Autoshortloop feedback regulation of pulsatile gonadotropin-releasing hormone (GnRH) secretion by its metabolite, GnRH-(1-5).

Given the central role of the decapeptide gonadotropin-releasing hormone (GnRH) in reproductive function, our long-term objective is to delineate the underlying mechanism regulating these reproductive processes. The outcome of GnRH secretion is in part dependent on the proteolytic metabolism of this decapeptide. In contrast to the belief that the metabolism of GnRH serves only as a degradative process that removes excess GnRH, we have shown that a metabolite of the decapeptide, GnRH-(1-5), can directly regulate GnRH gene expression and reproductive behavior. To further characterize the effect of GnRH-(1-5) on GnRH neuronal function, we determined whether GnRH-(1-5) can directly regulate GnRH secretion and pulsatility using an in vitro perifusion system. We compared the effect of GnRH-(1-5) on GnRH secretion in the immortalized GnRH neuron (GT1-7 cell line), whole rat hypothalamic explant, and enzymatically dispersed rat hypothalamic cells. Tissue preparations were perifused continuously for 9 h during which a 3-h challenge with GnRH-(1-5) was administered (4-6 h). The results show that treatment with GnRH-(1-5) increased (p < 0.05) the mean GnRH secretion and the amplitude of the pulses but not the pulse frequency. The present study supports the notion that GnRH-(1-5) is functionally capable of regulating the reproductive neuroendocrine system.

Impaired immune function in a premature infant with zinc deficiency after total parenteral nutrition.

The report describes a premature infant with necrotizing enterocolitis who developed symptoms of zinc (Zn) deficiency after three to four weeks of total parenteral nutrition (TPN). Clinical presentations included characteristic skin rash, alopecia, retarded growth, generalized edema and decreased serum alkaline phosphatase (ALP). Immune function studies revealed impaired neutrophil adhesion and mitogen-induced lymphoproliferation, whereas phagocytosis, chemotaxis and lymphocyte subsets remained normal. A high dose of elemental Zn (2.5 mg/kg/day), administered orally, improved the clinical symptoms and restored the immune function. In patients with Zn deficiency, impaired neutrophil adhesion and lymphocyte function may contribute to immunodeficiency which can be reversed with adequate Zn supplementation.

A priming effect of naloxone on in vitro LHRH release from the hypothalamus of mid-luteal ewes.

The possible involvement of endogenous opioid peptides (EOPs) in LHRH release from hypothalami of ewes during the breeding season was investigated using an in vitro perifusion system. Hypothalami were procured in December from ovariectomized (OVX; 62-65 days before the experiment; n = 6) and mid-luteal (ML; n = 7) Western White-Face ewes. Hypothalami were mid-sagitally sectioned into halves containing the preoptic area, mediobasal hypothalamus, and infundibulum (median eminence). The left half (treated) received two 30-min challenges (beginning at 130 and 250 min, respectively, after onset of perifusion) of 500 microM naloxone (NAL) followed by a 30-min 60-mM potassium (K) challenge (at 370 min after onset of perifusion). The right half served as the control, receiving only K at the same time as the treated tissue. Both NAL challenges elicited (p less than 0.05) LHRH release from tissues of both ML and OVX ewes. Release of LHRH by hypothalami from ML, but not from OVX, ewes was greater (p less than 0.01) after the second than after the first NAL challenge. These results are consistent with the view that an inhibitory opioid influence exists on LHRH release from ovine hypothalami. The release of LHRH in response to NAL was dependent on the ovarian status in vivo since the priming effect of NAL on subsequent NAL-induced LHRH release occurred only from the hypothalami of ML ewes. We suggest from these results that EOPs may modulate LHRH release from ovine hypothalami in an ovarian steroid-dependent and independent manner.

A new approach to suppress bucking before extubation--lidocaine through modified endotracheal tube.

The conventional endotracheal tube was modified with an epidural catheter adhered on the concave aspect of it. The opening of the catheter is at the proximal margin of the cuff. Local anesthetic can be injected into the trachea, then desensitize the tracheal mucosa nearby the cuff. Thirty-four female gynecological patients underwent abdominal total hysterectomy were studied and divided into three groups. In group 1, anesthesia was maintained without special management. In groups 2 and 3, 2 mL gentian violet stained 4% lidocaine solution was administered intratracheally by two different methods 60-120 minutes before the conclusion of the surgery. The peak cuff pressures generated by the awakening patients were 53.8 +/- 2.2 cm H2O (mean +/- SE) in group 1, 47.3 +/- 2.5 cmH2O (Group 2) and 36.4 +/- 1.6 cmH2O Group 3) respectively. Bucking before awakening was also evaluated clinically and showed 100%, 73% and 0% in each group. Intratracheal administration of lidocaine in dose of 2 mL 4% showed significant effect for the suppression of bucking during the recovery of general anesthesia in group 2 and 3 compared with the group 1. Lidocaine administered through the catheter of modified endotracheal tube also resulted in less increase in the peak cuff pressure and even no clinically observed bucking than direct administered through the endotracheal tube. Gag reflex was preserved in all patients and none had suffered from aspiration postoperatively.