d-ribose improves cardiac contractility and hemodynamics, and reduces expression of c-fos in the hippocampus during sustained slow ventricular tachycardia in rats

Background Moderate hypotension during hemodynamically stable ventricular tachycardia (VT), leads to cerebral ischemia. Supplementation of d-ribose has been shown to improve cardiac metabolism. We hypothesized that cerebral ischemia during slow VT may lead to the expression of immediate early genes related to neurodegeneration. This expression may be prevented by d-ribose substitution. Methods Slow VT was induced over 20 min by external left ventricular pacing after infusion of physiologic saline or d-ribose (450 mg/kg) in 44 rats. Different coloured microspheres were used for tissue blood flow measurements. Histochemistry of c-fos in cerebral tissue sections was performed. Results With the onset of VT, the mean arterial pressure (MAP) significantly dropped in both groups. However, the MAP in the d-ribose group was significantly higher (p < 0.05) than in the control group (111 ± 21 mm Hg vs. 80 ± 40 mm Hg). The rate pressure product (RPP) during VT was significantly higher in the d-ribose group than in the control group (75,000 vs. 59,000, p < 0.05). The occurrence of lethal VT was significantly higher in the control group and could be prevented by d-ribose. A stable activation of c-fos was observed in the control group. This ischemic stress response of the brain could not be seen after d-ribose infusion. Conclusion d-ribose improves hemodynamic parameters, cardiac contractility and prevents the activation of pro-apoptotic c-fos, demonstrating a neuroprotective effect of d-ribose during slow VT.