Heart rate and QT interval in streptozotocin-induced diabetic rat

Aim: Prolonged QT interval is a common finding in diabetic patients. The effects of streptozotocin [STZ]- induced diabetes on QT interval has been investigated by application of 4 standard QT correction algorithms

Methods: The electrocardiogram was recorded in STZ-treated [60 mg/kg bodyweight, ip] and age-matched control rats with a biotelemetry system for the period of the study$Results: Heart rate [HR] was significantly [P<0.01] reduced and QT interval was significantly [P<0.05] prolonged in diabetic rats compared to controls at 8, 10 and 12 weeks after STZ treatment. At 8 weeks HR was 260 +/- 16 BPM [n=5] in diabetic rats compared to 333 +/- 25 BPM [n=5] in controls and QT interval was 70 +/- 7 ms [n=5] in diabetic rats compared to 59 +/- 6 ms [n=5] in controls. When QT interval was corrected for HR there was no longer any significant difference in QT interval between diabetic and control rats. The effects of different correction techniques have been compared and the consequences considered

Conclusion: The rapid and dramatic reductions in HR observed after administration of STZ are associated with a prolongation of the QT interval. However, the magnitude of the difference of the QT interval between the STZ and control groups was not significant after QT interval correction for the difference in HR?

Effects of voluntary exercise on heart function in streptozotocin [STZ] - induced diabetic rat

Exercise training improves cardiac performance and has been utilized as an effective adjunct to pharmacotherapy in the management of diabetes mellitus. The aims of this study were to characterize voluntary exercise habits in streptozotocin [STZ]-induced diabetic rats and investigate whether attained levels of voluntary exercise induce effects on diabetic heart function. Diabetes was induced by a single intraperitoneal injection of STZ [60 mg/kg]. Animals were divided into 4 groups: Control Sedentary [CS], Diabetic Sedentary [DS], Control Running [CR] and Diabetic Running [DR]. DR and CR rats were provided with running wheels. Body weight and blood glucose were measured in running rats at the start and end of the 60-day exercise period. Ventricular action potentials were measured in spontaneously beating heart. Shortening and intracellular Ca[2+] were measured in electrically stimulated ventricular myocytes. DR rats exercised less than CR rats. At 60 days the mean distance covered by DR rats was 1027 +/- 289 m compared to 5975 +/- 1117min CR rats. CR gained whilst DR rats lost weight at the end of the exercise period. Mean blood glucose in CR and DR rats at the start of the exercise period was 71 +/- 4 and 426 +/- 21 mg/dl, respectively. Glucose levels were not altered in CR rats but were reduced in DR rats at the end of the exercise period. The time to peak shortening and peak Ca[2+] transient and time to half relaxation of the Ca[2+] transient were prolonged in myocytes from DS compared to CS rats and were not additionally altered by voluntary exercise. In conclusion, diabetic rats were less inclined to partake in voluntary exercise compared to controls and the levels and duration of exercise were insufficient to significantly alter cardiac performance in either control or diabetic rats

Contraction and intracellular free ca2+ concentrations in ventricular myocytes from rats recieving sucrose-enriched diet

Contraction and intracellular free Ca2+ concentrations [Ca2+]i in ventricular myocytes from rats receiving sucrose-enriched diets [SED's] were investigated. Groups of Wistar rats received normal rat chow together with either normal drinking water or water containing 500 mM sucrose ad libitum. Experiments were performed 12-14 weeks later. Rats receiving SED's responded differently to a st and ard glucose tolerance test. Fasting blood glucose levels in SED and control rats were 59.4 +/- 1.3 and 58.8 +/- 1.4 mg/dl, respectively. At 30 min after intraperitoneal administration of glucose [2g/kg body weight] concentrations of blood glucose were significantly [P<0.05] higher in rats receiving SED [256.2 +/- 32.7 mg/dl] compared to controls [136.6 +/- 14.7 mg/dl]. At 120 min blood glucose in SED [67.6 +/- 7.2] and control [63.0 +/- 2.4 mg/dl] rats were not significantly [P>0.05] different when compared to initial fasting blood glucose values. Blood plasma insulin concentrations in SED and control rats were 3.01 +/- 0.55 [5] and 0.29 +/- 0.05 [5] ng/ml, respectively. Amplitude and time to peak [TPK] of ventricular myocyte shortening and Ca@@@@@@ transient were not altered by SED. Time to half [THALF] relaxation of shortening was significantly prolonged in myocytes from SED [60.6 +/- 2.1 ms] compared to control [48.7 +/- 2.9 ms] rats. The TPK and THALF relaxation of the Ca2+ transient were not altered by SED. However, the amplitude of Ca2+ transient was significantly increased in myocytes from SED [0.36'0.02 RU] compared to control [0.31 '0.02 RU] rats. Altered myofilament sensitivity to Ca2+ may underlie the contractile defects seen in ventricular myocytes from rats fed diets that are supplemented with drinking water containing 500 mM sucrose for 12-14 weeks

Contraction and intracellular Ca2+ in ventricular myocytes from rats receiving fructose-enriched diets

Contraction and intracellular Ca2+ in ventricular myocytes from rats receiving fructose-enriched diets [FED] were investigated. Groups of male Wistar rats received normal rat chow together with either normal drinking water or water containing 500 mM fructose ad libitum. Experiments were performed 12-14 weeks later. Rats receiving FED responded differently to a st and ard glucose tolerance test. Fasting blood glucose levels in FED and control rats were 48.5 +/- 2.3 [4] and 47.0 +/- 1.9 [4] mg/dl, respectively. At 30 min after intraperitoneal administration of glucose [2g/kg body weight], concentrations of blood glucose were significantly [p<0.05] higher in rats receiving FED [206.3 +/- 19.5 mg/dl] compared to controls [150.3 +/- 8.5 mg/dl]. At 120 min, blood glucose in FED [87.3 +/- 4.2] and control [80.3 +/- 3.4 mg/dl] rats were still significantly [p<0.01] higher than initial values. Amplitude and time to half [THALF] relaxation of ventricular myocyte shortening and Ca2+ transient were not altered by FED. Time to peak [TPK] shortening was unaltered, however, the TPK Ca2+ transient was significantly prolonged in FED rats [65.1 +/- 3.4 ms] compared to controls [56.4 +/- 2.0 ms]. In conclusion, diets supplemented with drinking water containing 500 mM fructose for a period of 12-14 weeks did not have significant effects on ventricular myocyte shortening but did prolong the time course of the Ca@@@@@@ transient suggesting that defects in Ca2+ transport may precede defects in myocyte contractility in this experimental model