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Biomedical subjects

I A Greer

Publications and source records attributed to I A Greer.

At least 19 recordsLinked to original sources
PubMed1992

Gemeprost-induced cervical ripening: histological and biophysical effects.

The mechanism of prostaglandin-induced cervical ripening is not clear. The aim of this study was to measure the biophysical and histological effects of gemeprost on the cervix. Thirty-four women admitted for surgical termination of pregnancy in the first trimester were randomised in a double-blind manner to receive either gemeprost or placebo prior to surgery. In 20 (10 active, 10 placebo) a needle biopsy was taken from the anterior lip of the cervix prior to cervical dilatation for histology. The forces required to dilate the cervix from 3 mm to 10 mm were measured. A group of seventeen parous women undergoing surgical termination who did not receive gemeprost were also studied as a parous control group. A needle biopsy was obtained in eight of them and also in six non-pregnant parous women undergoing hysterectomy for benign conditions, the latter acting as a non-pregnant control group. Polymerised collagen was stained with Picrosirius red and glycosaminoglycans with alcian blue using a MgCl2 gradient. Optical densitometry was used as an objective measure of staining. Neutrophil concentration was assessed immunohistochemically. Gemeprost treatment increased free passibility (the size of the largest dilator which could be passed without encountering resistance) (P < 0.01), reduced the forces required to dilate the cervix (P < 0.01) reduced blood loss (P < 0.05), reduced the collagen concentration (P < 0.01) and was associated with a modest neutrophil influx (P < 0.02) as compared to placebo. The pregnant parous group had a significantly lower collagen concentration than the non-pregnant parous group (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Abortion, Induced↗
PubMed1992

Prostaglandins and the cervix.

The dramatic capabilities of prostaglandins to modify the condition of the uterine cervix have been exploited to the considerable benefit of patients who require therapeutic interventions for labour induction and termination of pregnancy. This will continue to be an important facet of clinical obstetric and gynaecologic practice, although further refinements and improvements in techniques seem certain to continue.

Abortion, Therapeutic↗
PubMed1992

The effect of pH on release of PGE2 from vaginal and endocervical preparations for induction of labour: an in-vitro study.

OBJECTIVE: To study the effect of pH and precoating with obstetric cream on the release of prostaglandin E2 (PGE2) from commercially available triacetin and starch based gels, lactose based vaginal tablets and sustained release hydrogel polymer pessaries in-vitro. DESIGN: A prospective observational study. METHODS: PGE2 preparations held in dialysis bags were placed in Ringers lactate buffer and release of PGE2 into the buffer was measured over 8-12 h by radioimmunoassay. The hydrogel polymer pessary was also assessed after precoating with obstetric cream. MAIN OUTCOME MEASURES: In-vitro PGE2 release at pH 7.4, pH 5.4 and pH 3.4. RESULTS The gel preparations provided rapid and reliable release, while the lactose based vaginal tablet provided much lower release of PGE2 with sudden and variable release occurring after 5-8 h, an effect which was enhanced at low pH. With the triacetin gel preparation, release of PGE2 was reduced at lower pH, while the starch based gel appeared to provide optimal release at pH 5.4. The hydrogel polymer pessaries provided linear release in-vitro and this was reduced at pH 3.4. In addition, precoating the sustained release hydrogel polymer pessaries with obstetric cream virtually abolished release of PGE2. CONCLUSIONS: As the vagina is normally acid, these results suggest that vaginal pH could influence PGE2 release and this may result in variable clinical responses. In view of this, pH should be taken into account in the development of preparations for clinical use. Furthermore, the use of obstetric cream should be avoided when administering PGE2 preparations for induction of labour.

Cells↗
PubMed1992

Doppler umbilical artery flow velocity waveforms in diabetic pregnancy.

OBJECTIVE: To assess the effect of uncomplicated diabetes on umbilical artery flow velocity waveforms (FVWs); to investigate the relation between glycaemic control and FVWs and the predictive value of umbilical artery FVWs for antenatal fetal compromise. DESIGN: Prospective descriptive study. SETTING: A large diabetic pregnancy clinic in a teaching hospital. SUBJECTS: 128 pregnancies complicated by diabetes mellitus. 170 non diabetic women with no pre-existing or pregnancy complications. INTERVENTIONS: In diabetic pregnancies, umbilical artery resistance index (RI) Doppler recordings and glycosylated haemoglobin were measured every 2 weeks from 28 weeks. MAIN OUTCOME MEASURES: Umbilical artery RI and antenatal fetal compromise defined as a non reactive, decelerative cardiotocograph and/or a biophysical profile score persistently less than 6 and leading to immediate caesarean section. RESULTS: Uncomplicated diabetic pregnancies had FVW values similar to those in the non-diabetic range. Glycaemic control was unrelated to umbilical artery FVW values. Abnormal umbilical artery RI was found in nine pregnancies, these were more likely to show evidence of fetal compromise and to be associated with birthweights of less than 50th centile. In seven pregnancies there was evidence of fetal compromise, but only three of these pregnancies had abnormal FVW values. CONCLUSIONS: The non-diabetic range of umbilical artery RI values is appropriate for diabetic pregnancies. Long-term glycaemic control, within the range in this study, does not seem to affect umbilical artery RI. Abnormal umbilical artery RI is a significant predictor of fetal compromise in diabetic pregnancy, but fetal compromise can occur in association with normal RI values. Undue reliance should not be placed on normal FVW values in diabetic pregnancies.

Apgar Score↗
PubMed1992

Dexamethasone inhibits basal and stimulated prostaglandin E2 output from human placental cells by inhibition of prostaglandin H synthase.

In view of the temporal relation between elevated concentrations of glucocorticoids and prostaglandins (PG) at the time of parturition, we have examined the effects of dexamethasone on PGE2 output by mixed cell preparations from human placentae at term maintained in short-term (48 or 96 h) culture. Dexamethasone inhibited placental PGE2 output in a dose-dependent fashion. The effect on placental cells was more marked than on short-term cultures of amnion cells and was not influenced by the presence of progesterone. Dexamethasone also inhibited stimulated PGE2 output after addition of arachidonic acid. These results suggest that glucocorticoids inhibit placental PG output by a mechanism involving attenuation of PG synthase activity or expression and do not support a direct causal role for elevated maternal or fetal glucocorticoids at term on increased placental PG biosynthesis.

Arachidonic Acid↗
PubMed1991

Haemorrhagic problems in obstetrics and gynaecology in patients with congenital coagulopathies.

OBJECTIVE: To review the obstetric and gynaecological problems in women with congenital coagulopathies. DESIGN: Retrospective review. SETTING: Regional Adult Haemophilia Unit, Glasgow Royal Infirmary. SUBJECTS: All women in contact with the Unit over a period of 30 years, comprising eight with von Willebrand's disease, 18 obligate carriers of haemophilia A and five obligate carriers of Christmas disease. Each woman was interviewed and details of their obstetric and gynaecological histories were obtained and their case records were reviewed. MAIN OUTCOME MEASURES: Haemostatic changes associated with pregnancy and gynaecological problems. RESULTS: In 14 pregnancies in seven patients with von Willebrand's disease, there were four primary and four secondary post-partum haemorrhages and a large perineal haematoma complicating an episiotomy. These problems arose despite the endogenous rise in factor VIIIc seen with pregnancy. All women seen with von Willebrand's disease complained of menorrhagia and had been referred to gynaecologists. Treatment included danazol, tranexamic acid and the contraceptive pill. Diagnostic curettage resulted in severe haemorrhage in one woman and two women with pelvic pain and dyspareunia were found to have spontaneous broad ligament haematomas, one requiring surgery. In 43 pregnancies in obligate carriers of haemophilia A and Christmas disease there were five post-partum haemorrhages and a large perineal haematoma. CONCLUSION: In von Willebrand's disease it should be noted that adequate laboratory correction of factor VIIIc levels does not ensure clinical haemostasis; hence platelet function should also be measured. Patients with congenital coagulopathies pose particular problems for the obstetrician and gynaecologist and should be managed in close association with the local haemophilia centre.

Blood Coagulation Disorders↗
PubMed1991

Immunocytochemical localization of neutrophil elastase in term placenta decidua and myometrium in pregnancy-induced hypertension.

OBJECTIVE: The aim of the study was to determine whether there was evidence of elastase containing neutrophils at the materno-fetal interface in women with pregnancy-induced hypertension (PIH). DESIGN: An observational prospective study. SETTING: The Simpson Memorial Maternal Pavilion Edinburgh. METHODS: Placentas were obtained at vaginal or abdominal delivery from 51 consecutive women, 23 had normal pregnancies (13 caesarean sections) and 28 had PIH (18 caesarean sections). An immunocytochemical technique was used to localize elastase containing neutrophils in the placenta, decidua and myometrium. MAIN OUTCOME MEASURES: The numbers of positively stained cells, estimated subjectively as minimal, moderate or heavy, in subchorionic plate, perivillous fibrin and decidua. RESULTS: In both normal and PIH pregnancies neutrophils were absent from the myometrium. However, elastase containing neutrophils were located in areas of fibrin in the subchorionic plate and around the villi although there was no significant difference between the normal and PIH group. Neutrophils were also located in the fibrin of the decidua and in this case the number was significantly greater in the PIH group than in the normal group and correlated with plasma urate. CONCLUSION: The release of neutrophil elastase in the decidua could contribute to the vascular damage evident in PIH.

Adult↗
PubMed1991

Neutrophil activation is confined to the maternal circulation in pregnancy-induced hypertension.

The aim of this study was to determine whether neutrophil activation occurs in the fetal circulation in pregnancy-induced hypertension and to correlate this with evidence of neutrophil activation in the maternal circulation. Twenty-one normal pregnancies and 23 complicated by pregnancy-induced hypertension were studied in the third trimester. The mean length of gestation at delivery was significantly shorter (P less than .01) and the mean birth weight percentile was significantly lower (P less than .05) in the hypertensive group; otherwise the groups were comparable. Blood was obtained before cesarean delivery or established labor in the mothers and immediately after delivery from the umbilical vein. Plasma neutrophil elastase, which is released after neutrophil activation, was measured by radioimmunoassay as a marker for neutrophil activation. The mean (+/- standard error) concentration of neutrophil elastase in maternal plasma in the hypertensive group (35.9 +/- 4.7 ng/mL) was significantly higher than in the normal group (20.8 +/- 0.87 ng/mL) (P less than .005). The concentration of neutrophil elastase in umbilical venous plasma was not significantly different between the normal and hypertensive groups. However, significantly higher concentrations of neutrophil elastase were found in the umbilical venous plasma of pregnancies delivered vaginally compared with those delivered by cesarean (P less than .05) regardless of diagnosis. There was no correlation between maternal venous and umbilical venous plasma neutrophil elastase concentrations, birth weight percentile, plasma urate, or platelet count. These data suggest that neutrophil activation is confined to the maternal circulation in pregnancy-induced hypertension where it may contribute to vascular damage and dysfunction in areas such as the placental bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Umbilical artery Doppler flow velocity waveforms and maternal prostaglandin E2 and F2 alpha metabolite concentrations during cervical ripening with prostaglandin E2.

In 20 women, the umbilical artery flow velocity waveform (FVW) was recorded immediately before and 30-40 min after administering vaginal or extraamniotic prostaglandin E2 to ripen the cervix. Maternal plasma concentrations of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) metabolites (bicyclo-PGEM and PGFM, respectively) were measured at the time of the Doppler recordings. The administration of prostaglandin E2 was associated with a significant rise in maternal plasma PGFM and bicyclo-PGEM concentrations, but there was no change in the umbilical artery FVW Pulsatility index (PI). These results suggest that cervical ripening with local prostaglandin E2 has no effect on the umbilical artery FVW.

Administration, Intravaginal↗
PubMed1990

Platelet function after intramuscular diclofenac.

A randomised double-blind controlled study was performed to examine the effect of diclofenac on skin bleeding time and in vitro whole blood platelet aggregation. Twenty thoracotomy patients were studied; 10 were given diclofenac 75 mg intramuscularly at induction of anaesthesia, and 10 formed a control group. Skin bleeding times and platelet aggregation tests were performed the day before and repeated one hour after induction of anaesthesia. Diclofenac prolonged skin bleeding time and reduced platelet aggregation. There were no significant changes in the control group.

Adult↗
PubMed1990

Vaginal administration of PGE2 for induction of labor stimulates endogenous PGF2 alpha production.

Prostaglandin E2 is effective for induction of labor but many preparations exist using a variety of vehicles from which the active ingredient may not be equally available. Plasma concentrations of bicyclic PGE2 metabolite (PGEM) and 13, 14-dihydro, 15-keto PGF2 alpha (PGFM) were measured following administration of a 3mg PGE2 vaginal tablet or 1mg PGE2 vaginal gel to twenty-four parous women with favorable induction features, randomly allocated to receive one or other preparation. PGEM increased rapidly following both administration of the 3mg PGE2 vaginal tablet and the 1mg PGE2 vaginal gel, reaching a peak within 40 minutes of PGE2 administration. The maximal rise in PGEM in the gel group correlated directly with the change in cervical score and inversely with the need for augmentation with oxytocin and the induction-delivery interval. A secondary rise in PGFM was noted in both groups 3-4 hours following PGE2 administration. The magnitude of the increase in PGE2 may be important in the clinical response to PGE2 administration, while PGE2 absorption may switch-on endogenous PGF2 alpha production, similar to what is seen in spontaneous labor.

Administration, Intravaginal↗
PubMed1990

Effects of ketorolac tromethamine on hemostasis.

Ketorolac tromethamine is a potent prostaglandin synthetase inhibitor useful in the treatment of postoperative pain. Since it is also known to have antiplatelet properties, we determined the effect of ketorolac, alone and in combination with low-dose heparin, on hemostasis. Each of 12 healthy male volunteers received the following drug combinations on a double-blind, crossover basis: ketorolac dummy/heparin dummy, ketorolac active/heparin dummy, ketorolac active/heparin active, and ketorolac dummy/heparin active. Ketorolac significantly prolonged bleeding time, and inhibited platelet aggregation and platelet thromboxane production. Heparin had no effect on bleeding time or platelet function, but significantly prolonged the kaolin-cephalin clotting time and increased anti-Xa levels. Ketorolac had no effect on the kaolin-cephalin clotting time or anti-Xa levels, and no interaction was found between ketorolac and heparin. The modest prolongation of bleeding time with ketorolac is unlikely to be of any major clinical significance, as the value remained within the normal range in almost all subjects. However, because of its antiplatelet properties, the drug should be used with caution in persons with hemostatic disorders.

Administration, Oral↗