A 75 g oral glucose tolerance test was carried out on 953 pregnant women who were identified on the basis of clinical risk factors. The tests were analysed by the WHO criteria: 826 were normal, 120 showed impaired glucose tolerance, and 7 identified diabetes. A number of obstetric and perinatal outcome measures were compared between the groups with normal and impaired glucose tolerance, and also with 135 women who had pre-existing Type 1 diabetes and delivered during the study period. There was no significant difference in the incidence of antenatal complications between mothers with normal and impaired glucose tolerance. There was a higher rate of induced labour ( p < 0.05) and caesarean section ( p < 0.01) in the impaired glucose tolerance group compared to the normal group, but no difference in fetal outcome or neonatal morbidity. All of these outcome measures were increased in the Type 1 diabetic pregnancies. KEY WORDS Pregnancy Impaired glucose tolerance Fetal outcomeA further 16 patients had an antenatal glucose tolerance test but were excluded from the analysis (10 tests were incomplete due to vomiting after the glucose load, 3 patients delivered at other hospitals, and the case records of a further 3 patients could not be traced). A standard

A 75 g oral glucose tolerance test was carried out on 953 pregnant women who were identified on the basis of clinical risk factors. The tests were analysed by the WHO criteria: 826 were normal, 120 showed impaired glucose tolerance, and 7 identified diabetes. A number of obstetric and perinatal outcome measures were compared between the groups with normal and impaired glucose tolerance, and also with 135 women who had pre-existing Type 1 diabetes and delivered during the study period. There was no significant difference in the incidence of antenatal complications between mothers with normal and impaired glucose tolerance. There was a higher rate of induced labour (p < 0.05) and caesarean section (p < 0.01) in the impaired glucose tolerance group compared to the normal group, but no difference in fetal outcome or neonatal morbidity. All of these outcome measures were increased in the Type 1 diabetic pregnancies.

Apoptosis is found in failing human hearts. Catecholamines are upregulated in heart failure and appear to cause cardiomyocyte apoptosis. Recent randomised c l i c a l studies show mortaliity benefit h m plselective-blockade in patients with heart failure. However it remains uncerhm ' if cardiomyocyte apoptosis is a pselective process. Method: Neonatal rat ventriculomyocytes (NRVM) were plated to subconfluence. Experiments were carried out in serum-five medium with ascorbic acid. Cells were incubated with wpdine(ISO.O.Ol-lpM), with or without CGP20712A (plblocker) and 1C1118,551 (p2blocker); with or without IBMX(phosphodiesterase inhibitor). Apoptosis was quantified by an anti-DNNanti-histone ELISA k i t (ROCHE) and confirmed with time-lapse. videomicroscopy, H33342 stain for nuclear morphology and DNA electrophoresis. Adenylyl cyclase (AC) assay using a recovery method with a-AW and 'H-CAMP was performed on human atrial-and neonatal rat ventricular-membrane preparations incubated with IS0 with or without CGP, ICI and pertussis toxin (PTX). Results. IS0 increased apoptosis in a dose-dependent manner up to 1 . 6~ control (pd.05). Degree of apoptosis with ISoeCGP was equivalent to control @=0.09). ISOtICl however augmented apoptosis up to 2% control(p4.01). Apoptosis was augmented in all groups by IBMX. In NRVM membrane preps AC activity with lSOcCGP was augmented 2 . 5~ H3Kn PTX was added (pd.05). This augmentation was not seen in the human atrialmembrane preps. Conclusion: In NRVM IS0 upregulates apoptosis via a plselective pathway appears to be CAMP-related. p2AR appear to be protective via a PTX-sensitive inhibition of AC activity. However p2 protection may not be present in human 2 MONOCYTE APOPTOSIS IN ATHEROGENESIS