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Biomedical subjects

E B Flink

Publications and source records attributed to E B Flink.

At least 19 recordsLinked to original sources
PubMed1992

High-dose magnesium sulfate attenuates pulmonary oxygen toxicity.

BACKGROUND AND METHODS: Rats rapidly develop respiratory distress when exposed to 100% oxygen and die within a few days. Autopsy of the lung shows severe histologic damage characteristic of the adult respiratory distress syndrome. The purpose of this study was to evaluate the effects of magnesium sulfate loading in a rat model of acute oxygen toxicity. Thirty-four rats were divided into three groups. Group 1 (n = 18) served as a control (no magnesium therapy), while group 2 (n = 8) and group 3 (n = 8) received varying amounts of magnesium sulfate. All animals were exposed to 100% oxygen for 96 hrs or until death. Lung damage was quantitated by measuring the lung injury score on histologic examination. RESULTS: Administering magnesium sulfate in moderate doses at infrequent intervals to rats (group 2) resulted in less severe oxygen-induced lung damage than that which occurred in rats not receiving magnesium (control group). However, the difference was not statistically significant. Rats (group 3) given doses of magnesium sulfate in amount and frequency adequate to maintain a serum magnesium concentration recognized as therapeutic in eclampsia significantly reduced oxygen-induced lung damage. CONCLUSION: High-dose magnesium sulfate therapy can reduce lung injury caused by acute oxygen toxicity in rats.

Animals↗
PubMed1992

Cardioskeletal mitochondrial myopathy associated with chronic magnesium deficiency.

A 3-year-old boy presenting with convulsions and carpopedal spasm had hypomagnesemia and hypermagnesuria due to congenital magnesium-losing nephropathy. Despite chronic oral and intermittent intravenous magnesium supplementation, he remained chronically hypomagnesemic. At age 4, he developed a progressive proximal myopathy and dilated hypertrophic cardiomyopathy that ultimately contributed to his death at age 14 years. Skeletal and cardiac muscle specimens showed a mitochondrial myopathy with increased numbers of enlarged, structurally abnormal mitochondria. Muscle magnesium content was markedly decreased. Chronic oral and intermittent intravenous magnesium supplementation may be inadequate to prevent the progressive cardioskeletal myopathy associated with the chronic magnesium deficiency of congenital magnesium-losing nephropathy.

Biopsy↗
PubMed1990

Magnesium deficiency.

Over the past 40 years, human magnesium deficiency has become recognized as a world-wide clinical problem. In 1926, Leroy (1), demonstrated the absolute need of magnesium for growth and life in mice, and the need for magnesium in plants was demonstrated in 1860. Although clinical deficiency was first reported in 1934, it was not until the 1950s that interest in clinical magnesium deficiency developed rapidly. Before the 1950s, textbooks of medicine, pediatrics and biochemistry did not mention magnesium disturbances. In this paper I shall emphasize the recognition and treatment of magnesium deficiency by giving details of the setting, i.e. illnesses, the multifaceted manifestations, the laboratory findings and safe protocols for treatment.

Animals↗
PubMed1987

Hypomagnesemia.

Explore the source record for details and available documents.

Humans↗
PubMed1986

Magnesium deficiency in alcoholism.

Significant magnesium deficiency occurs in chronic alcoholism. The evidence depends on a number of related lines of evidence: hypomagnesemia, a number of clinical symptoms in common with patients with nonalcoholic causes of magnesium deficiency, induction of magnesium excretion by alcohol ingestion (167-260% of control values), positive magnesium balance on alcohol withdrawal (average 1.15 meq/kg), decreased exchangeable magnesium (28Mg, mean deficit 1.12 meq/kg), a mean deficit of 11.4 meq/kg of fat-free dry weight of muscle of alcoholic patients, and hypocalcemia responsive only to magnesium therapy. When alcohol is withdrawn, free fatty acids rise sharply and plasma magnesium falls. Respiratory alkalosis occurs abruptly also on alcohol withdrawal. The alkalosis and rise of free fatty acids with concomitant fall of magnesium produces an acute instability of the internal milieu and could result in acute symptoms. There also are a number of nutritional deficiencies which need to be cared for, but magnesium, thiamine, and other B vitamins need to be administered immediately. Potassium and phosphorus should be supplied when they are low.

Alcoholism↗
PubMed1985

Hirsutism. Pathophysiology, clinical evaluation, treatment.

Hirsutism is generally an androgen-mediated disorder. Tremendous progress has been made in elucidating the numerous clinical disorders that can cause it. Systematic evaluation of hirsute women must be directed at determining the cause of hyperandrogenemia, which in turn allows specific and effective therapy to be initiated.

Adenoma↗
PubMed1985

Magnesium deficiency in human subjects--a personal historical perspective.

Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.

Adolescent↗
PubMed1979

Relationship of free fatty acids and magnesium in ethanol withdrawal in dogs.

A group of dogs was conditioned to drink 4-6 g ethanol/kg/day for long periods. Ethanol ingestion was interrupted at monthly intervals in order to study some metabolic changes of the withdrawal period. Plasma long chain free fatty acids (FFA) increased by a maximum mean of 1.4 meq/liter (threefold), and magnesium (Mg) decreased by a maximum mean of 0.4 meq/liter (75% of control during the first 24 hr of simple ethanol withdrawal. Because magnesium salts of FFA are very insoluble, these divergent changes of Mg and FFA suggest that lipolysis may be responsible for the hypomagnesemia that occurs in ethanol withdrawal. In order to control lipolysis, glucose-insulin, glucose alone, and fructose alone were given intravenously for a 4-hr period beginning 14 hr after withdrawal. FFA fell by a maximum of 65% or 0.44 meq/liter and Mg fell by a maximum of 0.31 meq/liter during the glucose-insulin infusions. Nicotinic acid (10-20 mg/kg) in saline produced an identical drop in FFA and a slight rise in Mg. After stopping the nicotinic acid infusion, a sharp rebound rise in FFA and a sharp fall in Mg occurred similar to the simple withdrawal experiments. The sharp divergent changes in FFA and Mg after cessation of nicotinic acid infusion support the prime role of FFA-effecting movements of Mg and the thesis that FFA bind Mg. Control of lipolysis is theoretically sound in therapy of the ethanol withdrawal syndrome.

Alcoholism↗