家兔死后眼玻璃体液镁，铁含量与PMI关系的研究

目的寻找一种精确推定PMI的方法。方法应用电感耦合等离子体质谱(ICP-MS),检测家兔死后96h内眼玻璃体液镁、铁元素含量,探讨其与PMI的相关性。结果家兔死后0～48h眼玻璃体液镁元素含量与PMI显著相关,6～48h铁元素含量与PMI显著相关,其二项式回归方程分别为y=0.0738x2+0.6997x+11.45(R2=0.9119)、y=0.0411x2-0.3148x+1.4113(R2=0.9594)。结论家兔死后眼玻璃体液Mg、Fe含量变化可作为推定48h内PMI的参考指标之一。     

The Role of Vitreous Magnesium Quantification in Estimating the Postmortem Interval

The use of magnesium as a parameter to estimate the time of death is controversial. In 32 traumatic deaths with known postmortem intervals (PMIs), small quantities of vitreous humor (VH) were sampled repetitively every 3 h until 24 h postmortem. The bodies were kept at the constant ambient temperature of 20°C (68°F). The concentrations of magnesium were in the range of 0.47–1.15 mM. A statistically significant correlation of the concentration of magnesium with the PMI was observed (r = 0.453, p < 0.01), but with small predictive value—coefficient of variation for regression was 45.5%; the average of the paired differences between the estimated and actual PMIs was 5.24 + 3.19 h. Although useful results might be expected due to the large transmembrane gradient for magnesium, the results of this study strongly disprove the usefulness of measuring magnesium in VH to estimate the time of death.     

Alcohol intoxication may exacerbate the effects of blunt cranial trauma through changes in brain free magnesium levels

Moderate to high levels of alcohol decrease brain intracellular free magnesium concentration, a factor known to be critical in brain injury. Phosphorus magnetic resonance spectroscopy was used to examine changes to brain free magnesium concentration after blunt cranial trauma in alcohol-intoxicated rats. Rats exposed acutely or chronically to alcohol sufficient to increase blood alcohol levels to between 150 and 350 mg/dL demonstrated a brain free magnesium level that was 20-50% less than in nonintoxicated animals (p < 0.01). After injury, brain free magnesium levels declined more rapidly and to a greater extent in alcohol-affected animals than in nonintoxicated control animals (p < 0.001). As both preinjury depletion of magnesium and degree of magnesium decline after brain injury have been associated with poor recovery, these findings suggest that moderate to severe alcohol intoxication may predispose the brain to a worse outcome by reducing brain free magnesium levels, both before and after injury.