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Biomedical subjects

A A Calder

Publications and source records attributed to A A Calder.

At least 73 records · Page 4Linked to original sources

Units for the evaluation of uterine contractility.

An improved system of units is proposed for evaluating the contractile activity of the myometrium. Mean active pressure (in kPa) provides the best overall measure of contractility. This measure is broadly compatible with studies quoting 'uterine activity integral' in kPa s per 15 min, but may be applied to any period of time. Units are suggested for measuring the amplitude, frequency and duration of contractions. It is shown that these are independent variables, and that mean active pressure is the numerical product of these three components.

Female↗

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↗

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↗

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↗

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↗

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↗

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↗

The predictive value of three pregnancy-associated proteins in the detection of the light-for-dates baby.

Three pregnancy-associated proteins, human placental lactogen, pregnancy-specific beta 1-glycoprotein and pregnancy-associated plasma protein-A have been measured in two groups of pregnant women. One group subsequently gave birth to children of normal birthweight, the other group were all delivered of a child with a birthweight less than the 10th centile. From the results obtained the values of the tests in predicting intrauterine growth retardation have been calculated. Human placental lactogen proved to be the most useful of the tests compared in predicting intrauterine growth retardation in the individual patient.

Female↗

The effect of exogenous hormones on the resistance of the early pregnant human cervix.

The force required to dilate the cervix to a diameter of 8 mm (cervical resistance index) has been measured in 355 patients undergoing suction termination in the first trimester of pregnancy. The cervical resistance index (CRI) was significantly lower in multigravid patients compared with primigravid patients. Prior treatment with prostaglandin E2 pessaries produced a consistent reduction in CRI in multigravidae but not in primigravidae. The effect of the prostaglandin was more pronounced on the compliance of the cervical tissue than on the diameter of the cervical canal. Treatment with pessaries of oestradiol, progesterone and medroxy-progesterone acetate produced no changes in the CRI.

Cervix Uteri↗

Blood rheology in pre-eclampsia and intrauterine growth retardation: effects of blood pressure reduction with labetalol.

Blood viscosity ( Contraves L S 30) and its determinants were measured in 23 patients with mild/moderate pre-eclampsia, 10 patients with intrauterine growth retardation and 22 control subjects, matched for age and gestation. Both abnormal groups had a significantly increased blood viscosity at high shear rate (94 s-1) associated with increased haematocrit. Fibrinogen levels were also increased, but there were no significant differences between groups in plasma viscosity, low shear viscosity (0.94 s-1) or red cell deformability, measured by a low-shear washed cell system of filtration through 5-micron pore diameter Nuclepore filters. In the pre-eclamptic group, measurements were repeated after 1-2 weeks in nine patients treated with labetalol (a combined alpha and beta adrenergic blocker) and in 10 patients treated with bed rest. Labetalol reduced blood pressure but no change in rheology was seen in either group. Control of blood pressure by labetalol does not adversely affect rheology, in contrast to diuretics which are known to cause haemoconcentration and increased blood viscosity.

Adult↗

Posture in labour: patients' choice and its effect on performance.

In a study to assess the influence of maternal posture on the progress and efficiency of labour, 275 parturients were asked to choose between remaining in bed during labour or being ambulant. Among primigravidae in spontaneous labour those who remained ambulant throughout had the shortest labours; they also had shorter labours than others who were only partially ambulant. Analysis of the data, based on original preference, however, suggests that an easy labour allows ambulation rather than vice versa. Radiotelemetry was used to transmit the fetal heart signal in all ambulant patients and provided satisfactory fetal surveillance in both high- and low-risk labours.

Female↗