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

1. Oral administration of DL-alpha-tocopheryl nicotinate (EN) (0-04 or 0-2 mmol day-1 kg-1) or DL-alpha-tocopharyl acetate (EA) (0-2 mmol day-1 kh-1) delayed the progress of hypertension in unilaterally nephrectomized rats, which were treated with deoxycorticosterone and salt, and in genetically hypertensive rats (SHR) which were given sodium chloride solution. Suppression of body weight gain, incidence of pneumonia and mortality were reduced by treatment with EN or EA. 2. Severe hypertension in old SHR (9 months) further progressed, when drinking water was replaced by sodium chloride solution, and four out of ten of these animals died of cerebral haemorrhage during 4 weeks. The administration of EN or EA prevented the increase in blood pressure and incidence of stroke.
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PMID:Anti-hypertensive action of DL-alpha-tocopharyl esters in rats. 107 97

Fifty-three patients with traumatic shock were injected 200-400 ml of a 10% solution of sodium chloride in combination with 100 ml of the 40% solution of glucose. The continuous, for 1-2 h, elevation of arterial pressure, increased minute blood circulation volume, cardiac index, stroke volume were noted. At the same time base deficiency in blood was growing. So, in the last 5 patients the infusion therapy at the prehospital stage was completed by injecting 200 ml of 3% sodium solution and the acid-base state in them was thus leveled. When using the "internal autotransfusion" lethality was reliably less than in patients who were treated by routine (polyglucon, gelatinole) infusion therapy.
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PMID:[The use of the "internal autotransfusion" method in complex shock-control measures at the prehospital stage]. 130 53

Septic shock in young children is often characterized by clinical findings consistent with a reduction in cardiac index (CI) and elevation of systemic vascular resistance index (SVRI). In this context, infusion of inotropic agents, alone or in combination with vasodilators, has been recommended. We have utilized group B streptococcal (GBS) infusion in piglets to develop a model of low-CI/high-SVRI septic shock, and report here the effects of the combination of epinephrine (EPI) plus either nitroglycerin (NG) or nitroprusside (NP) in this model of infant sepsis. Piglets were anesthetized, intubated, and ventilated. All piglets received GBS continuously for 90 minutes and were further divided into three experimental groups. Group 1 received NG 16 micrograms/kg.min plus EPI 2 micrograms/kg.min; group 2 received NP 10 micrograms/kg.min plus EPI 2 micrograms/kg.min, and group 3 received 0.9% sodium chloride (saline) only. CI, which fell for all three groups at the onset of GBS infusion, rose significantly in group 2 animals (but not in groups 1 and 3). This effect was mediated entirely by an increase in myocardial stroke volume. Aortic blood pressure, initially unaffected by GBS infusion, rose significantly in both group 1 and 2 compared with group 3. SVRI, which rose for all three groups at the onset of GBS infusion, was further markedly elevated in group 1 (but not in groups 2 and 3). Pulmonary artery pressure and pulmonary vascular resistance index, both significantly increased after GBS infusion, were reduced in group 2 but not groups 1 and 3. These observations illustrate the potential for unexpected, and possibly detrimental, hemodynamic consequences when vasoactive agents are combined in young septic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of combining epinephrine with nitroglycerin or nitroprusside during group B streptococcal sepsis in piglets. 141 51

A newborn is described, who was born in term with 3250 g weight, after intrauterine hypoxia. She was born with vacuum extraction, and suffered from birth trauma and intrauterine infection. At age of one day manifested an eclampsia, which was hardly diminishable. The serum Na level was 118 mmol/l. Bilateral adrenal apoplexy was visible with ultrasound. The newborn was treated with infusion of sodium chloride and glucose, with antibiotic and glucocorticoid hormone. Her condition improved rapidly. Her serum cortisol level at 8 and 15 day after stopping of 12 days prednisolon therapy was below 2.5 micrograms/dl, marking hypadrenia. At age 3 months the function of adrenals was normal: the serum cortisol level was 11.4 micrograms/dl, and after ACTH stimulation it run up to 44.5 micrograms/dl. By screening of 1491 newborns, 13 adrenal apoplexy was found. The other 12 were one-sided and symptomless.
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PMID:[Bilateral neonatal adrenal hemorrhage associated with hypoadrenalism]. 158

The effect of salt intake on the hypertensive response to long-term infusion of endothelin-1 was investigated. Chronically instrumented male Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that included 3 control days followed by 7 days of endothelin-1 infusion at 5.0 pmol.kg-1.min-1 and 5 days of recovery. Rats were maintained on either a normal sodium chloride intake (2.0 meq Na+ per day; normal sodium) or a high sodium chloride intake (6.0 meq Na+ per day; high sodium) throughout the protocol. Control rats received normal or high sodium intakes but not endothelin-1. In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Cardiac output, stroke volume, water balance, and urinary sodium and potassium excretion remained unchanged. Termination of endothelin-1 infusion resulted in rapid normalization of both arterial pressure and peripheral resistance. In contrast, normal sodium rats exhibited no alteration in mean arterial pressure, heart rate, total peripheral resistance, stroke volume, water balance, or urinary sodium and potassium excretion throughout the endothelin-1 infusion protocol. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension.
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PMID:Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 159 49

1. To determine the effect of chloride ion on the development of hypertension and the incidence of cerebral lesions in stroke-prone spontaneously hypertensive rats (SHRSP), groups of 10 rats were administered chronically with either 171 mmol/L sodium chloride or equimolar sodium provided as sodium citrate in the drinking water from the age of 12 weeks. 2. The life span was significantly extended in SHRSP given sodium citrate (336 +/- 28 vs 246 +/- 26 days, mean +/- s.e.m., P less than 0.05) but their development of hypertension was not different from SHRSP given sodium chloride. 3. In order to determine the role of calcium homeostasis, calcium in urine was collected. Urinary calcium in SHRSP given sodium citrate was significantly decreased (1.0 +/- 0.12 vs 1.8 +/- 0.18 mg/24 h urine, P less than 0.05). 4. If the normal life span is 320 +/- 35 days, this suggests that chloride ion ingested with sodium accelerates the development of cerebrovascular diseases, and that increased urinary calcium excretion may be related to this adverse chloride effect on the development of hypertension in SHRSP.
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PMID:Chloride ion ingested with sodium affects the development of cerebral lesions in stroke-prone spontaneously hypertensive rats. 191 41

The relation between dietary intake of sodium chloride and blood pressure levels remains controversial. The critical questions concern whether there is a susceptible subgroup at risk of elevated blood pressure because of sodium chloride consumption. If there is such a subgroup, what is its size and how can it be identified? Further clinical trials are needed to determine the long-term effects of sodium chloride reduction on blood pressure. The risk of disease, including stroke and coronary heart disease, is linear with blood pressure levels. A small change in blood pressure can have a relatively large impact on disease, even within the normal range of blood pressure.
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PMID:Research and policy directions. Salt and blood pressure. 198 7

To evaluate the role of plasma chemistry in the genesis of electrical impedance of blood, a laboratory simulation was performed using solutions prepared so as to mimic plasma chemistry abnormalities that are seen in the critically ill. There was a 15% increase of impedance due to decrease in sodium chloride concentration from 140 mmol/L to 120 mmol/L, and a 12% decrease of impedance due to increase in sodium chloride to 160 mmol/L. Impedance changes secondary to other chemistry abnormalities were small and probably not significant, with the exception of a change of albumin concentration from 80 gm/L to 50 gm/L, which induced a 6% increase in impedance. Using this data, a model was constructed to predict changes in whole blood resistivity, and this was extrapolated in two simulations of plasma chemistry abnormalities to predict alterations of calculated impedance stroke volume in excess of 5%.
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PMID:The electrical impedance of plasma: a laboratory simulation of the effect of changes in chemistry. 204 72

We studied the effects of dietary Ca2+ on blood pressure, survival, and calcium channel function to investigate cardiovascular disease mechanisms in stroke-prone spontaneously hypertensive rats. Beginning at 3 weeks of age, rats were fed high sodium chloride diets (8.0%) in combination with either high (2.0%) or low (0.2%) Ca2+ diets for 8 weeks. At 12 weeks of age, survival was 90% in the high Ca2+ group and 30% in the low Ca2+ group. The higher blood pressure and lower survival in the low Ca2+ group suggest an intensification of altered vascular muscle cell mechanisms by a dietary Ca2+ deficit. Nimodipine (1-10 nM) effectively blocked L-type Ca2+ currents in isolated vascular muscle cells from both groups. Contraction of isolated cells that were not patch clamped to high potassium solutions were also blocked by 1 nM nimodipine. Disappearance of the L-type Ca2+ channel current was accelerated by holding at depolarizing potentials (positive to -50 mV) and by depolarizing steps to 0 mV. Nimodipine block of the L-type Ca2+ currents in vascular muscle is believed to contribute substantially to antihypertensive properties and stroke prevention, actions that may develop fully only in stroke-prone spontaneously hypertensive rats on a diet of at least normal Ca2+.
Stroke 1990 Dec
PMID:Effects of dietary calcium on nimodipine-sensitive calcium channel function in stroke-prone spontaneously hypertensive rats. 217 63

Stroke is a major cause of morbidity and mortality in the United States with 250,000 cases per year. Cerebral ischemia is the largest category of stroke with cardiac arrest, profound hypotension, and vascular occlusion the principal causes. Traditional approaches to the treatment of ischemic stroke focus on maintaining cardiac output, blood pressure, cerebral blood flow, and on preventing thrombosis. Recently, attention has been focused on developing new therapies that are directed toward abnormal biochemical events at excitatory synapses. Ischemia causes impairment of brain energy metabolism and the release of excessive amounts of glutamate into the extracellular space. This process secondarily excites neurons and further depletes energy stores. The excitotoxic hypothesis of brain injury proposes that glutamate is a principal cause of damage in ischemia. Three components of this hypothesis have been tested and largely proved in experimental studies in tissue culture and in animal models of stroke. First, elevated concentrations of glutamate cause excessive excitation at a subset of glutamate receptors, the N-methyl-D-aspartate (NMDA) receptor. Second, excitation at this receptor leads to excessive influx of sodium chloride and water which causes acute neuronal damage, and calcium which causes delayed and more permanent damage. Third, pharmacologic blockade at the NMDA receptor-ion channel complex prevents ischemic neuronal damage. Studies using specific pharmacologic compounds that block glutamate's action hold particular promise for treating stroke in humans, including competitive antagonists at the NMDA glutamate binding site (for example, 2-amino-5-phosphonovalerate, AP5), noncompetitive antagonists at the calcium channel (for example, MK-801, dextromethorphan, ketamine), and agents that might be directed at the glycine, zinc, and magnesium sites.
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PMID:Selective vulnerability of the brain: new insights into the pathophysiology of stroke. 254 55


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