[Frontiers in Bioscience 2, a9-12, May 15, 1997]

	[Frontiers in Bioscience 2, a9-12, May 15, 1997] CAVEAT LECTOR
	MAGNESIUM PROTECTS AGAINST COCAINE-INDUCED HEMORRHAGIC STROKE IN A RAT MODEL: A ³¹P-NMR IN-VIVO STUDY Burton M. Altura^1,2,3, Asefa Gebrewold¹, Bella T. Altura^1,3, And Raj K. Gupta⁴ Departments of Physiology¹ and Medicine², and The Center for Cardiovascular and Muscle Research³, State University of New York, Health Science Center at Brooklyn, 450 Clarkson Avenue, Brooklyn, New York 11203 and Department of Physiology and Biophysics⁴, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461 Received 4/2/97; Accepted 5/5/97; On-line 5/15/97 2. INTRODUCTION Cocaine abuse results in an increased incidence of aneurysmal subarachnoid hemorrhages, intracerebral hemorrhages, brain edema and occlusion-type strokes in humans (for reviews see 1-3). Recently, it has been reported that cocaine administration to anesthetized rats can produce subarachnoid and intracerebral hemorrhagic strokes which result in rapid, significant deficits in whole brain intracellular free magnesium ions ([Mg²⁺]_i, falls in intracellular pH (pHi), progressive loss of phosphocreatine (PCr) and elevation of inorganic phosphate (Pi) up until death (4). Other studies demonstrate that cocaine can produce direct vasospasm of cerebral blood vessels (5,6) concomitant with rapid loss of [Mg²⁺]_i (3) and cellular uptake/release of Ca²⁺ (8). In vivo ³¹P-NMR spectroscopic studies were undertaken to determine whether: 1. systemic administration of Mg²⁺ could protect animals against cocaine-induced hemorrhagic stroke; and 2. a relationship exists between basal levels of brain [Mg²⁺]_i and stroke risk. Since most cocaine abusers imbibe at least two or more doses of cocaine separated by intervals of time, in order to trigger the stroke (2,3,9), we developed a rat model to simulate the clinical experience.

[Frontiers in Bioscience 2, a9-12, May 15, 1997]
CAVEAT LECTOR

MAGNESIUM PROTECTS AGAINST COCAINE-INDUCED HEMORRHAGIC STROKE IN A RAT MODEL: A ³¹P-NMR IN-VIVO STUDY

Burton M. Altura^1,2,3, Asefa Gebrewold¹, Bella T. Altura^1,3, And Raj K. Gupta⁴

Departments of Physiology¹ and Medicine², and The Center for Cardiovascular and Muscle Research³, State University of New York, Health Science Center at Brooklyn, 450 Clarkson Avenue, Brooklyn, New York 11203 and Department of Physiology and Biophysics⁴, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461

Received 4/2/97; Accepted 5/5/97; On-line 5/15/97

2. INTRODUCTION

Cocaine abuse results in an increased incidence of aneurysmal subarachnoid hemorrhages, intracerebral hemorrhages, brain edema and occlusion-type strokes in humans (for reviews see 1-3). Recently, it has been reported that cocaine administration to anesthetized rats can produce subarachnoid and intracerebral hemorrhagic strokes which result in rapid, significant deficits in whole brain intracellular free magnesium ions ([Mg²⁺]_i, falls in intracellular pH (pHi), progressive loss of phosphocreatine (PCr) and elevation of inorganic phosphate (Pi) up until death (4). Other studies demonstrate that cocaine can produce direct vasospasm of cerebral blood vessels (5,6) concomitant with rapid loss of [Mg²⁺]_i (3) and cellular uptake/release of Ca²⁺ (8).

In vivo ³¹P-NMR spectroscopic studies were undertaken to determine whether: 1. systemic administration of Mg²⁺ could protect animals against cocaine-induced hemorrhagic stroke; and 2. a relationship exists between basal levels of brain [Mg²⁺]_i and stroke risk. Since most cocaine abusers imbibe at least two or more doses of cocaine separated by intervals of time, in order to trigger the stroke (2,3,9), we developed a rat model to simulate the clinical experience.