In this study was evaluated the effect of chronic hyperglycemia in the vascular response of thoracic aorta and pulmonary trunk in two strain rats. Chronic hyperglycemia was induced in male Wistar Kyoto (WK) and Sprague Dawley (SD) rats for single injection of streptozotocin (60 mg/kg, ip.). After 8 weeks, body weight, glucose, systemic arterial blood pressure (SABP) and right ventricular systolic pressure (RVSP) were measured. Thoracic aorta and pulmonary trunks were removed for vascular reactivity studies. Cumulative concentration‐response curves with phenylephrine (Phe) and Acetylcholine (ACh) were made in aorta and pulmonary rings. Glucose blood levels (mg/dl) were similar in both groups, 525±2 vs. 502±3. SABP in mmHg was increased in hyperglycemic SD compared to WK rats 160±2 vs. 140±2, while RVSP was higher in WK than SD rats 41±2.6 vs. 22±1.5 (P<0.001). Maximal tension contraction (g) response with Phe was higher in hyperglycemic SD against hyperglycemic WK aortic rings (2.1±0.1 vs. 1.2±0.1, P</a><0.001), with similar response in the pulmonary rings in both groups. ACh‐induced relaxation (%) response was reduced in SD aorta and pulmonary rings, 58±3 vs 66±4, and this response was attenuated inaorta 78±3, and pronounced in pulmonary rings, 49±3, from WK rats (P<0.001). The results shown that chronic hyperglycemia induce vascular damage predominantly in pulmonary artery in WK rats as consequence pulmonary hypertension, whereas in SD rats, systemic hypertension consecutive to aorta damage is mainly developed suggesting that a genetic factor determine the vascular damage induced by chronic hyperglycemia.

Autonomic innervation of heart is abnormal in diabetes and produces altered cardiovascular parameters. Cerebrolysin is a neurotrophic factor that improves the dendritic tree and synapses in the central nerve system after brain damage. The aim of this study was to evaluate if cerebrolysin can improve the cardiac neuropathy generated in diabetic rats. Male Sprague-Dawley rats two months old were injected with streptozotocin (70 mg/Kg/, ip). Hyperglycemia and altered cardiac rate were confirmed after eight weeks of STZ injection, and cerebrolysin treatment was started in control and diabetic rats for two months (1 ml/kg/day, ip). Body weight, heart rate, heart rate variability, arterial blood pressure, and blood glucose levels were measured. Also heart weight and levels of nitrites, NGF and VEGF were measured in left ventricle homogenates. The results show that body weight was reduced and blood glucose levels were increased significantly in diabetic rats. Cerebrolysin treatment produced no significant changes in body weight either in blood glucose level in control and diabetic rats. Cerebrolysin treatment in diabetic rats shows an improvement in the altered basal cardiac rate (306 ± 6.5 lat/min) compared to diabetic saline group (272 ± 8.9 lat/min: P < 0.05), without changes in control rats. Levels of nitrites, VEGF, and NGF in the left ventricle increased in diabetic cerebrolysin treated rats. In conclusion, the results show that cerebrolysin improves some abnormalities observed in the diabetic cardiac neuropathy in rats and suggest that could be considered an additional treatment to prevent or reduce the cardiac autonomic alterations generated in diabetes.

Autonomic denervation is a late complication of diabetes mellitus and is considered a cause of different cardiovascular disorders. In this study we evaluated the effect of Cerebrolysin (CBL) a neurotrophic factor, on cardiovascular hemodynamic parameters in rats with chronic hyperglycemia. Male Sprague Dawley rats were administered with streptozotocin (single dose, 60mg/Kg,ip). Hyperglycemic and normoglycemic rats were administered during 8 weeks with vehicle (saline 0.9 %) or Cerebrolysin (2ml/Kg/day, ip), at 60 days, after the induction of hyperglycemia. At the end, different parameters were measured in conscious rats: body weight (BW), heart rate (HR), heart rate variability (HRV), systolic arterial blood pressure (SABP), and blood glucose (BG). Heart weight (HW) and the ratio HW/BW were obtained after euthanized rats. The results shown that in the hyperglycemic rats the administration of CBL produce an increase in BW and HW, HR and HRV and a decreases in SABP as compared with hyperglycemic vehicle rats (BW 315±1 vs. 258±4), HW 1.4±0.07 vs. 1.1±0.05), ratio HW/BW 0.47±0.03 vs. 0.31±0.05), HR 322±8 vs. 278±1 beat/min), SABP 168±12 vs. 145±9 mmHg) (p< 0.001 for all comparison). The results suggest that the neurotrophic factor CBL, could improve the cardiovascular parameters in rats with chronic hyperglycemia and could be considered and adjacent treatment to patients with diabetes mellitus.