Abstract
Surgical procedures lead to profound and sustained (up to 1–2 weeks) activation of the pituitary gland, resulting in changes in endocrine function. Questions remain on whether activation of the pituitary influences the threshold and development time-course of postoperative pain. To address these questions, we evaluated postoperative hypersensitivity in female and male rats with ablated pituitary and gonadal hormone productions via hypophysectomy, ovariectomy and gonadectomy, respectively. Plantar incision, a model of acute postoperative pain, or sham operation was performed on rat hind paws. Hypophysectomy, ovariectomy and gonadectomy were achieved by surgical disconnection of pituitary, ovaries and testicles, respectively. Postoperative thermal and mechanical hypersensitivity were monitored for 7 days post incision. Hypophysectomy on female and male rats produced statistically similar thermal and mechanical postoperative hypersensitivity thresholds and time-courses as compared to intact estrous female and male rats. Moreover, ovariectomy and gonadectomy did not significantly change postoperative hypersensitivity observed in control female and male animals. Our experiments demonstrate that hypophysectomy, ovariectomy and gonadectomy do not significantly impact postoperative hypersensitivity observed in normal female and male animals. These data suggest that surgery-induced changes in the endocrine system via activation of pituitary and subsequently gonadal tissues have little impact on the threshold and development of postoperative pain in female and male rats.
Highlights
It is well documented that surgical intervention profoundly modulates the endocrine system leading to complex metabolic events [1,2,3]
As expected [30, 31], HYPO, which leads to substantial decrease of luteinizing hormones (LH) and to a lesser extent follicle stimulating hormone (FSH) [32, 33], reduced serum estradiol levels (Table 1)
We evaluated whether postoperative mechanical hypersensitivity was altered in male and female rats that have undergone hypophysectomy
Summary
It is well documented that surgical intervention profoundly modulates the endocrine system leading to complex metabolic events [1,2,3]. Tissue injury and psychological stress associated with surgeries and/or anesthetics used during surgical procedures could be major contributors in modulating the endocrine system [4]. There is evidence that the response of the endocrine system to surgical intervention is mediated through the hypothalamic-pituitary-adrenal (HPA) axis [5]. Major and some minor surgeries usually result in systemic sustained increase of adrenocorticotropin (ACTH), growth hormone (GH) and prolactin (PRL), whereas plasma estradiol and testosterone levels are decreased for up to 1-2 weeks after surgery [1,6,7,8]. Plasma levels of some hormones correlate with severity of postoperative pain [13,14]. Successful management of postoperative pain restores the normal serum levels of these hormones [10,13]. Systemic elevation of hormones after surgery could stimulate the immune system [9,15,16], which plays a critical role in regulating pain development and threshold [17]
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