100umol/L of COP can invoke a positive ionotropic effect that is glucose dependent and a slight negative chronotropic effect when oxygen is in the range of normoxia, and helped the recovery of cardiac contractility after ischemia (lack of oxygen) which is thought to be via a glycolytic mechanism.[1]
One study that used isoprenaline (beta-adrenergic agonist) in a dose that was able to induce cardiac lesions noted that pretreatment of 200mg/kg COP (injections) was able to significantly attenuate the degree of cardiac lesions[3] and doses up to 1000mg/kg have been shown to dose-dependently reduce death induced by an overdose of isoprenaline in mice (16% reduction at 250mg/kg, 50% reduction at 1000mg/kg).[4] Low doses can increase in efficacy over 4 days of loading when compared to the same dose taken 4 hours acutely prior to the isoprenaline insult,[5] and these effects may occur in a rehabilitative manner as evidence by 3060mg of Creatinol O-Phosphate given for three days (IV) to persons who recently suffered a Myocardial infarction, where serum cardiac enzymes decreased by 33-46% relative to control.[6]
Injections of Creatinol O-Phosphate have an apparent cardioprotective effect against beta-adrenergic induced lesions and may possibly be rehabilitative as well; no studies on oral ingestion at this time
A reduction in the time required for atropine to induce cardiac arrythmia in guinea pigs has also been noted.[4] Anti-arrythmic properties have been noted in vivo with COP supplementation[7] even after three days of 2040mg (twice daily 1020mg injections).[8]
Administration of COP, as well as the reference drug atropine, have been shown to improve A-V conduction of the heart in a small sample (n=6) pilot study; atropine's benefits were more evidence.[9]
Injections of COP appear to be beneficial for arrythmia disturbances, no studies on oral ingestion
