groups III and IV, Pdi at 20-Hz stimulation decreased to less than baseline (P < 0.05), whereas Pdi at 100-Hz stimulation did not change. After administering propofol in Group IV, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05). At 20 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to fatigued values. We conclude that reduced contractility in nonfatigued and fatigued canine diaphragm induced by propofol recovers within 20 min after the cessation of administration.     

The effect of sedative drugs on diaphragmatic contractility in dogs: propofol versus midazolam

Implications: a sedative dose (0.1 mg x kg(-1) x h(-1)) of midazolam, compared with a subhypnotic dose (1.5 mg x kg(-1) x h(-1)) of propofol, decreases the contractility of the diaphragm in dogs.     

RETRACTED ARTICLE: Dobutamine increases contractility of fatigued diaphragm in dogs: The relationship between dose and diaphragmatic contractility

The dose-related effects of dobutamine (DOB) on the contractility of fatigued diaphragm were studied in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups of eight: the control (group C) and the DOB (group D). Diaphragmatic fatigue was induced by intermittent supramaximal electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (P_di). After the induction of diaphragmatic fatigue, P_di at low-frequency (20-Hz) stimulation decreased significantly compared with the prefatigue values (P<0.05), whereas no change in P_di was observed at high-frequency (100-Hz) stimulation. In group D, after producing fatigue, P_di at 20-Hz stimulation increased significantly with a continuous infusion of DOB (5 and 10 μg·kg⁻¹·min⁻¹) i.v. (P<0.05). The P_di at 100-Hz stimulation increased significantly with administration of DOB 10 μg·kg⁻¹·min⁻¹ i.v. (P<0.05). There was a significant correlation between dose of DOB and P_di at both stimuli (P<0.05). In group C, the speed of P_di recovery at 20-Hz stimulation was relatively slower. The integrated diaphragmatic electric activity (E_di) in each group did not change at any frequency of stimulation throughout the study. It is concluded that DOB increases the contractility of fatigued diaphragm in a dose-dependent manner.     

Effect of halothane on diaphragmatic muscle function in pentobarbital-anesthetized dogs

The mechanism underlying the decrease in minute ventilation (VE) observed under halothane anesthesia was investigated in nine spontaneously breathing dogs. Anesthesia was induced with pentobarbital sodium and was maintained with halothane. Inspired fraction of halothane (FIhal) was increased every 30 min, from 0.005 to 0.02. VE decreased from 8.1 +/- 0.9 to 4.8 +/- 0.4 l . min-1 (P less than 0.001), as FIhal increased from 0 to 0.02. This resulted from a decrease in both mean inspiratory flow (VT/TI) and the duty ratio (TI/TTOT). Transdiaphragmatic pressure (Pdi) and the integrated electrical activity of both hemidiaphragms (Edi) were measured during normal breathing, and during breathing against closed airways (P0di, E0di), in order to obtain an index of the inspiratory neuromuscular output of the diaphragm. With increasing FIhal, there was a significant decrease in Pdi, P0di, Edi, and E0di. The authors measured Pdi and Edi generated during supramaximal stimulation of the two phrenic nerves (PSdi, Esdi) at frequencies of 10, 20, 50, and 100 Hz, in order to eliminate in this decrease the role played by a decrease in the neural drive to breathing. PSdi and ESdi decreased significantly with increasing FIhal, and had not returned to the control values 30 min after discontinuation of halothane administration. The authors conclude that, in pentobarbital-anesthetized dogs, halothane is responsible for a diaphragmatic dysfunction, which may be located either at the neuromuscular junction, on the contractile processes of the muscle, or on both, and for a decrease in the activation time of the inspiratory muscles. Both of these effects contribute to the decrease in VE observed under halothane anesthesia.     

Effects of sevoflurane on ischaemic myocardium in dogs

We studied the effect of sevoflurane on ischaemic myocardium in terms of myocardial energy and carbohydrate metabolism. Mongrel dogs were anaesthetized initially with sodium pentobarbitone, and then inhaled sevoflurane at 0% (0 MAC), 2.4% (1.0 MAC) or 4.7% (2.0 MAC) of inspired concentration for 60 min. Ischaemia was then induced for 3 min by ligating the left anterior descending coronary artery. The tissue levels of energy and carbohydrate metabolites were determined before and after sevoflurane inhalation, and after 3 min of ischaemia. Sevoflurane significantly decreased systolic and diastolic blood pressures, heart rate, and rate-pressure product in a dose dependent manner. When the animals did not inhale sevoflurane (0 MAC), ischaemia significantly decreased adenosine triphosphate and creatine phosphate levels, and produced alterations of carbohydrate metabolism. These metabolic changes induced by ischaemia were lessened by inhalation of sevoflurane. To exclude the influence of haemodynamic changes, blood pressure and heart rate were maintained during 1.0 MAC sevoflurane inhalation. Significant attenuation of ischaemia-induced metabolic changes caused by sevoflurane was still observed in some metabolites. These results indicate that the ischaemic influences on the myocardium may be reduced by sevoflurane, and this protective effect can be explained not only by its haemodynamic effect.     

七氟醚对犬颅内压影响的实验研究

１２只成年杂种犬，观察了０．５、１．５ＭＡＣ七氟醚对颅内压的影响。七氟醚吸入顺序Ａ组：０．５→１．５ ＭＡＣ，Ｂ组：１．５→０．５ ＭＡＣ。结果表明：Ａ组吸入０．５ＭＡＣ七氟醚（呼末浓度）５、１５、３０分钟颅内压分别上升２８％、１６％、１５％（Ｐ＜０．０１），吸入１．５ＭＡＣ时分别上升３７％（Ｐ＜０．０１）、１１％、１１％；Ｂ组吸入１．５ＭＡＣ时颅内压分别上升４９％、３１％、２３％（Ｐ＜０．０１），吸入０．５ ＭＡＣ时其接近基础值；与正常ＰａＣＯ２相比，吸入 ０．５ＭＡＣ七氟醚，过度通气后颅内压下降 １３％（Ｐ＝０．０５４），吸入１．５ＭＡＣ时颅内压无显著性变化。结果提示：七氟醚对颅内压影响轻微；低吸入浓度保留了脑血管对ＣＯ２的反应性．高吸入浓度可能抑制脑血管对ＣＯ２反应性。     

Different effects of halothane and enflurane on diaphragmatic contractility in vivo

We examined the effects of halothane and enflurane on diaphragmatic contractility in 12 anesthetized, mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. Animals were randomly assigned to two groups, a halothane group (n = 6) and an enflurane group (n = 6). The Pdi stimulus-frequency relationship was compared at anesthetic levels of 1, 1.5, and 2 MAC (minimum alveolar concentration) in each group. The sequence of changing anesthetic concentration was randomized. In addition, the Pdi-frequency relationship was also compared between 1 MAC of halothane and enflurane in 8 of 12 dogs. In animals anesthetized with enflurane, Pdi significantly decreased with 50- and 100-Hz stimulation in the presence of increasing MAC values, whereas Pdi at 10-Hz stimulation was not affected by the depth of anesthesia. Pdi with 20-Hz stimulation during 2 MAC enflurane also decreased significantly below Pdi levels seen at 1 and 1.5 MAC. By contrast, with halothane there was no difference in Pdi at any of the stimulation frequencies during any of the three levels of anesthesia. There was no statistical difference, however, between Pdi-frequency relationships during 1 MAC of halothane and enflurane in eight animals. From these results, we conclude that halothane does not impair diaphragmatic contractility any more than enflurane does, but enflurane decreases force generation of the diaphragm at high stimulation frequencies in a dose-related fashion. This depressant effect of enflurane occurs mainly through the impairment of neuromuscular transmission and/or membrane excitability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dose-response characteristics of midazolam for reducing diaphragmatic contractility

A sedative dose of midazolam decreases contractility of the diaphragm, but no data are available concerning the relationship between dose and diaphragmatic contractility. We studied the dose-response characteristics of midazolam for reducing the diaphragmatic contractility in dogs. Animals were divided into three groups of eight each: Group 1 received no study drug, Group 2 was infused with a sedative dose of midazolam (0.1 mg/kg initial dose plus 0.1 mg x kg(-1) x h(-1) maintenance dose), and Group 3 was infused with an anesthetic dose of midazolam (0.1 mg/kg initial dose plus 0.5 mg x kg(-1) x h(-1) maintenance dose). We assessed the diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of midazolam in Groups 2 and 3, Pdi at low-frequency (20 Hz) and high-frequency (100 Hz) stimulation decreased from the baseline values (P < 0.05), and the integrated electrical activity of diaphragm (Edi) at 100-Hz stimulation decreased from the baseline values, whereas Edi at 20-Hz stimulation did not change. Compared with Group 1, Pdi and Edi for each stimulus decreased during midazolam infusion in Groups 2 and 3 (P < 0.05). The decrease in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that midazolam decreases, in a dose-dependent manner, contractility of the diaphragm in dogs.