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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of elevated temperatures and the time-temperature combinations for irreversible damage are outlined. Coagulation abnormalities and the effects on the kidney, liver, heart, brain and serum enzymes, the role of electrolytes and water, including salt deficiency and the controversial question of salt supplements, potassium deficiency, changes in other electrolytes and sweat solutes, and rhabdomyolysis (including a discussion of experimental work on dogs) are reviewed. The section ends with a discussion of the effects of drugs and an account of a recent fatal case of heat stroke which may have been triggered by chlorpromazine therapy.
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PMID:Heat illness. II. Pathogenesis. 32 Jul 24

Medical disorders related to environmental heat exposure are exceptionally common in persons who perform hard work in hot climates. They are also common in competitive athletes as well as in persons who participate in casual exercise to maintain health. The important issue of salt and water disturbances consequent to heavy sweating in hot climates is discussed in detail as are mechanisms of potassium deficiency and its implications. The major forms of environmental heat illness including heat syncope, heat cramp, heat exhaustion, and heat stroke are presented in detail with relevant clinical examples. A discussion of the differential diagnosis of hyperthermia and rhabdomyolysis follows. Because of the difference in treatment and complications, heat stroke is subdivided into the classic variety that affects the elderly and very young and that form that follows heavy physical work and is always associated with rhabdomyolysis. Because severe heat exhaustion and heat stroke are life-threatening disorders, the chapter includes a detailed discussion of complications and plans for treatment.
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PMID:Heat stroke and related heat stress disorders. 265 54

Considerable experimental evidence has accumulated to indicate that brain ischemia or stroke-like events will lead to rapid losses of brain potassium, magnesium, ATP, creatine phosphate and glucose. These events are usually followed by an uptake of sodium and calcium ions. Increased uptake or excess Ca2+ uptake in neuronal cells is thought to be the prime cause of neuronal death in the brain. Mg2+ deficiency is known to produce a host of neurological disturbances in man; experimentally, Mg2+ deficiency leads to excess uptake of Ca2+ in the brain. Strokes and transient ischemic attacks also are known to be associated with neurological disturbances and ionic changes in the brain. Stroke patients have been reported to exhibit deficits in serum and CSF [Mg]. Acute Mg or K deficiency can produce cerebrovasospasm, at least experimentally. The lower the extracellular concentration of either Mg2+ or K+, the greater the magnitude of cerebral arterial contraction. These cerebrovascular contractions induced by lowering either the [Mg2+]0 or [K+]0 cannot be antagonized or attenuated by known pharmacologic antagonists. The cerebrovasospasms produced upon lowering [Mg2+]0 can be modulated by [K+]0 and vice versa; e.g. the lower the [K+]0, the greater the degree of vasospasm upon withdrawal of [Mg2+]0 and vice versa. Lowering [Mg2+]0 in situ and in vitro results in increased uptake of Ca2+ in the brain and the cerebral arteries. Cerebrovasospasms induced by substances that are known to be released in the brain on injury, such as prostanoids and serotonin, are relaxed dramatically by addition of [Mg2+]0. Infusions of MgSO4 into the brain via the internal carotid artery produces dose-dependent lowering of systolic and diastolic blood pressure as well as dose-dependent vasodilatation of arterioles (17-30 micron) and venules (18-40 micron) in the cerebral microcirculation, as observed by direct in situ high-resolution TV image-intensification microscopy. In clinical studies, infusion of MgSO4 has been reported to alleviate cerebrovasospasms. Epidemiological evidence is accumulating to suggest that consumption of fruit and vegetables (foodstuffs relatively high in K and Mg, and low in Na) is associated in certain geographic regions with a lower than normal incidence of strokes, particularly that of cerebral hemorrhage. On the basis of such data, and the findings reported herein, we believe one must consider that certain types of cerebrovascular accidents, transient ischemic attacks and 'classical' migraine attacks may be associated with a 'true' Mg deficiency and altered fluxes of K+ ions in the brain and CSF.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of Mg and K on cerebral vessels--aspects in view of stroke. Review of present status and new findings. 639 42

Twenty nine full term haemophiliac neonates and babies, aged eight months with acute intracerebral haemorrhage are reported: four babies with haemophiliac status, one with intracerebellar bleeding due to microvascular malformation, and 24 babies in whom the cause of bleeding could not be established (probably vitamin-K deficiency). Fourteen surgeries were performed in ten babies. When dramatic neurological signs of spontaneous cerebral stroke develop in a term newborn or a baby they require immediate ultrasonographic examination. This noninvasive method can be repeated without risk to disclose all changes into the bleeding focus before and after surgical treatment. Selective cerebral angiography was exceptionally recommended for detection of suspected vascular malformation. Lumbar puncture was performed in more than one third of patients to confirm subarachnoid bleeding. However, this method has not been accepted being the purposeless and risky. Pharmacotherapy should be quickly used to correct the supposed vitamin-K deficiency and for replacement of relevant missing plasma factor of the prothrombin complex. To stop bleeding and to secure surgery the replacement substitute must raise the factors' level at least by 50 percent. The treatment of choice is vitamin-K1, 1-3 mg and fresh frozen plasma 10ml/kg of body weight. The neurological recovery was in general satisfactory after the stabilization of acute clotting disorder was achieved. Eight babies died (28 percent), five of them were admitted in deep comatose state.
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PMID:[Spontaneous intracranial hemorrhage in term neonates and infants]. 771 42

Significant reduction in bone mineral density (BMD) occurs in stroke patients on the hemiplegic and contralateral sides, correlating with the degree of paralysis and vitamin D and K deficiency due to malnutrition, and increasing the risk of hip fracture. We evaluated the efficacy of vitamin K2 (menatetrenone: menaquinone-4; MK-4) in maintaining BMD by comparing serum biochemical indices of bone metabolism between treated and untreated patients. In a random and prospective study, of 108 hemiplegic patients following stroke, 54 received 45 mg menatetrenone daily (MK-4 group, n = 54) for 12 months, and the remaining 54 (untreatment group) did not. Nine patients excluded from the study. The BMD in the second metacarpals and serum indices of bone metabolism were determined. BMD on the hemiplegic side increased by 4.3% in the MK-4 group and decreased by 4.7% in the untreated group (p < 0.0001), while BMD on the intact side decreased by 0.9% in the MK-4 group and by 2.7% in the untreated group (p < 0.0001). At baseline, patients of both groups showed vitamin D and K1 deficiencies, high serum levels of ionized calcium, pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), and low levels of parathyroid hormones (PTH) and bone Gla proteins (BGP), indicating that immobilization-induced hypercalcemia inhibits renal synthesis of 1, 25-dihydroxyvitamin D (1, 25-[OH]2D) and compensatory PTH secretion. Both vitamins K1 and K2 increased by 97.6% and 666.9%, respectively, in the MK-4 group. Correspondingly, a significant increase in BGP and decreases in both ICTP and calcium were observed in the MK-4 group, in association with a simultaneous increase in both PTH and 1, 25-[OH]2D. One patient in the untreated group suffered from a hip fracture, compared with none in the MK-4 group. The treatment with MK-4 can increase the BMD of disused and vitamin D- and K-deficient hemiplegic bone by increasing the vitamin K concentration, and it also can decrease calcium levels through inhibition of bone resorption, resulting in an increase in 1, 25-[OH]2D concentration.
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PMID:Menatetrenone ameliorates osteopenia in disuse-affected limbs of vitamin D- and K-deficient stroke patients. 973 52

Compared to the prehistoric diet, the modern human diet contains not only excessive NaCl and deficient K+, but also deficient precursors of HCO3- and sometimes excessive precursors of nonvolatile acid. The mismatch between the modern diet and the still ancient biological machinery of humans subtly but chronically disorders their internal milieu, giving rise to a prolonged state of low-grade potassium deficiency and low-grade metabolic acidosis whose severity increases with age. Supplemental KCI cannot redress this mismatch and correct this state. However, the mismatch is redressed and the state corrected by restoring intakes of K+ and HCO3- to levels approaching those in the diet of our prehistoric forebearers, with either fruits and vegetables or with supplemental KHCO3. So restored, KHCO3 can: 1) attenuate hypertension and possibly prevent its occurrence by suppressing the phenomenon of normotensive NaCl-sensitivity, in part by its natriuretic effect; (2) prevent kidney stones by reducing urinary excretion of calcium and increasing urinary excretion of citrate; (3) ameliorate and protect against the occurrence of osteoporosis by increasing the renal retention of calcium and phosphorus, and by suppressing bone resorption and enhancing bone formation; and (4) likely prevent stroke.
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PMID:Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. 1051 88

NXY-059, an alpha-phenyl-N-tert-butyl nitrone derivative, is a free radical-trapping agent presently in late clinical trials as a potential neuroprotectant limiting reperfusion injury following acute stroke. Two recent trials suggest that NXY-059 causes hypokalemia and associated cardiac disturbances. With regard to the mechanism of such association, most investigators agree that potent trapping of free radicals leads to the 11 beta-hydroxysteroid dehydrogenase blockade in kidneys, diminishing renal hydrocortisone oxidation and increasing K(+) ion urine excretion. Importantly, potassium deficiency represents the major avoidable cause of the array of serious cardiac adverse reactions: QT-prolongation, Torsades de pointes and other life-threatening arrhythmias, and higher risks for perioperative cardiopulmonary resuscitation and cardiac death. Because a prime target for NXY-059 use will likely be acute strokes in the emergency room environment, the potential combination of the drug with intensive therapy including fluid infusions, particularly with diuretics, might be especially harmful because of the synergic depletion of potassium, which might also jeopardize the fate of the novel nitrone neuroprotectant.
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PMID:Hypokalemia, cardiac failure, and reporting NXY-059 safety for acute stroke. 1722 Apr 68

Dietary potassium intake has been demonstrated to significantly lower blood pressure (BP) in a dose-responsive manner in both hypertensive and nonhypertensive patients in observational studies, clinical trials, and several meta-analyses. In hypertensive patients, the linear dose-response relationship is a 1.0 mm Hg reduction in systolic BP and a 0.52 mm Hg reduction in diastolic BP per 0.6 g per day increase in dietary potassium intake that is independent of baseline potassium deficiency. The average reduction in BP with 4.7 g (120 mmol) of dietary potassium per day is 8.0/4.1 mm Hg, depending race and on the relative intakes of other minerals such as sodium, magnesium, and calcium. If the dietary sodium chloride intake is high, there is a greater BP reduction with an increased intake of dietary potassium. Blacks have a greater decrease in BP than Caucasians with an equal potassium intake. Potassium-induced reduction in BP significantly lowers the incidence of stroke (cerebrovascular accident, CVA), coronary heart disease, myocardial infarction, and other cardiovascular events. However, potassium also reduces the risk of CVA independent of BP reductions. Increasing consumption of potassium to 4.7 g per day predicts lower event rates for future cardiovascular disease, with estimated decreases of 8% to 15% in CVA and 6% to 11% in myocardial infarction.
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PMID:The importance of potassium in managing hypertension. 2140 95