What causes hypercapnia? Won't breathe, can't breathe or something in between?

摘要

Obesity and the mechanical impediments it imposes on the respiratory muscles explains why some patients with obstructive sleep apnea (OSA) develop hypercapnia, but only a fraction of obese patients with OSA develop persistent elevation of arterial PCO_2. Why is that? Only a few years ago a promising answer to this question was leptin deficiency. In a rodent model of obesity, the ob/ob mouse, functional leptin is not produced and ventilation is depressed particularly during sleep. Leptin administration improves CO_2 chemosensitivity, raises ventilation across all sleep stages and reduces the elevated arterial PCO_2 . There is more evidence. Leptin exerts its effects by acting on melanocortin-4 receptors in the hypothala-mus. Chemosensitivity is depressed in agouti yellow mice with blocked melanocortin pathways . All this suggests that leptin deficiency may be responsible for hypercapnia in OSA particularly when it occurs with obesity and led to examinations of leptin levels in patients with OSA [e.g. 3,4].