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Aim: This study aims to identify the clinical factors that can predict the requirement of massive transfusion among patients with postpartum hemorrhage (PPH)., Methods: Consecutive anonymized patients with PPH who were treated at the emergency department of our perinatal medical center were examined. Patients who had received transfusions before admission, those who had cardiac arrest on arrival, and those without history of blood gas analysis were excluded. Our primary outcome was the requirement of massive transfusion defined as packed red blood cells of ≥10 units/24 h. Univariable logistic analysis was carried out to identify the odds ratio and 95% confidence interval (CI) of the explanatory variables for the outcome., Results: A total of 31 patients (massive transfusion, n  = 19) were included in the main analysis. The crude odds ratio for fibrinogen per mg/dL and lactate per mmol/L were calculated as 0.98 (95% CI, 0.97-0.99) and 1.62 (95% CI, 1.08-3.02), respectively. The area under the curves for fibrinogen and lactate were 0.814 and 0.734, respectively, and optimal cut-off values for fibrinogen and lactate were 211 mg/dL and 4 mmol/L, respectively., Conclusion: These findings suggest that lactate and fibrinogen can be predictors for the requirement of massive transfusion in patients with PPH., (© 2019 The Authors. Acute Medicine & Surgery published by John Wiley & Sons Australia, Ltd on behalf of Japanese Association for Acute Medicine.)

This study was conducted to examine the correlation between uterine vascularity and natural history of uterine leiomyoma. Seventy women with leiomyoma participated in this study. Measurements of uterine and leiomyoma volume, as well as blood flow characteristics of the main uterine artery and leiomyoma arteries, were made every 3 months for 1 year. Leiomyoma arteries could be detected in 52 (51.5%) of 101 leiomyomas. Leiomyoma volume increased in 24 (46.2%) of 52 leiomyomas with leiomyoma artery. However, the leiomyoma volume increased in only three (6.1%) of 49 leiomyomas without leiomyoma artery. No difference was found between the pulsatility index of the leiomyoma artery in the group with increased size and in the group with stable size. This study shows the vascularity of leiomyoma to be useful as a predictor of leiomyoma growth.

This study was conducted in order to evaluate the influence of low calcium intake on the vascular response to angiotensin II (A-II) in pregnant and non-pregnant rabbits. Both were fed on a regular and a low calcium diet, respectively, for a period of at least 25 days. By using the common iliac arterial rings of each of the rabbits, and further classifying the respective arterial rings into those with intact endothelium and those with denuded endothelium, the response to A-II in the rings was compared. A greater degree of refractoriness to A-II was observed in the intact endothelial rings than in the denuded rings regardless of the difference in calcium intake, in both pregnant and non-pregnant rabbits. The refractoriness was however, particularly remarkable in the pregnant arterial rings. Therefore refractoriness to A-II in arterial rings on a low calcium diet is higher than that in the rings on a regular calcium diet regardless of the presence of endothelial cells, in both pregnant and non-pregnant rabbits. It is clear that reduction in the calcium intake results in an increase in the response to A-II, which is caused by increased reactivity of the vascular smooth muscle layer.

Recently we demonstrated that the vascular response to angiotensin II (A-II) was attenuated in an endothelium-dependent manner by using the isolated ring specimen iliac arteries of pregnant rabbits. In this paper we investigated the possibility that three vasoactive substances, thromboxane A2(TXA2), prostacyclin (PGI2), and endothelium-derived nitric oxide (EDNO), might be involved in this refractoriness to A-II during pregnancy, by measuring the changes in the vascular response to A-II (pA2, intrinsic activity) of the isolated arterial rings of rabbits before and after the addition of an inhibitor specific for each of these three substances. Sodium ozagrel, TXA2 synthetase inhibitor, decreased the vascular response to A-II more in the blood vessels of pregnant rabbits, regardless of whether the endothelium was intact or denuded, than in the blood vessels of non pregnant rabbits. Tranylcypromine, a PGI2 synthetase inhibitor, significantly increased contractility in the blood vessels with intact endothelium of pregnant rabbits (i.a. = 1.39 +/- 0.099, n = 11, mean +/- SEM), compared to that in the blood vessels with intact endothelium of non pregnant rabbits (i.a. = 1.08 +/- 0.090, n = 7). Methylene blue, a guanylate cyclase inhibitor which blocks the effect of EDNO, amplified the vascular response in blood vessels with intact endothelium of both groups, and more intensely in the blood vessels of pregnant rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

The criteria for pregnancy induced hypertension (PIH: hypertensive type of toxemia) have been determined by the Japanese Obstetrics and Gynecology Society. Mild PIH is classified into two types. One is "Absolute PIH (A-PIH)" diagnosed by (1) systolic blood pressure (SBP) greater than or equal to 140 mmHg and less than 160 mmHg or (2) diastolic blood pressure (DBP) greater than or equal to 90 mmHg and less than 110 mmHg. The other one is "relative-PIH (R-PIH)" diagnosed by (3) an increase in SBP greater than or equal to 30 mmHg compared to the usual SBP or (4) an increase in DBP greater than or equal to 15 mmHg compared to the usual DBP (In this paper, blood pressure prior to the 12th gestational week is considered as "usual" blood pressure). However, there has been no report in which two types of PIH are assessed. Our hypothesis is that the pathophysiology of the two types of PIH is different. We have already reported the clinical background of two types of PIH. The purpose of this study is to clarify the pathophysiological difference by evaluating the blood pressure change during pregnancy. We evaluated 963 nullipara and 747 multipara whose pregnancies were recorded from the 1st trimester (multiple pregnancy and pre-term delivery before the 32nd gestational week were excluded). Among the nullipara, 765 women (79.4%) were diagnosed as having normal blood pressure (N-group), 7.1% as A-PIH, and 13.0% as R-PIH. Among the multipara, the N-group consisted of 632 women (84.6%), the A-PIH: 4.6% and R-PIH: 10.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

The criteria for pregnancy induced hypertension ("PIH" which is a hypertensive type of toxemia) have been determined by the Japanese Obstetrics and Gynecology Society. Mild PIH is classified into two types. One is "Absolute PIH (A-PIH)" diagnosed by (1) systolic blood pressure (SBP) greater than or equal to 140 mmHg and less than 160 mmHg or (2) diastolic blood pressure (DBP) greater than or equal to 90 mmHg and less than 110 mmHg. The other one is "relative-PIH (R-PIH)" diagnosed by (3) an increase in SBP greater than or equal to 30 mmHg compared to usual SBP or (4) an increase in DBP greater than or equal to 15 mmHg compared to usual DBP (In this paper, blood pressure prior to the 12th gestational week is considered as "usual" blood pressure). We have already investigated the pathophysiological difference through the background and the change in blood pressure throughout pregnancy and puerperium in these two types of PIH. The purpose of this study is to clarify the pathophysiological difference by evaluating the influence of hypertension on fetal growth. We evaluated 963 nullipara and 747 multipara whose pregnancies were recorded from the 1st trimester (multiple pregnancy and pre-term delivery before the 32nd gestational week were excluded). Among nullipara, 765 women (79.4%) were diagnosed as having normal blood pressure (N-group), 7.1% as A-PIH, and 13.0% as R-PIH. Among multipara, the N-group consisted of 632 women (84.6%), A-PIH: 4.6% and R-PIH: 10.3%. There is no difference among the three groups in gestational days but the body weight, the chest circumference, and the abdominal girth at birth of A-PIH show a significant difference from those of the R-PIH and N-groups in both nullipara and multipara.(ABSTRACT TRUNCATED AT 250 WORDS)

The criteria for pregnancy induced hypertension (PIH) have been determined by the Japanese Obstetrics and Gynecology Society. Mild PIH is classified into two types. One is "Absolute-PIH (A-PIH)" diagnosed by 1) systolic blood pressure (SBP) greater than = 140mmHg and less than 160mmHg or 2) diastolic blood pressure (DBP) greater than = 90mmHg and less than 110mmg. Another one is "Relative-PIH (R-PIH)" diagnosed by 3) an increase in SBP greater than = 30mmHg compared to normal SBP or 4) an increase in DBP greater than = 15mmHg compared to normal DBP. However, there has been no report in which two types of PIH are assessed. Our hypothesis is that the pathophysiology of two types of PIH is different. The purpose of this study is to clarify the pathophysiological difference by evaluating the clinical backgrounds. We evaluated 963 nullipara and 747 multipara whose pregnancies were recorded from the 1st trimester (multiple pregnancy and pre-term delivery before 32 gestational weeks were excluded). Among 765 nullipara women, 79.4% were diagnosed as having normal blood pressure (N-group), 7.1% as A-PIH, and 13.0% as R-PIH. In the multipara N-group, the figures were 632 women (84.6%), A-PIH, 4.6% and R-PIH, 10.3%. Clinical backgrounds showed that the incidence of hypertensive family history, high hematocrit (greater than = 39.0) before the 12th gestational week or obesity (Kaup index greater than = 24 before pregnancy) was significantly higher in A-PIH than in the N-group of nullipara and higher in the A-PIH than in the R-PIH and N-groups of multipara.(ABSTRACT TRUNCATED AT 250 WORDS)

During pregnancy, vascular sensitivity to A-II is reduced and it was clarified that this refractoriness to A-II is due to a change in EDRF output in pregnant rabbits. The present study aimed at elucidating whether estrogen or progesterone is responsible for the augmentation of EDRF output. 17-OH-estradiol was administered (200 micrograms/kg/day) for 7 days to 8 non-pregnant rabbits, while progesterone was similarly administered (2,000 micrograms/kg/day) to 8 other non-pregnant rabbits. Twenty-four nonpregnant rabbits were employed as the controls. Common iliac arterial rings prepared from each group were compared for the isometric response to A-II. The arterial rings with intact endothelium prepared from the progesterone-treated group were found to have a smaller pD2 value and a smaller maximum response to A-II than the estrogen-treated group. On the other hand, no differences between the progesterone group and estradiol group were observed in these values for the endothelium-denuded arterial rings. These findings indicated that the augmentation of EDRF output during pregnancy is brought about by progesterone.

Vascular refractoriness to angiotensin-II (A-II) during pregnancy is well recognized. The present study was designed to evaluate how the response of endothelial cells of arterial rings to A-II changes in pregnant rabbits (n = 24) when compared with non-pregnant rabbits (n = 24). The response of the arterial rings with intact endothelium to A-II was markedly decreased in the pregnant rabbit group in comparison with the non-pregnant rabbit group. In contrast, in the case of the arterial rings whose endothelium had been removed, there was no difference between the two rabbit groups in the response to A-II. However, the maximum response of arterial rings to A-II was significantly lower in the pregnant group than the non-pregnant group under the presence of the endothelium. This study revealed that the arterial rings with intact endothelium prepared from the pregnant group shows markedly increased refractoriness to A-II, while no such difference is seen with rings from which the endothelium had been removed. That is, this study indicated that an endothelium-derived relaxing factor (EDRF) is deeply involved in refractoriness to A-II in pregnant rabbits.

An effect of E-Trp6-LH-RH (superactive LH-RH agonist) in the pituitary and ovarian function was examined. Four regularly cycling baboons were used for this study. After determination of control values of plasma levels of LH, oestrogen and progesterone during the entire menstural cycle, D-Trp6-LH-RH was infused subcutaneously for 7 days during the early luteal phase in these four baboons. An infusion of D-Trp6-LH-RH increased plasma LH and oestrogen, but it failed to alter the plasma level of progesterone. From these results, it seems unlikely that 1) D-Trp6-LH-RH has a luteolytic effect, and 2) an increased ovarian oestrogen causes luteolysis in the baboon.

Continuous illumination (LL) beginning at 22 days of age caused precocious puberty followed by persistent estrus with anovulation in female offspring originating from mother rats exposed to a 14L:10D light-dark cycle prior to and during pregnancy. However, LL had no deleterious effect on reproductive cycles of offspring reared in LL and originating from mothers exposed to LL prior to and during pregnancy. These rats had a normal onset of puberty in LL, a normal 4-day estrous cycle, a periodic rise of plasma estrogen prior to the periodic appearance of the preovulatory luteinizing hormone (LH) surge, and spontaneous ovulation in LL continued until at least 300 days of age. Also, the female offspring of these rats showed a similar resistance to the deleterious effects of LL on cyclic ovulation. These results support the following interpretation: 1) offspring from mother rats exposed to LL prior to and during pregnancy become insensitive to the deleterious effects of LL on cyclic ovulation, 2) neural elements controlling cyclic release of LH are not totally photoperiod (14L:10D)-dependent, and 3) in the absence of daily 14L:10D signals, an endogenous clock, possibly timed by daily laboratory signals (temperature, noise, taking of vaginal smears), may provide time cues for cyclic LH release.