Search PubMed⌕ Search

Biomedical subjects

I A Greer

Publications and source records attributed to I A Greer.

At least 163 records · Page 9Linked to original sources
PubMed1987

Maternal plasma bicycling PGE2 levels following vaginal administration of prostaglandin E2 pessaries in full term pregnancies.

Plasma levels of bicyclic PGE2 (PGE2M) were measured after administration of a 5mg, PGE2 slow release hydrogel pessary and a 3mg vaginal tablet (Upjohn). Twenty-four women of low parity with favourable induction features were randomised to receive either the hydrogel pessary or the vaginal tablet. A single pessary was administered and amniotomy was performed after 4 hours. Augmentation with oxytocin was carried out after amniotomy if required. Both groups showed a rise in plasma PGE2 levels in keeping with the release profiles of the pessaries. Wide interindividual differences in absorption were found.

Administration, Intravaginal↗
PubMed1986

Inhibition of whole blood platelet aggregation by nicardipine, and synergism with prostacyclin in-vitro.

Platelets are involved in the pathogenesis of vascular disease, and calcium channel blocking agents (CCB) such as nicardipine, are being used in the treatment of such disorders. CCB's are known to have minor anti-platelet actions from studies performed in platelet rich plasma (PRP). Recently it has become possible to study platelet aggregation in whole blood. The effects of nicardipine on whole blood platelet aggregation were studied in-vitro using the Clay-Adams Ultra Flo 100 whole blood platelet counter. Nicardipine inhibited aggregation to 0.5 micrograms/ml collagen, and 0.5 mM arachidonic acid in a dose dependent manner, but had minimal effects on aggregation to 10 microM ADP. Nicardipine also acted synergistically with prostacyclin to inhibit aggregation. The effect of nicardipine on generation of PGI2 and TxA2 from whole blood was studied. Nicardipine did not affect TxA2 production, but significantly increased PGI2 production at high concentration. The effect of nicardipine on vascular PGI2 production was also assessed using umbilical artery rings, but nicardipine had no effect on PGI2 production. This study confirms that CCBs have inhibitory actions on platelet aggregation, and this may be of value in the treatment of vascular disease.

Adenosine Diphosphate↗
PubMed1986

Endothelial stimulation by DDAVP in von Willebrand's disease and haemophilia.

Desamino-D-arginine vasopressin (DDAVP) is known to stimulate factor VIII (FVIII) and plasminogen activator release from endothelial cells, and has been shown to stimulate prostacyclin (PGI2) production in normal and haemophilic subjects. In von Willebrand's disease (vWd) some patients have a dissociate response with regard to FVIII and plasminogen activator. The aim of our study was to compare the PGI2, FVIII and plasminogen activator response to DDAVP infusion in vWd with the response to DDAVP in normal and haemophilic subjects. PGI2 metabolites thromboxane B2 (TxB2), factor VIII coagulant activity, factor VIII-related antigen and plasminogen activator were measured before and after DDAVP infusion. There was a significant increase in PGI2 metabolites, factor VIII-related antigen and plasminogen activator in all groups following DDAVP, but no effect on TxB2 was found, and there was no evidence of any dissociate response to DDAVP in any of the groups. Basal levels of PGI2 metabolites, however, were significantly lower in vWd as compared to normal and haemophilic subjects. Post-DDAVP levels of PGI2 metabolites were also significantly lower in vWd as compared with normal subjects. This may be due to a reduced stimulus to PGI2 production in vWd secondary to defective platelet adhesion.

Antigens↗
PubMed1985

Inhibition of platelet aggregation in whole blood by adrenoceptor antagonists.

It has recently become possible to study platelet aggregation in whole blood which may more closely resemble the in-vivo situation as the platelets are left in their natural milieu with red and white cells present which themselves can influence aggregation. The effects of 4 adrenoceptor antagonists on platelet aggregation in whole blood were studied in-vitro using the Clay-Adams Ultra Flo 100 whole blood platelet counter. Labetalol, pindolol and propranolol inhibited aggregation to 0.5 microgram/ml collagen in a dose dependent manner, and were synergistic with prostacyclin in inhibiting collagen induced aggregation. These 3 drugs also promoted reversal of aggregation induced by 10 microM ADP, but only inhibited 0.5 mM arachidonic acid induced aggregation at high drug concentrations. Atenolol had no effect on either collagen, ADP or arachidonic acid induced aggregation. The anti-platelet effect of these drugs may be of value in the treatment of vascular disease.

Adenosine Diphosphate↗
PubMed1985

A comparative study of the effects of adrenoceptor antagonists on platelet aggregation and thromboxane generation.

Platelet aggregation and thromboxane A2 have been implicated in the pathogenesis of several forms of vascular disease. The aim of this study was to determine the effect of a wide range of adrenoceptor antagonists on platelet aggregation, and thromboxane A2 production, from normal human platelet rich plasma in vitro. Labetalol, pindolol and propranolol inhibited platelet aggregation to collagen in a dose dependent manner. Increasing the concentration of collagen "shifted" the dose response curve to the right. These 3 drugs also significantly inhibited thromboxane A2 generation in response to collagen but not to arachidonic acid. This effect was independent of any inhibitory effect of these drugs on platelet aggregation, and occurred at a drug concentration close to that obtained in vivo. Atenolol, metoprolol, prazosin and timolol were similarly assessed but had no effect on either platelet aggregation or thromboxane A2 generation. This ability of labetalol, pindolol, and propranolol to inhibit platelet aggregation and thromboxane generation, may be of clinical benefit in view of the increasing evidence implicating thromboxane A2 in the pathogenesis of vascular disease.

Adrenergic beta-Antagonists↗
PubMed1985

Effect of stanozolol on factors VIII and IX and serum aminotransferases in haemophilia.

The treatment of haemophilia has been dramatically improved since the introduction of factor VIII and IX concentrates, however these concentrates have brought new problems such as hepatitis and A.I.D.S. An oral agent which could raise endogenous levels of factor VIII and IX would be of great benefit. Danazol, an anabolic steroid, has recently been shown to increase levels of factors VIII and IX in haemophilia. We therefore studied the effect of stanozolol, a closely related anabolic steroid, in 15 patients with haemophilia A or Christmas disease over a 2-4 week period. There was no consistent change in factor VIIIc or factor IX, and fibrinolysis was significantly enhanced. No effect was apparent on the incidence of spontaneous bleeds. However serum aminotransferases which were abnormal in 11 of the 15 patients at the start of the study fell significantly with stanozolol therapy. This raises the interesting possibility that anabolic steroids may be beneficial in patients with chronic liver diseases.

Blood Viscosity↗
PubMed1985

Inhibition of thromboxane and prostacyclin production in whole blood by adrenoceptor antagonists.

There is increasing evidence implicating thromboxane A2 (TxA2) in vascular disease. Adrenergic blocking agents have been used with success in the secondary prevention of myocardial infarction. The aim of this study was to determine whether adrenergic blocking agents had any effect on the production of TxA2 and prostacyclin (PGI2) from whole blood in vitro. Fresh whole blood without anticoagulant was placed in glass tubes containing either drug or vehicle, the latter acting as control, and allowed to clot at 37 degrees C for 30 minutes. The serum PGI2 metabolites (PGI2M) and TxB2 (the stable hydration product of TxA2) were determined by radioimmunoassay. Labetalol, pindolol and propranolol all inhibited both PGI2M and TxB2 production in a dose dependent manner, while atenolol had no effect. Labetalol was the most potent significantly inhibiting TxB2 production at a drug concentration compatible with that found in-vivo. This inhibitory effect on TxB2 production may be of benefit in the treatment of vascular disease.

Adrenergic alpha-Antagonists↗
PubMed1985

Immunoreactive prostacyclin and thromboxane metabolites in normal pregnancy and the puerperium.

Prostacyclin and thromboxane have been implicated in the pathophysiology of several disorders of pregnancy, but there is little information on concentrations of these prostaglandins in normal pregnancy. The aim of our study was to determine the range of values throughout normal pregnancy and the puerperium and to compare this with concentrations in normal non-pregnant women. Measurement was by radioimmunoassay of prostacyclin and thromboxane metabolites. We observed a significant difference in prostacyclin metabolites in the first trimester, (mean 19.9, SEM 0.96 pg/ml) compared with the normal non-pregnant group (mean 15.9, SEM 0.68 pg/ml). There were no significant differences between values in the normal non-pregnant group and those in the second and third trimester or postnatally. The increase in prostacyclin in the first trimester may be associated with placentation and physiological vasodilation, and insensitivity to angiotensin II seen in early pregnancy. We noted a significant reduction in thromboxane metabolites in the second (mean 133, SEM 14.9 pg/ml) and third (mean 123, SEM 10.7 pg/ml) trimesters and the puerperium (mean 119, SEM 6.3 pg/ml) compared with the values in the normal non-pregnant group (mean 142, SEM 4.9 pg/ml). This may be due to increased platelet stability or decreased thromboxane synthesis.

Epoprostenol↗
PubMed1984

Topical pramoxine and hydrocortisone foam versus placebo in relief of post partum episiotomy symptoms and wound healing.

A double-blind randomised controlled trial, comparing pramoxine hydrochloride 1 per cent and hydrocortisone acetate 1 per cent in a mucoadhesive foam base, with simple aqueous foam (B.P.), in relieving episiotomy discomfort and episiotomy healing in 40 patients was carried out. Simple aqueous foam was more effective with regard to wound healing and episiotomy discomfort as measured by analgesic consumption. Pramoxine and hydrocortisone foam offers no advantage over simple aqueous foam in the treatment of post partum episiotomy discomfort.

Administration, Topical↗