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Biomedical subjects

I A Greer

Publications and source records attributed to I A Greer.

At least 145 records · Page 8Linked to original sources
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↗
PubMed1989

Neutrophil activation in pregnancy-induced hypertension.

Human neutrophil elastase may be a major mediator of vascular damage and could contribute to the vascular damage seen in women with pregnancy-induced hypertension (PIH). Elevated plasma levels of this substance will reflect neutrophil activation in vivo. To determine neutrophil activation in PIH, we studied 30 normal non-pregnant women, 32 women with normal pregnancies, 19 with mild/moderate PIH and 16 with severe PIH between 28 and 39 weeks gestation. Plasma neutrophil elastase was measured by radioimmunoassay. There was a significantly higher concentration of plasma neutrophil elastase in both mild/moderate and severe PIH than in normotensive pregnancies and this may contribute to the vascular lesion associated with PIH. Concentrations were also significantly higher in normal pregnancy than in non-pregnant women which suggests that neutrophil activation and degranulation are increased in normal pregnancy.

Adult↗
PubMed1989

Increased neutrophil activation in diabetic pregnancy and in nonpregnant diabetic women.

Human neutrophil elastase may be a mediator of vascular damage, and enhanced neutrophil reactivity could contribute to the susceptibility of pregnant diabetic women to vascular complications. Elevated plasma levels of neutrophil elastase will reflect neutrophil activation in vivo. The aim of this study was to determine whether neutrophil activation occurs in uncomplicated diabetic pregnancy. We studied 30 normal nonpregnant women, 20 nonpregnant diabetic women, 32 nondiabetic women with normal pregnancies, and 17 insulin-requiring pregnant diabetic patients. Plasma neutrophil elastase was measured by radioimmunoassay. There was a significantly higher concentration of plasma neutrophil elastase in normal pregnant women compared with the nonpregnant group (P less than .001). The nonpregnant diabetic group had significantly higher concentrations than the normal nonpregnant group (P less than .002). The pregnant diabetic group had significantly higher concentrations than the nonpregnant diabetic group (P less than .001) and the normal pregnant group (P less than .05). The high concentrations of plasma neutrophil elastase may contribute to the greater sensitivity of pregnant diabetic patients to vascular complications.

Adult↗
PubMed1988

Haemostatic effects of ketorolac with and without concomitant heparin in normal volunteers.

Ketorolac is a potent cyclo-oxygenase inhibitor used for the treatment of postoperative pain. It is known to have anti-platelet properties. The aim of this study was to determine the effect of ketorolac on haemostasis both alone and in combination with low dose heparin in 12 healthy male volunteers. Each volunteer received the following drug combinations in a double blind, placebo controlled, cross over manner: ketorolac placebo/heparin placebo, ketorolac active/heparin placebo, ketorolac active/heparin active and ketorolac placebo/heparin active. Ketorolac significantly prolonged bleeding time, inhibited platelet aggregation to arachidonic acid and collagen 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 in any of the investigations. The prolongation of bleeding time seen with ketorolac is unlikely, to be of any major clinical significance as almost all subjects remained within the normal range; however, it should be used with caution in subjects with haemostatic problems.

Adult↗
PubMed1988

Effect of maternal ketorolac administration of platelet function in the newborn.

Ketorolac is a potent analgesic agent with antiplatelet properties which is known to cross the placenta. The aim of this study was to determine whether maternal administration of ketorolac in labour had any effect on neonatal platelet function as compared with maternal administration of pethidine and prochlorperazine. Eighteen parous women were studied in labour, twelve received pethidine (control) and six received ketorolac for analgesia. Immediately after delivery, blood was taken from the umbilical vein and anticoagulated with citrate. Platelet aggregation in whole blood was studied. Ketorolac significantly inhibited aggregation in response to arachidonic acid and collagen but not ADP. These findings confirm that ketorolac crosses the placenta. The antiplatelet effects are likely to be related to ketorolac's inhibitory effect on TxA2 production which is required for arachidonic acid and collagen-induced aggregation, but not the primary aggregation response induced by ADP. These effects suggest that ketorolac should be used with caution in patients whose neonates are at risk of haemostatic problems.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Therapeutic progress--review XXVIII. Platelet function and calcium channel blocking agents.

Platelets play a major role in the pathogenesis of vascular disorders such as coronary heart disease. The control of platelet function centres on the concentration of free intra-cellular Calcium ions (Ca2+). Increases in intracellular Ca2+ will result in platelet activation and release of substances such as thromboxane A2 which will stimulate further platelet activation and vasoconstriction, leading to vascular damage, thrombosis and ischaemia. Calcium channel blocking agents (CCB's) have the ability to reduce Ca2+ availability and may have potentially beneficial effects on platelet function. CCB's have been convincingly shown to have anti-platelet properties in vitro. They have also shown anti-platelet properties in vivo although this finding has not been consistent. In addition they have been shown to act synergistically with other anti-platelet agents. In the light of the available information it is likely that CCB's have only minor anti-platelet properties in vivo when used alone. Combining CCB's with other anti-platelet agents, however, may allow lower doses of drugs to be used to achieve a satisfactory inhibitory effect on platelet function. Such combination therapy may be of value in the treatment of vascular disorders; however, further studies are required to evaluate these effects in the clinical situation.

Arteriosclerosis↗