A comparison between atria from control and streptozotocin‐diabetic rats: The effects of dietary myoinositol

Abstract

1 Atria, isolated from control rats, six-week streptozotocin-diabetic rats and from similarly diabetic rats treated with myo-inositol (MI) were compared. The MI treatment was shown to reverse the depressed sciatic nerve MI which was observed in the untreated diabetic group. 2 Spontaneously beating atria from the untreated diabetic animals beat more slowly, and with greater force than tissues from the control group. When electrically driven at 4 Hz they were found to be less sensitive to the negative inotropic effect of acetylcholine. No differences between the two groups were observed in responses to isoprenaline. 3 Intramural nerve stimulation in the presence of 10-6M propranolol (vagal stimulation) had a greater negative inotropic effect in the untreated diabetic rat atria than in the controls. Positive inotropic responses to nerve stimulation in the presence of 10-6 M atropine (sympathetic stimulation) were not significantly different between the two groups. 4 Atria from the MI-treated diabetic animals were found to have a lower spontaneous contractile force and greater sensitivity to acetylcholine than tissues from the untreated diabetic animals. The values obtained in both cases were similar to those from the controls. No significant effect of MI treatment on spontaneous contractile rate or on responses to nerve stimulation was demonstrated. 5 Atrial (mainly myocardial) MI was measured in additional control, six-week diabetic and six-week MI-treated diabetic animals. A significantly higher concentration was observed in the MI supplemented group compared to the untreated diabetic group. The mean MI content in the latter group was lower than that obtained from control tissues but not significantly so. 6 The results implicate MI depletion either in the neurones or in the myocardium in at least some of the changes observed. Possible mechanisms involved are discussed.

Diabetes increases mortality after myocardial infarction by oxidizing CaMKII

“…Although reduced heart rate variability, a feature of SND, could be due to intrinsic SAN defects, loss of normal autonomic function, or a combination of both, our ex vivo findings indicate that STZ treatment directly affects SAN, causing intrinsic SND by increased apoptosis, fibrosis, and subsequent electrical source-sink mismatch between SAN and myocardium. Our findings do not dispute a role for autonomic dysfunction in diabetes-induced defects in heart rate but appear consistent with other evidence showing diabetes causes pathological effects on SAN (44)(45)(46).…”

Polyol pathway‐mediated changes in cardiac muscle contractile properties: studies in streptozotocin‐diabetic and galactose‐fed rats

“…Similar findings have been reported for diabetic (Pfaffman, 1980;Kofo-Abayomi & Lucas, 1988), but not galactosaemic rats. Action potentials and repolarization are prolonged in diabetic atria.…”

“…Contraction in papillary muscles and atria were examined. There have not been any reports on atrial contractile properties in diabetes, although some dysfunction was expected because resting beat rate is reduced, and sensitivity to autonomic agents is changed (Foy & Lucas, 1978;Tomlinson & Yusof, 1983;Kofo-Abayomi & Lucas, 1988 (Special Diet Services, Manea, Cambs). A third group of normal onset controls was also used; previous studies have shown that their contractile properties do not differ from those of age-matched control rats ).…”

Long‐term effects of streptozotocin‐induced diabetes on the electrocardiogram, physical activity and body temperature in rats

“…Defective Ca 2+ signalling mechanisms, including reductions in L‐type Ca 2+ channel current, depressed sarcoplasmic reticulum Ca 2+ uptake and release mechanisms, and reduced rate of Ca 2+ efflux on the Na + –Ca 2+ exchange, partly underlie these contractile defects (Lagadic‐Gossmann et al 1996; Chattou et al 1999; Choi et al 2002). Reductions in heart rate (HR) in isolated perfused heart (Li et al 1989; Nicholl et al 1991; Imai et al 1991; Ravingerova et al 1996; De Angelis et al 2000; Nemeth et al 2001) and spontaneous beating rate in right atria (Goyal & McNeill, 1985; Ramanadham & Tenner, 1986; Kofo‐Abayomi & Lucas, 1988; Nagamine et al 1989; Booth & Hodgson, 1993; Hicks et al 1997; Sellers & Chess‐Williams, 2000) from STZ‐treated rats suggest that intrinsic defects are partly responsible for heart rhythm disturbances. In vivo studies have also demonstrated reduced HR and reductions in heart rate variability (HRV), suggesting that extrinsic control of heart rhythmicity may also be defective in STZ‐treated rats (Hicks et al 1998; Fazan et al 1999; Lo et al 2002; Howarth et al 2005).…”