Laser-assisted tubal anastomosis.

OBJECTIVE: To determine if laser-assisted anastomosis is superior to microsurgical anastomosis and laser welding for tubal reconstruction. STUDY DESIGN: Sixty uterine tubes from 30 rabbits were transected and then anastomosed with a microsurgical technique, laser welding and laser-assisted anastomosis using a microscope. The rabbits were mated one month postoperatively and examined for implantation sites and adhesion formation three to seven days postpartum. RESULTS: The amount of time required to perform laser-assisted anastomosis as well as laser welding was significantly shorter than for microsurgery. All the tubes withstood the distension pressure of pregnancy with the exception of 1 of the 20 laser-welded tubes, which had 30% of its circumference dehisced. There was no difference in the number of implantation sites per tube between the different groups. The anastomotic sites were well healed and were nonidentifiable except for holding stitches and microsurgical sutures. CONCLUSION: Laser-assisted anastomosis and laser welding took less time to perform than microsurgery. Laser-assisted anastomosis resulted in excellent healing, as did microsurgery. With the protection of serum albumin, laser-assisted anastomosis did not cause any thermal damage, and the anastomotic sites could tolerate the distension pressure of pregnancy and parturition without problems. Laser welding without protection of serum albumin could cause thermal damage and dehiscence. The implantation and pregnancy rates were comparable The implantation and pregnancy rates were comparable with all three types of procedure.

Comparison of laser-assisted anastomosis, laser welding, and microsurgical anastomosis of rabbit uterine tubes.

OBJECTIVE: To assess laser-assisted anastomosis in fallopian tube reconstruction. METHODS: Fifty-two rabbit uterine tubes were transected and subjected to laser welding or to microsurgical or laser-assisted anastomosis in a randomized paired design, and compared with the contralateral side. The time required for the procedure, patency of the uterine tubes, amount of adhesion formation, and quality of scar tissue (grossly and histologically) were evaluated 4 weeks after surgery. RESULTS: Traditional microsurgical procedures required significantly longer operative time than laser-assisted anastomosis (64.4 +/- 2.2 versus 41.3 +/- 2.2 minutes) or laser welding (47.8 +/- 3.0 versus 24.5 +/- 3.0 minutes). Patency was established in all 52 uterine tubes. Adhesion formation was animal-dependent rather than procedure-dependent. All scars healed well and most were not visible beyond residue suture. Inflammatory cells were noted around the suture sites; however, gross observation revealed that all mucosal surfaces over the scars were smooth. One of 18 laser-welded uterine tubes developed dehiscence, whereas there was no dehiscence in laser-assisted or microsurgically anastomosed uterine tubes. CONCLUSION: Laser-assisted anastomosis is superior to laser welding or microsurgical anastomosis in rabbit uterine tubes. Laser-assisted anastomosis has potential use in fallopian tube reconstruction.

Inhibition of steroid 5 alpha-reductase in vivo: effect on suppression of luteinizing hormone and stimulation of accessory sex organs by testosterone in the orchidectomized rat.

An inhibitor of 5 alpha-reductase, the 17 beta-carboxylic acid derivative of testosterone (testosterone-17 beta CA), has been used to evaluate the importance of the 5 alpha-reduction of testosterone in its action on the suppression of LH secretion in male rats. The potential of testosterone-17 beta CA to inhibit the formation of 5 alpha-dihydrotestosterone (DHT) was first demonstrated in vitro. When homogenates of hypothalami or anterior pituitary glands were incubated with [3H]Testosterone in the presence of a 50-fold excess of testosterone-17 beta CA, the formation of labelled DHT was inhibited by more than 80%. Adult male rats that had been castrated for 1-2 months were fitted with chronic intravenous catheters and implanted with silicone elastomer sheets: one group received one sheet, 0.5-2.0 cm2 in size containing 1.6% testosterone, a second group received one 50 cm2 sheet containing 1.6% testosterone-17 beta CA and a third group received two sheets, one sheet 50 cm2 in size containing 1.6% testosterone-17 beta CA and the second ranging in size from 0.5 to 2.0 cm2 and containing 1.6% testosterone. Blood was withdrawn daily from each rat over a 4-5 day period after implantation of the steroids and the level of LH in the plasma was measured by radioimmunoassay. The seminal vesicles and the ventral prostate gland were removed at autopsy on day 4 or 5; the weights of these organs were shown to have increased progressively as the size of the implant of testosterone increased. In contrast, the level of LH in the plasma was suppressed to a comparable extent by implants of testosterone between 0.6 and 2 cm2, whereas a 0.5 cm2 implant of testosterone had no effect. Implants of testosterone-17 beta CA alone did not influence the weight of the accessory organs or the level of LH. When testosterone-17 beta CA and testosterone were implanted together, the growth-promoting effect of the latter on the accessory sex organs was significantly reduced. The effectiveness of testosterone in suppressing the level of LH in the plasma of these animals was not influenced by the presence of testosterone-17 beta CA and in certain instances the level was raised.

Steroid metabolism by the lung: conversion of dihydrotestosterone to 5 alpha-androstan-3 alpha, 17 beta-diol by rat lung tissue in vitro.

The potential of lung tissue of adult male rats metabolize dihydrotestosterone (DHT) in vitro was examined. Within 3 min, a homogenate of 100 mg lung tissue, cleared of blood by perfusion before homogenization, metabolized 90% of the [3H]DHT substrate. Appoximately 80% of the DHT was converted to 5 alpha-androstan- alpha, 17 beta-diol. The amount of 5 alpha-androstan-3 alpha, 17 beta-diol formed during a 5-min incubation increased linearly, with substrate concentrations ranging from 3.3 x 10(-8) to 3 x 10(-6) M. Thus, the capacity of rat lung tissue to metabolize DHT in vitro and the rate of 3 alpha-reduction of DHT are sufficiently great to consider the possibility that lung may be responsible for the rapid clearance of DHT from the circulation in this species.

Release of gonadotrophin-releasing hormone (Gn-RH) from isolated, perifused medial-basal hypothalamus by melatonin.

Basal release of Gn-RH from perifused medial-basal hypothalami of rats was at or below levels detectable by radioimmunoassay. Infusion of norepinephrine, dopamine, acetylcholine or serotonin (0.1-10 mM) as 10-20 min pulses was not associated with a detectable increase of Gn-RH in the effluent. However, 10-20 min pulses of melatonin (0.1-1.0 mM) consistently caused release of Gn-RH.

Direct effect of testosterone and its 5alpha-reduced metabolites on pituitary LH and FSH release in vitro: change in pituitary responsiveness to hypothalamic extract.

A continuous flow incubation (perifusion) system was used to examine the effect of testosterone (T) and three of its 5alpha-reduced metabolites, dihydrotestosterone (DHT), 5alpha-androstane-3alpha, 17beta-diol (3alpha-Adiol) and its 3beta-epimer (3beta-Adiol) on LH and FSH release, induced by hypothalamic extract (HE). In the absence of steroids, successive identical pulses of HE, of 10 min duration each, administered at hourly intervals over a 8-hr period, caused highly reproducible release of LH and FSH. In experimental perifusions, the amounts of LH and FSH released in response to standard 10-min pulses of HE administered at hourly intervals during the continuous infusion of steroid for 4-6 hr were compared with the responses of the same pituitaries to the standard test pulses of HE given before the start of the steroid infusion and after its cessation. All the androgens tested altered pituitary responsiveness. At the 0.1 and 1.0 mug/ml dose level there were differences between the steroids in the way they influenced the responsiveness of the pituitary overtime. Their effects at these two doses fell into three categories depending on whether there was initially: 1) an augmentation of HE induced LH release (T and 3beta-Adiol), 2) augmentation of both FSH and LH release (DHT), OR 3) NO AUGMENTATION IN THE RELEASE OF EITHer gonadotrophin (3alpha-Adiol). All the androgens ultimately suppressed pituitary responsiveness to HE and all were associated with changes in the ratios of LH and FSH released. When the dose of T and 3 beta-Adiol was raised to 10 mug/ml or that of DHT lowered to 0.01 mug/ml the initial stimulatory phase was not seen. Epitestosterone, the biologically inactive epimer of T, did not alter the responsiveness of the pituitary of HE.