Gere S. Dizerega

Prevention of postoperative tubal adhesions: comparative study of commonly used agents.

Tubal abrasions were surgically induced in 25 rhesus monkeys following demonstration of tubal patency. Five monkeys received dexamethasone, promethazine, and ampicillin perioperatively, five received intraperitoneal 10% dextran 40, five received intraperitoneal 32% dextran 70, and 10 received no additional therapy. Fimbrial biopsies were obtained from two additional monkeys treated with 32% dextran 70 before and postoperatively on days 2, 5, and 7. Only those treated with 32% dextran 70 retained tubal patency and avoided development of adhesions, involving fimbria, omentum, ovary, uterus, and bladder. Histologic examination of fimbrial biopsies demonstrated sufficient epithelial repair to have occurred during the 5 days 32% dextran 70 remained in the pelvin cavity to prevent adhesion formation.

Follicular phase treatment of luteal phase dysfunction

Previously, we demonstrated that selective suppression of serum follicle-stimulating hormone (FSH) in monkeys treated with charcoal-extracted porcine follicular fluid (pFF) in the early follicular phase induced luteal defects resembling those which occur spontaneously in women and monkeys. Here, we assessed whether luteal phase defects arising in association with induced FSH deficiencies during the early follicular phase can be treated by early FSH therapy. Rhesus monkeys were treated with pFF and human menopausal gonadotropin (hMG) (FSH:luteinizing hormone [LH], 3:1) on cycle days 1 to 3 or day 4, respectively. Daily femoral blood samples were analyzed for LH, FSH, and estradiol by radioimmunoassay. In the monkeys treated with the pFF-hMG combination, a single ovulation was uniformly noted at laparoscopy, and initial luteal phase elevations in serum progesterone levels were nearer those of normal ovulatory cycles than after pFF alone. These results suggest that FSH/LH treatment in the early follicular phase compensated, in part, for the pFF-induced deficiency in endogenous FSH levels.

Pregnancy-associated ovarian refractoriness to gonadotropin: A myth

Ovulation was induced in three of five rhesus monkeys during midpregnancy using human menopausal gonadotropin/human chorionic gonadotropin therapy. No evidence of ovarian refractoriness to gonadotropic stimulation was found. It is concluded that cyclic ovarian function in these primates is suspended during gestation and into the puerperium because pituitary gonadotropin secretion is insufficient to support folliculogenesis.

Selection and Maturation of the Dominant Follicle and Its Ovum in the Menstrual Cycle

The specialized investments of the growing preovulatory follicle, and its successor the corpus luteum, establish and maintain the changing hormonal milieu which nurtures the ovum through maturation, fertilization, and the initial stages of embryogenesis. Indeed, it is the ovarian cycle which modulates hypothalamic-pituitary function through both negative and positive feedback on gonadotropin release, as well as temporal regulation of proliferative and secretory phases within the uterus during the menstrual cycle. No wonder, then, that the sequelae to aberrancies during folliculogenesis (spontaneous or induced) include abnormalities of the cervical mucus, endometrium, circulating gonadotropins, the corpus luteum, and even the ovum. Accordingly, fertility in the female depends most fundamentally on an underlayment of intra-ovarian processes which account for timely follicular growth culminating in ovulation of a fertilizable oocyte.