Schlenker E H, Farkas G A
Department of Physiology and Pharmacology, University of South Dakota, Vermillion 57069, USA.
Respir Physiol. 1995 Jan;99(1):97-103. doi: 10.1016/0034-5687(94)00085-e.
This study evaluated the modulatory role of endogenous opioids on ventilation in young and mature, lean and obese male Zucker rats. Naloxone, an opioid receptor antagonist, and saline (control) were administered subcutaneously to awake rats, and ventilation in air and in response to an hypoxic and an hypercapnic gas challenge measured. In response to naloxone young, obese but not lean rats exhibited a marked increase of ventilation in all three conditions. Older obese Zucker rats that were morbidly obese breathed at a frequency of over 200 breaths per minute and showed only a modest increase of ventilation in response to naloxone. Older lean rats increased ventilation with naloxone only when exposed to hypercapnia. Unlike the stimulatory effects hypoxia and hypercapnia had on ventilation in older, lean rats, the ventilatory responses of the obese, older rats to hypoxia and to hypercapnia were blunted. We conclude that the obese Zucker rat may be a good animal model to assess how chest wall loading and endogenous opioids interact in the development of ventilatory control abnormalities.
本研究评估了内源性阿片类物质对年轻和成熟、瘦型和肥胖雄性 Zucker 大鼠通气的调节作用。对清醒大鼠皮下注射阿片受体拮抗剂纳洛酮和生理盐水（对照），并测量在空气中以及对低氧和高碳酸血症气体刺激的通气情况。在纳洛酮作用下，年轻肥胖但非瘦型大鼠在所有三种情况下通气均显著增加。患有严重肥胖症的老年肥胖 Zucker 大鼠呼吸频率超过每分钟 200 次，对纳洛酮的反应仅表现为通气适度增加。老年瘦型大鼠仅在暴露于高碳酸血症时，纳洛酮会使其通气增加。与低氧和高碳酸血症对老年瘦型大鼠通气的刺激作用不同，肥胖老年大鼠对低氧和高碳酸血症的通气反应减弱。我们得出结论，肥胖 Zucker 大鼠可能是评估胸壁负荷和内源性阿片类物质在通气控制异常发展中如何相互作用的良好动物模型。
