Panic Disorder (PD) is a psychological disorder of significant importance in human health but principally in women's health since the prevalence of PD in females is twice as high as in males. The reason why PD is more prevalent in women is unknown, but an association of the ovarian reproductive hormones variation during woman's menstrual cycle with the pathophysiology of PD implicated in the female organism is suggested. Panic attack (PA) stems from a probable altered chemosensitivity of encephalic chemoreceptors to CO2 which appear to be hypersensitive in patients with PD. It has already been reported that women with PD experience more respiratory symptoms during PA compared to men which suggests a greater sensitivity of the female organism to CO2. Ovarian hormones exert a positive influence on respiratory function, and progesterone has been pointed out as a potent respiratory stimulant because promotes the decline of the partial pressure of CO2 (PCO2) in the blood through hyperventilation. Thus, progesterone seems to act in regions of the brain involved in chemosensitivity. Retrospective studies pointed out a worsening of panic during the premenstrual period in patients with PD when there is an abrupt decrease in circulating progesterone concentrations. However, these findings have not been confirmed in prospective studies. Despite the lack of homogeneous data in the literature, progesterone may be involved in the pathophysiology of PD in women. In this sense the present project aims to investigate the influence of ovarian hormones in the panic index and in the ventilatory and metabolic response to hypercapnic panicogenic stimulus.
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