Cardiopulmonary reflex impairment in experimental diabetes in rats

The aim of the present study was to evaluate the sensitivity of the cardiop ulmonary receptors in experimental diabetes induced by streptozotocin by th e use of 2 different methods: (1) administration of increasing doses of ser otonin to analyze peak changes of arterial pressure and heart rate for each given dose in conscious intact normal and diabetic rats; (2) expanding blo od volume with the use of dextran (6%) to produce similar increases in left ventricular end-diastolic pressure to quantify the arterial pressure, hear t rate, and renal sympathetic nerve activity in sinoaortic, denervated, ane sthetized normal and diabetic rats. Blood samples were collected to measure blood glucose. Diabetic rats showed hyperglycemia (22+/-0.7 versus 7+/-0.2 mmol/L), reduced body weight (226+/-12 versus 260+/-4 g) and heart rate (2 94+/-14 versus 350+/-10 bpm), and similar arterial pressure (104+/-4 versus 113+/-4 mm Hg) when compared with control rats. Serotonin induced signific ant bradycardia and hypotension, which were similar and proportional to the dose injected in both groups, Mean arterial pressure and heart rate decrea ses in response to volume overload were significantly lower in diabetic tha n in control rats. The reflex reduction of the renal sympathetic nerve acti vity as expressed by percentage changes in nerve activity in response to in creasing left end-diastolic pressure was abolished in diabetic animals (1.9 +/-0.8% versus -14+/-4%/mmHg in controls). These results showed an impairme nt of cardiopulmonary reflex control of circulation in diabetes during acut e volume expansion. The normal responses to serotonin administration indica ted that the cardiopulmonary reflex is still preserved in diabetic rats.