In-vivo 31P-nuclear magnetic resonance (NMR) studies were undertaken with anesthetized rats to determine: a. whether systemic administration of MgCl2 could protect animals against cocaine-induced hemorrhagic stroke, and b. whether a relationship exists between basal levels of brain intracellular free magnesium ions ([Mg2+]i), phosphometabolites, and stroke risk. Repeat 31P-NMR spectra were obtained at various intervals of time (3-120 min, or up until death) after administration of cocaine (5 + 30 mg/kg). Ion selective electrodes were used to measure plasma Mg2+, K+, Na+ and Ca2+. Forty percent of animals died in the absence of Mg2+ infusion following high dosage of cocaine. Only 13% died with cocaine following Mg2+ infusion (p <0.005). In the Mg2+-protected animals, neither brain [Mg2+]i,intracellular pH (pHi), [phosphocreatine-PCr]/[ATP], nor brain [inorganic phosphate-Pi]/[ATP] fell when toxic and lethal doses of cocaine were given. Low basal brain [Mg2+]i (275 +/- 24 vs. 466 +/- 35 microM, p <0.01) and low basal brain [PCr] (3.36 +/- 0.35 vs. 4.26 +/- 0.24 mM, p <0.01) were found to be associated with a 3-fold increased incidence of stroke. A positive correlation (r = 0.31, p <0.03) between brain [Mg2+]1 and [PCr]/[ATP] was found. It is possible that both brain [Mg2+]i and [PCr] may be useful as important predictors of susceptibility to cocaine-induced hemorrhagic stroke.

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However, despite more than 80 years of intensive research, it remains to be determined how this angiopathy and widened PP develop. The lack of highly sophisticated in-vivo, non-invasive biophysical and biochemical techniques which are needed to diagnose, early, the microvascular structural and hemorheological alterations in the heart and brain, unfortunately, has often missed the potential underlying changes which can lead to cardiac failure and/or stroke in people over 60 years of age. About seven in 10 people over 65 with diabetes will die of heart disease and one in six from a stroke.

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