To study whether ventricular overdrive pacing (VOP) induces preconditioning, rabbits were equipped with right ventricular electrode catheters for pacing and intracavital recording and polyethylene cannulas in the left ventricle and right carotid artery to measure intraventricular pressure and blood pressure. One week after surgery in conscious animals, VOP at 500 beats/min over 2, 5, or 10 min resulted in an intracavital S-T segment elevation, shortening of ventricular effective refractory period, decrease in maximum rate of pressure development and blood pressure, and increase in left ventricular end-diastolic pressure proportional to the duration of stimulation. A 5-min preconditioning VOP applied 5 or 30 min before a 10-min VOP markedly attenuated ischemic changes, whereas a 2-min VOP had no effect. In anesthetized rabbits, a 5-min VOP slightly increased guanosine 3',5'-cyclic monophosphate (cGMP) and profoundly elevated adenosine 3',5'-cyclic monophosphate (cAMP) content in left ventricular samples. When this VOP was preceded (5 or 30 min) by a preconditioning VOP, the cAMP increase was significantly attenuated, whereas the cGMP increase was amplified. We conclude that a single 5-min VOP induces preconditioning in association with alterations in cardiac cyclic nucleotide contents.

A preceding right ventricular overdrive pacing (VOP) of 500 b.p.m. for 5 min, markedly reduced the severity of global myocardial ischaemia produced by a subsequent 5-min VOP in conscious rabbits. This VOP-induced preconditioning developed in parallel with an increase in cardiac cyclic guanosine 3':5'-monophosphate (cyclic GMP) content. VOP-induced preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of nitroglycerin (NG). In the heart of the NG-tolerant rabbits, neither VOP nor preconditioning increased cyclic GMP content. This suggests that changes by NG tolerance of cyclic GMP metabolism may account for the loss of VOP-induced preconditioning.

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To evaluate the role of fructosamine/albumin ratio as an alternative screening parameter for gestational diabetes mellitus (GDM), serum fructosamine, albumin, protein, fructosamine/albumin ratio, and oral glucose tolerance were measured in 56 non-pregnant control healthy subjects, and in 96 pregnant women who screened positive after a 50 g glucose challenge-test. Oral glucose tolerance test (OGTT) identified 12 of 96 pregnant women as having GDM. Fructosamine concentration of 1.98 +/- 0.32 mmol/L (mean +/- SD) and fructosamine/albumin ratio of 47 +/- 10 mumol/g (mean +/- SD) has been obtained in nonpregnant control subjects. During the second trimester a lower fructosamine level (1.84 +/- 0.29 mmol/L, p < 0.05) and a higher fructosamine/albumin ratio (62 +/- 15 mumol/g, p < 0.001) occurs in pregnant women, when compared to non-pregnant healthy control subjects, most likely due to the low serum albumin concentration (30 +/- 6 g/L). The serum fructosamine levels and fructosamine/albumin ratio were only slightly higher in the pregnant women with GDM than in normal pregnant women (2.05 +/- 0.47 mmol/L versus 1.84 +/- 0.29 mmol/L, 67 +/- 16 mumol/g versus 62 +/- 15 mumol/g, respectively) but the differences were not statistically significant. The fructosamine and fructosamine/albumin ratio values for normal and GDM groups overlapped considerably. Sensitivity, specificity, positive predictive and negative predictive values for fructosamine were 41.7%, 85.7%, 29.4% and 91%, and for fructosamine/albumin ratio 25%, 79.8%, 15% and 88% respectively. This suggests that both fructosamine and fructosamine/albumin ratio have low sensitivity as predictors of GDM and can therefore not be used as screening tests.

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