F-4-05-04
RESPIRATORY MUSCLE TRAINING IN CHRONIC TETRAPLEGIA-THE EFFECT AND INFLUENCE IN SLEEP BREATHING DISORDER
Tyng-Guey Wang (National Taiwan University, Taipei, Taiwan), Yen-Ho Wang (National Taiwan University, Taipei, Taiwan), Fuk-Tan Tang (Chang Gung Medical College, TaoYuan, Taiwan), Jin-Shin Lai (National Taiwan University, Taipei, Taiwan), I-Nan Lien (National Taiwan University, Taipei, Taiwan)
Objective: To define the effect of respiratory muscle training in sleep breathing disorder of chronic spinal cord injury (SCI) patients.
Method: Fifteen cervical cord injury patients (13 men, 2 women),injured at lease six months, were included in our study. The pulmonary functions, including forced vital capacity (FVC), maximum voluntary volume (MVV), maximum inspiratory pressure (Pimax) and maximum expiratory pressure (Pemax), were performed by compact II spirometry (Vitalograph LTd, England) and the data was corrected by Chinese norm. Using novometric capnography (Novomtrix Medical Systems Inc., USA) to monitor patients' respiratory status during sleep. The machine could record 24 hours' end-tidal carbon dioxide (EtCO2) and oxygen saturation (O2 sat) and analyzed the percentile of abnormal EtCO2 and 02 sat. The respiratory muscle training program consisted of' (1) mode: DHD inspiratory muscle trainer (model DHD 22-7500, DHD Diemolding Healthcare division., USA) (2) intensity: 60 % of Pimax (3) frequency: 5 days a week (4) duration: 15 minutes twice each day (4) training period: 6 weeks.
Result: The training program improved Pimax and MVV of our patients significantly (Pimax from -68.7±27.4cmHg to -77.3±24.0cmHg, p<0.05; MVV from 62.7±33.2 L/min to 73.2±31.3 L/min, p<0.05) but not their Pemax and FVC as previous report. For those patients with increased Pimax, their duration of EtCO2 above 48 mm Hg of sleep time decreased from 2.2±3.3% to 1.0±2.0% (p<0.05) and period of O2 sat below 90 % during sleep reduced from 1.8±2.8 % to 1.3±2.4% (p<0.05).
Conclusion: The inspiratory muscle training is effective in increasing Pimax and MVV of patients with cervical cord injury, it further improves their breathing condition of sleep, and reduces pulmonary complications.
F-4-05-05
DISABILITY PREVENTION OF CHRONIC HEART FAILURE: INTRODUCTION OF AN ANIMAL HEART FAILURE MODEL TO THE STUDY OF REHABILITATION MEDICINE
Masahiro Kohzuki, Kazunori Yoshida, Masahiro Kamimoto, Xue-Min Wu, Mika Hashimoto, Tokutaro Sato. (Section of Internal Medicine & Disability Prevention, Tohoku University Graduate School of Medicine, Sendai, Japan)
The treatment of congestive heart failure includes the administration of diuretics, which reduces preload and relieves the symptoms and signs of venous congestion. Despite the widespread use of diuretics for the treatment of left ventricular dysfunction following myocardial infarction, information concerning the evolution of heart failure is still scarce and data on survival are largely unknown. By contrast, angiotensin converting enzyme (ACE) inhibitors have been shown to prevent progressive cardiac enlargement or reverse its course and to increase survival in animals and man. Coronary artery ligation in the rat (rat CHF) is a reliable model of ventricular dysfunction which closely mimics left ventricular failure due to myocardial infarction (MI) in man. Rats with infarction develops cardiomegaly, and impaired hemodynamics in proportion to infarct size. We examined the effects of diuretics on cardiac hypertrophy and lung congestion, plasma atrial natriuretic peptide (ANP) in rat CHF. We also assessed the changes in cardiac angiotensin converting enzyme (ACE) and endothelin-1 (ET-l) receptor and the responses to ANP infusion in this model. Rats with infarction had significant cardiac hypertrophy. In rats with infarction, enalapril significantly attenuated cardiac hypertrophy (P<0.01), left ventricular hypertrophy (P<0.01) and lung congestion (P<0.05). We found that attenuated response to ANP in rat CHF and successful treatment of heart failure by an ACE inhibitor enalapril tend to normalize ANP level. In contrast, chlorothiazide had no effect on cardiac or left ventricular hypertrophy. At I month after MI, ACE increased markedly in the infarct area and moderately in hypertrophied myocardium without changing the affinity compared to the sham-operated rats. On the contrary, cardiac ET-1 receptor in M1 rats did not change. The present study confirms the beneficial effects of enalapril in this model. The present study indicates that cardiac ACE but not ET-1 may participate in the pathophysiology of cardiac hypertrophy in chronic heart failure. These results indicate that characteristics and responses of this model are very similar to those of human CHF. Studies using this model may offer insight into the rehabilitation medicine, such as effects of exercise on cardiac autonomic tone.
