ACTA ENDOCRINOLOGICA (BUC)

Context. Studies of platelet function in diabetics are inconsistent, some studies reporting higher platelet reactivity, while others showed no change. Objective. We aimed to evaluate platelet indices and in vitro platelet aggregation in rats with long-lasting (28 weeks) diabetes mellitus. Design. Twelve controls and 14 diabetic rats were investigated. Diabetes was induced in 11-week-old rats using streptozotocin (60 mg/kg,i.p.). Platelet indices and in vitro adenosine diphosphate (ADP)-, protease-activated receptor 4 (PAR4) agonist-, and arachidonic acid (AA)-induced platelet aggregation were assessed at the age of 38 weeks. Results. Compared to controls, diabetic rats presented lower platelet count and plateletcrit (both p≤0.001), and higher mean platelet volume (p<0.01). ADP- (p=0.04) and AA-induced (p<0.01) platelet aggregation were lower in diabetic compared with control rats, whereas PAR4 agonistinduced platelet aggregation was similar between the two groups (p=1.00). Conclusions. This study demonstrates a paradox of high intrinsic platelet reactivity and low in vitro ADP- and AA-induced platelet aggregation in diabetic rats compared with non-diabetic controls. The relevance of in vitro platelet aggregation to the contribution of platelets to in vivo thromboembolic events in diabetic rats remains questionable.

Context. Endothelial and vascular muscle dysfunctions are incriminated in the pathogenesis of diabetes mellitus (DM)-related vascular complications. However, the time-course of these changes remains unclear. Objective. We aimed to assess the time-dependency of changes that occur in vascular reactivity in aortic rings of rats with streptozotocin (STZ)-induced DM with shortversus long-term DM durations and in age-matched controls. Design. Wistar rats were assigned to young control (n=6), young DM (n=9), aging control (n=6), and aging DM (n=8) groups. DM was induced at 11 weeks of age using STZ (60 mg/kg, i.p.). Methods. At the end of the study (15 weeks of age for young controls and diabetics and 38 weeks of age for aging controls and diabetics), KCl - and phenylephrineinduced vascular contractility, and acetylcholine - and sodium nitroprusside (NTP)-induced relaxation were studied to assess endothelium-dependent and –independent vasodilation. Results. Young and aging controls presented similar vascular reactivity parameters. Acetylcholineinduced vasodilation was reduced in both young and aging diabetics compared to age-matched controls. Furthermore, acetylcholine-induced relaxation was significantly lower in aging compared to young diabetics. Meanwhile, NTPinduced vasodilation and both KCl- and phenylephrineinduced vasoconstriction were only diminished in aging diabetics. Conclusions. These results suggest that endothelial dysfunction is an early, progressive, event in the large arteries of diabetic rats that precedes the dysfunction of vessel musculature. The lack of any change in aortic reactivity in aging controls indicates that the changes observed in aging diabetics are probably due to prolonged, severe hyperglycemia, with a negligible participation, if any, of the advancing age.

Context. Non-psychogenic polydipsia-induced hyponatremia is a rare clinical finding. The effects of severe hyponatremia on the electrical activity of the heart in this setting are far from clear. Case report. Resting ECG and 24-h ambulatory ECG monitoring performed in an 80-year-old hypertensive female accusing nonspecific symptoms of confusion, lethargy, disorientation, nausea, and palpitations, demonstrated significant intraatrial and atrioventricular conduction disorders and numerous atrial tachyarrhythmia episodes. Laboratory analysis revealed severe hyponatremia (108 mEq/L) as only significant disorder. Extensive endocrine, neurological, cardiology, and pulmonary examinations excluded the most common causes of hyponatremia, including the inappropriate antidiuretic hormone secretion syndrome. Careful history revealed excessive voluntary water intake of up to 6 L/day and low sodium intake, associated with long-term thiazidelike diuretic treatment. Correction of sodium levels was associated with complete resolution of both atrial arrhythmias and conduction disorders. Conclusions. This report presents the first case of severe hyponatremia caused by combined non-psychogenic polydipsia and thiazide-like diuretic use complicated with reversible cardiac conduction disorders and atrial arrhythmias. The close temporal relationship between the fully reversible cardiac electric abnormalities and severe hyponatremia strongly indicates hyponatremia as key feature in the pathogenesis of these electric abnormalities.