| PART Ⅰ A method for recording diaphragm EMG in rabbitsObjective: To establish a method for recording the diaphragm EMG in rabbits.Background: The diaphragm is the crucial muscle for respiration，which is mainlyregulated by respiratory center.The diaphragm EMG is a principal method ofassessing neural respiratory drive. Recent studies suggest that many respiratorydiseases are associated with abnormal neural respiratory drive. Accuraterecording of the diaphragmatic EMG could be useful to investigate neuralrespiratory drive in some diseases.Methods: The experiments were performed on7rabbits, which were anaesthetizedintravenously with nembutal (30mg/kg).A custom-made thin wire electrode(Enameled copper wire0.12mm in diameter,3mm in uninsulation length,2.5–3mminter-electrode distance) was threaded through a hypodermic needle（22-gauge,1.5in）.The thin wire electrodes were inserted into the crucial of the diaphragmthrough costovertebral angle in anesthetized7rabbits. Diaphragm EMG wererecorded immediately and one week after placement of electrode.Results: Satisfactory diaphragm EMG was recorded in5rabbits immediately andin4rabbits over a week.Conclusion: Satisfactory diaphragm EMG could be reliably obtained from crucialof the diaphragm with thin wire electrode inserted through costovertebral angle. PART Ⅱ Effect of diaphragm fatigue induced by electricalstimulation of the phrenic nerves on neural respiratory drive inrabbitsObjective: The purpose of this study was to establish an animal models ofdiaphragmatic fatigue induced by electrical stimulation of the phrenic nerves inrabbits, and assessed the effect of neural drive and neuromuscular transmissionduring the development of diaphragmatic fatigue, to determine whether change inneural drive and/or neuromuscular transmission to the diaphragm were importantfactors for diaphragmatic fatigue observed during electrical stimulation of thephrenic nerves.Background： It has been hypothesized that respiratory muscle fatigue plays animportant role in development of respiratory failure. The diaphragm is the mostimportant muscle of inspiration. Diaphragmatic fatigue leads to respiratoryfailure especially in severe chronic obstructive pulmonary disease or/andneuromuscular diseases. Therefore, investigation of the diaphragmatic fatigue isof interest not only for its theoretical aspects, but also for its applied aspects.Muscle fatigue is divided into central and peripheral types, representingdifferent site and mechanism of fatigue development. Central fatigue refers tothe condition in which muscle failure to generate force owing to reduced centralmotor output，and peripheral fatigue owing to failure of transmission at theneuromuscular junction or distal to this structure. The technique of twitchocclusion is the only test used to detect respiratory muscle fatigue that candistinguish central from peripheral fatigue. Fatigue is a complex physiologically phenomenon which mechanisms are influenced by the characteristics of the taskbeing performed.Up to now, the role of change in neural respiratory drive and/orneuromuscular transmission during diaphragmatic fatigue remains controversial.The neuromuscular system will to adapt to effort to sustain force generationduring muscle fatigue， whivh may increases neural drive to increase musclecontractile or to prevent their self-destruction by excessive activation throughdecrease in neural drive. Peripheral muscle fatigue can be restored throughstopping working, but respiratory muscle stopping working will belife-threatening. The study on neural respiratory drive after respiratory musclefatigue will help to understand the pathophysiology of related diseases ofrespiratory muscle strength decreased. Diaphragmatic fatigue has beendemonstrated in experiments in animals and humans. However, it is difficult togenerate severe diaphragmatic fatigue with respiratory loaded breathing in human.In the present study, we examined the effect of neural drive and neuromusculartransmission during the development of diaphragmatic fatigue induced byelectrical stimulation of the phrenic nerves in rabbits, also to determine thechange of neural drive and/or neuromuscular transmission after diaphragmaticfatigue induced by electrical stimulation of the phrenic nerves in rabbits.Methods: The experiments were performed on16rabbits, which were anaesthetizedintravenously with Nembutal (30mg/kg) and intubated with an endotracheal tube.Diaphragm EMG (EMGdi) were recorded from the crus of the diaphragm by a thin wireelectrode when rabbits in the supine position. Esophageal pressure (Pes), gastric pressure (Pga) and transdiaphragmatic pressure (Pdi) were recorded from a catheterwith two rubber balloons. Expiratory flow was recorded from pneumotachographconnected to intubation. Diaphragmatic fatigue was produced by sustainedsupramaximal electrophrenic stimulation of bilateral phrenic nerve.Diaphragmatic contractility were assessed with Twitch Pdi(TwPdi) generated byphrenic nerve stimulation. Diaphragm compound muscle action potentials (CMAP),EMGdi, expiratory flow, maximum Pdi (Pdimax), maximum Pga (Pgamax), maximum Pes(Pesmax), TwPdi, twitch Pga (TwPga), twitch Pes (TwPes) were measured at baseline,0min,10min,30min,60min and120min after diaphragmatic fatigue.Results:1) TwPdi was reduce by more than20%in all rabbits after electriclystimulation of phrenic nerve,which reduced from98.70%±3.68%at baseline to53.48%±10.04%at0min after diaphragmatic fatigue (p <0.05), after120minrecovered to77.23%±15.45%(Compared with baseline and0min p <0.05); Pdimax、tidal breathing Pdi were reduced from57.33%±19.66%vs19.16%±8.61%at baselineto33.39%±12.13%vs11.7%±7.19%at0min（P＞0.05），and recoveryed after120minto43.63%±15.63%（P＞0.05）vs11.79%±4.94%（P＞0.05）, respectively.（2）RMSdi、 RMSdi-max、 CMAP were reduced from43.37%±24.25%、94.4%±12.15%、97.29%±7.67%at baseline to43.37%±24.25%、94.4%±12.15%、97.29%±7.67%by postfatigue, and by120min were27.82%±14.11%、50.71%±29.44%、73.75%±21.75%ofinitial value(P＞0.05). The correlation of TwPdi and CMAP was significant, andthe related coefficient of seven rabbits in eight have statisticalsignificance,the minimum of which was0.722.(3) Respiratory rate(times/min)、 tidal volume（ml）、minute ventilation（ml）and expiratory flow（L/min）had noobvious changes(42.41±11.51vs41.14±15.27、18.84±3.36vs19.43±5.13、771.93±154.13vs741.94±219.13、4.18±0.6vs4.01±0.72，P＞0.05).Conclusion:⑴Diaphragmatic fatigue can be induced by supramaximal electricalstimulation of the phrenic nerves (peripheral fatigue).⑵In anesthetizedunbounded rabbits, TwPdi generated by phrenic nerve twitches have been proposedas a gold standard to assess diaphragmatic Contraction function,Pdimax can notreflect diaphragmatic Contraction function.⑶Neural respiratory drive andneuromuscular transmission have been significantly decreased, and the decreasingof neural respiratory drive might be protective for function of diaphragm.⑷Thecorrelation between CMAP and TwPdi after diaphragmatic fatigue indicated thattransmission fatigue probably plays a major role in rabbit diaphragmaticfatigue.⑸Diaphragmatic fatigue dose not significantly affect respiratorypattern in rabbits. |
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