Summary:To clarify the effect of extracellular magne sium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2 + concentration on the contractile and endothe lium-dependent dilatory responses were investigated in vitro. The contractions, induced by 1O-8_IO-s M norepi nephrine, were significantly potentiated at low Mg2 + (0,8 mM v. the normal, 1.2 mM). High (1.6 and 2.0 mM) Mg2 + exhibited an inhibitory effect on the contractile re sponses, No significant changes, however, in the EC so values for norepinephrine were found. The endothelium dependent relaxations induced by 1O-8_10-s M acetyl choline were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilDuring the past decade, a considerable amount of data has been generated concerning the effect of extracellular magnesium ions (Mg2 + ) on vascular smooth muscle tone and reactivity. Acute with drawal of Mg2 + elevates the basal tone of the arter ies, and contractile responses to various agonists are enhanced in Mg2+ -deficient solutions. Eleva tion of Mg2+ , however, relaxes the smooth muscle and attenuates vasoconstriction (see Altura and Al tura, 1981,1984,1985. Abbreviations used: ECso, 50% effective concentration; EDRF, endothelium-derived relaxing factor. From the original observations of Furchgott and ------------ 161atory responses also shifted the ECso values for acetyl choline to the right. The present results show that the contractile responses of the cerebral arteries are ex tremely susceptible to the changes of Mg2 + concentra tions. In response to contractile and endothelium dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endo thelial receptor. Since Mg2 + deficiency might facilitate the contractile but not the endothelium-dependent relax ant responses, the present study supports a role for Mg2 + deficiency in the development of the cerebral vasospasm.

The aim of this study was to investigate the effect of small alterations in the extracellular magnesium concentration on the tone of feline middle cerebral arteries and to examine the role of the endothelium in these responses. We measured the isometric tension of isolated arterial rings placed between two stainless steel wires in a tissue chamber containing Krebs-Henseleit solution aerated with a gas mixture containing 95% O 2 and 5% CO 2 at 37°C. After precontraction with noradrenaline, a decrease of the extracellular magnesium concentration from 1.2 mM to 1.0 and 0.8 mM resulted in sustained relaxations, whereas elevation of the extracellular magnesium concentration from 0.8 mM to 1.2 mM caused an increase in vascular tone when the endothelium was intact The magnesium deficiency-related dilations were absent in endothelium-denuded vessels and were inhibited by 5 x 10"' M oxyhemoglobin and 1 0 s M methylene blue, suggesting the involvement of an endothelium-derived relaxing factor in this vascular response. However, 5 x l 0~7 M nifedipine or 3xlO~s M dichlorobenzamil did not affect the magnesium deficiency-related relaxations. Therefore, nifedipine-sensitive calcium channels or the sodium/calcium antiport system are not involved in this vascular action of magnesium. We conclude that small alterations in the extracellular magnesium concentration, possibly within the physiological range, are able to modify the basal formation and release of endotheliumderived relaxing factor and thus alter arterial smooth muscle tone in this vascular bed. This endothelium-and magnesium-dependent system appears to be more sensitive than the direct smooth muscle actions of magnesium and might exert a protective effect against magnesium deficiency-induced direct cerebrovascular contraction. (Stroke 1991;22:785-789)

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Measurements of DNA concentrations by fluorescence of the DNA--bisBenzimide complex in the plasma of normal subjects, patients with disorders of cerebral circulation of different severity caused by atherosclerotic involvement of the carotid and/or spinal arteries (after the acute stage of brain stroke), and patients with lateral amyotrophic sclerosis showed a significant increase in its content vs. the norm. Electrophoresis of DNA isolated from plasma showed that in the patients it is represented not only by long fragments of at least 20,000 bp (which is typical of normal subjects), but also by shorter fragments. Key Words: DNA; fluorometry; bisBenzimide; cerebral circulation disorders; lateral amyotrophic sclerosisThe blood-brain barrier is always involved in organic diseases of the nervous system; the degree of such involvement can vary from metabolic to mechanical. This involves the development of pathological process, including autoimmune reactions toward brainspecific proteins of neurons, myelin, and glial elements. There are no published reports about changes in the plasma level of DNA which may be caused by destruction of nervous tissue and by DNA excretion by activated lymphocytes [2] because of developing autoimmune reactions.We compared plasma DNA levels in two types of nervous system involvement associated with destruction of brain structures of different extent: ex-

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