Source: Annual Congress 2011 - Physiology of human pulmonary hypertension
Disease area: Pulmonary vascular diseases

Abstract

Background: Right ventricular heart failure in COPD is thought to be a result of pulmonary hypertension due to increased pulmonary vascular resistance. Exercise, and especially interval training has been shown to be effective in improving left ventricular function, but the same is not shown for right ventricular function in COPD. The goal of this study was to examine the effects of aerobic interval training on cigarette smoke-induced right ventricular heart dysfunction in a mouse model for COPD.
Methods: 42 female A/J-OlaHsd mice were exposed to either cigarette smoke (CS) or fresh air (FA), for 14 weeks, 6 hours/day, 5 days/week. For the next four weeks they were either kept sedate (Se) or put through interval treadmill running (IT) for 1 hour/day, 5 days/week. After this period the mice were sedated with light isoflurane anaesthesia and the heart function was evaluated with echocardiography. Tricuspid annular plane systolic excursion (TAPSE) was used as a measurement of right ventricular function.
Results:

	Mean VO2max (mL/kg^0,75/min)	Mean TAPSE (mm)
FA-Se	32,1	0,71
FA-IT	40,5	0,82
CS-Se	32,9	0,46
CS-IT	41,6	0,75

Maximal oxygen uptake was higher for the IT groups compared to the Se groups (p<0,05). TAPSE was reduced for the CS-Se group compared to all other groups (p<0,001). There were no significant difference between the CS-IT group and the FA-Se group (p=0,35). The FA-IT group had significantly increased TAPSE compared to the FA-Se group (p<0,05), but not the CS-IT group (p=0,2).
Conclusion: Smoke exposure of A/J-OlaHsd mice causes a significant reduction in right ventricular function measured by echocardiographic TAPSE. This reduction seems to be normalized by intensive interval training.

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Citations should be made in the following way:
E. Hassel, A. M. Ormbostad, U. Wisløff, S. Steinshamn (Trondheim, Norway). Effects of interval exercise on cigarette smoke-induced right ventricular dysfunction in mice. Eur Respir J 2011; 38: Suppl. 55, 2316

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