ST segment elevation in patients with Brugada syndrome was augmented by selective stimulation of alpha-adrenoceptors or muscarinic receptors or by class IA drugs but was mitigated by beta-adrenoceptor stimulation or alpha-adrenoceptor blockade. These responses might be explained by postulating the presence of an area of early repolarization or a local "depolarized" area in the ventricle causing ST segment elevation in this syndrome. Because only a small number of patients were studied, these possibilities need further evaluation.

No abstract

We examined the effects of insulin-like growth factor (IGF)-I on follicular growth, oocyte maturation, and ovarian steroidogenesis and plasminogen activator (PA) activity in vitro, using a perfused rabbit ovary preparation in order to determine whether the follicle-stimulating effects of growth hormone (GH) are mediated by IGF-I. The addition of IGF-I to the perfusate stimulated follicular growth and the resumption of meiosis in follicular oocytes in a dose-dependent manner. There was no significant difference in the production of progesterone by perfused rabbit ovaries between IGF-I-treated and control ovaries, whereas IGF-I increased the production of estradiol (E2) by perfused rabbit ovaries in a dose-dependent manner. The concomitant addition of a monoclonal antibody recognizing the type I IGF receptor, alpha IR-3, to the perfusate significantly blocked IGF-I-stimulated follicular growth, oocyte maturation, and E2 production. Intrafollicular PA activity increased significantly 4 h after exposure to 10 or 100 ng/ml of IGF-I and reached maximal levels at 6 h. The percentage increase in follicle diameter at 6 h after exposure to IGF-I was significantly correlated with the intrafollicular PA activity. Treatment with GH resulted in a 2.7-fold increase in intrafollicular levels of IGF-I mRNA. The binding of [125I]-IGF-I to rabbit ovarian membrane preparations was inhibited by unlabeled IGF-I and IGF-II in a concentration-dependent manner. The relative affinity of the IGF-I receptor for IGF-I, IGF-II, and insulin was typical of type I binding (IGF-I > IGF-II > insulin). Affinity cross-linking of ovarian membranes with [125I]-IGF-I revealed a radiolabeled band corresponding to a molecular weight of 135,000, the alpha subunit of the type I IGF receptor. This band was totally displaced by IGF-I and alpha IR-3. It was concluded that IGF-I stimulated follicular development, E2 production, and oocyte maturation by interacting with its specific receptor located in rabbit ovarian membranes.

The potential role of oxygen free radicals in hCG-induced ovulation was investigated using the free radical scavenging enzymes superoxide dismutase (SOD) and/or catalase with the in-vitro perfused rabbit ovary preparation. SOD (25 micrograms/ml) and SOD + catalase (25 micrograms/ml) significantly reduced the % of large follicles that ovulated during perfusion (P less than 0.005). Neither maturity nor degeneration of ovulated ova and follicular oocytes was affected by SOD and/or catalase. Progesterone concentration in the perfusate was significantly increased in the SOD + catalase treatment group (P less than 0.01). These results indicate a significant role for oxygen free radicals in the process of ovulation.

Becausesonography is nowcapable of achieving increased resolution, ovarian tumors are more fre quently found in early pregnancy. In this case, we describea patientin the secondtrimester with ovarian endometriosis, which enlarged and was accompanied by structural changes inside the tumor. Case ReportA 28-year-old primigravidawas first seen in our antenatal clinic at 5 weeks of gestation. She had a history ofovarian endometriosis and had been treated with a gonadotropin-releasing hormone analogue before the pregnancy. A sonographic examination showed an intrauter me gestationsac and a right ovariantumor.The tumor was a unilocular cyst with fine in ternal echoesand a maximum diameter of 45 mm (Fig. 1A). Because the patient had a his tory of endometriosis, the tumorwasbelieved to represent an endometrial cyst and was treated conservatively.At 16 weeks ofgestation, sonographic exam ination revealeda fetus appropriatefor the ges tational age and showed an increase in size of the ovariancyst, which had reacheda maximum diameter of 85 mm. On transvaginalsonogra phy, irregularhyperechogenicrepresentingpap illary excrescences structures were seen inside the cyst. Color-flow Doppler sonography de picted vascularity within the solid irregular ar eas (Fig. 1B). These sonographic changes became more remarkable at i8 weeks of gesta flon. For further evaluation of a possible malig nancy, MR imaging was performed.The high signalintensityon TI-andT2-weightedimages was in the cystic portion of the tumor, suggest ing blood products. The solid portion was dark on Tl-weighted images and bright on 12-weighted images, suggesting malignancy that may have arisenfrom the endometriosis (Figs. lCand lD).On exploratory laparotomy performed at 20 weeksof gestation,a right ovariantumor adher ingtotheposterior wall ofthe uteruswasfound. A smallamountof asciteswasalsonoted.The tumor, which contained chocolatelike bloody fluid,hadalreadyraptured. After suctioning the fluid from the tumor, a right salpingo-oophorec tomy was performed.Papillaryexcrescences werefoundprotruding intothelumenof thetu mor. Final histopathologicexamination re vealed ovarian endometnosis with marked decidual changes and hemorrhage and without evidenceof malignancy (Fig. 1E). The patient recovered promptly and delivered a 3704-g healthymale infant at 40 weeksof gestation. during human pregnancy;thus, we did not use this contrast material in our patient. The clinical findings were indicative of malig nancy;however,final histopathologic exami nation of the tumor merely revealed solid tissue representing massive decidualization and hemorrhage. To our knowledge, ovarian endometriosisincreasingin size and accom panied by marked decidual bleeding during pregnancyis a rareoccurrence. The malignant transformation of endometri osis has been well documented, and persistent estrogenic stimulation has been implicated as a cause [4,5]. Becauseof this,ovarianendometri osis in pregnant women should be treated with special attention to structural changes that occur during pregnancy. Disc...

In the present study we investigated the role of angiotensin II (Ang II) receptor subtypes in gonadotropin-induced ovulation, oocyte maturation, and ovarian steroidogenesis and prostaglandin (PG) production in in vitro-perfused rabbit ovaries. The addition to the perfusate of PD123319, a nonpeptide Ang II antagonist with a high affinity for AT2 receptors, inhibited hCG-induced ovulation in a dose-dependent manner, whereas CV-11974, a nonpeptide AT1 receptor antagonist, had no effect. The majority of ovulated ova and follicular oocytes resumed meiotic maturation in response to hCG; and PD123319, but not CV-11974, significantly inhibited hCG-induced oocyte maturation. The addition of both Ang II receptor antagonists to the perfusate had no significant effect on the concentration of progesterone in the perfusate of hCG-treated ovaries, whereas PD123319 inhibited the hCG-stimulated production of estradiol. The production of PGE2 and PGF2 alpha was significantly increased at 6 h in hCG-treated ovaries compared with ovaries before hCG administration. PD123319 inhibited the hCG-stimulated production of PGs by perfused rabbit ovaries in a dose-dependent manner, indicating that hCG-induced PG synthesis is mediated, at least in part, via the activation of AT2 receptors. Ovulatory efficiency in ovaries perfused with or without PD123319 in the presence of hCG was significantly correlated with PG production by perfused rabbit ovaries 12 h after exposure to hCG (r = 0.6553 for PGE2, p < 0.001; r = 0.4758 for PGF2 alpha, p < 0.05). In conclusion, Ang II exerts complex and coordinated control on at least two distinct aspects in the normal ovulatory process, ovulation and oocyte maturation. Ang II produced locally by gonadotropin exposure may be a part of a novel intraovarian paracrine or autocrine control mechanism that operates via the AT2 receptor in the ovary.

We present a case of congenital midgut volvulus detected by prenatal sonography and ultrafast magnetic resonance (MR) imaging. At 34 weeks of gestation, enlarged hyperechogenic loops without peristalsis was identified by sonographic examination. On ultrafast T2-weighted single-shot fast-spin echo MR imaging, enlarged loops exhibited a lower signal intensity than the surrounding bowel loops, suggesting intraluminal hemorrhage. At explorative laparotomy following delivery, midgut volvulus causing hemorrhagic necrosis was found. Combined use of sonography and ultrafast MR imaging is useful to identify fetal midgut volvulus with hemorrhagic change.

The effects of angiotensin II (AII) and its receptor blocker, saralasin (SAR), on ovulation and oocyte maturation were investigated in an isolated, in-vitro perfused rabbit ovary. Ovulation and oocyte maturation were induced by AII in the absence of human chorionic gonadotrophin (hCG). SAR inhibited ovulation induced by AII or hCG, but not oocyte maturation. AII appears to play a critical role in follicle rupture, but not in resumption of oocyte meiosis.