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

The activities of monoamine biosynthetic enzymes were measured in brain regions of several hypertensive rat models at various ages. The types of hypertensive rats were the spontaneously hypertensive rat (SHR) and a stroke-prone substrain of the SHR as well as DOCA-salt and renal hypertensive rats. The genetically hypertensive rats had significantly elevated blood pressures as compared to the Wistar-Kyoto control rat after 5 weeks of age. During the early development of hypertension in the SHR, the activities of tyrosine hydroxylase in the hypothalamus and corpus striatum and of dopamine-beta-hydroxylase in the hypothalamus and pons-medulla were significantly higher than in the control rats. Tryptophan-hydroxylase was also elevated in the hypothalamus in SHR. From 3 to 8 weeks of age there appeared to be a significant correlation between hypothalamic dopamine-beta-hydroxylase activity and blood pressure in the hypertensive rats. In contrast, the activities of tyrosine hydroxylase and dopamine-beta-hydroxylase were slightly decreased in the DOCA-salt and renal hypertensive rats. It is suggested that noradrenergic or adrenergic neurons in the hypothalamus may participate in the initiation of elevated blood pressure in the genetic, but not in the DOCA-salt or renal hypertensive rats.
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PMID:Regional changes in the activities of aminergic biosynthetic enzymes in the brains of hypertensive rats. 1 54

Activities of aortae to produce prostaglandin (PG) I2-like substance in stroke-prone spontaneously hypertensive rats (SHRSP), stroke-resistant SHR (SHRSR) and normotensive control rats from the Wistar-Kyoto (WK) colony were compared. PGI2-like substance was produced by the incubation of the aortic ring in pH 9.0 borate-buffered saline and the amount produced was estimated by comparison of its anti-aggregatory activity with that produced by known amounts of the sodium salt of synthetic PGI2. Before the development of stroke, amounts of this substance generated in SHRSP and SHRSR were significantly higher than those in WK rats (p less than 0.01 and p less than 0.02, respectively). Remarkably reduced capacity to generate PGI2-like substance was observed in some SHRSP after the development of stroke.
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PMID:Production of prostacyclin-like substance in stroke-prone and stroke-resistant spontaneously hypertensive rats. 3 17

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

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

Twelve patients with clinical and hemodynamic evidence of severe congestive heart failure, unresponsive to the usual therapy of salt restriction, oxygen, bed rest, digitalis, and massive doses of diuretics, were studied during a control period and after intravenous dopamine. Seven patients survived and 5 died with intractable failure and shock despite transiently improved hemodynamic indices. At control period and after optimal dose of dopamine, there were no significant changes in heart rate (HR) and mean systemic arterial pressure. The mean pulmonary artery (PA) and pulmonary capillary wedge (PCW) pressures decreased slightly. Cardiac index (CI), stroke volume (SVI), and stroke work indices (SWI) rose (p less than 0.005) from the control values of 1.4 +/- 0.1, 15.3 +/- 5, and 13.6 +/- 1.7 to 2.2 +/- 0.1, 24.1 +/- 4, and 24 +/- 2.3, respectively; pulmonary arteriolar (PAR), total pulmonary vascular (TPVR), and systemic vascular (SVR) resistances fell (p less than 0.01). Urine output increased from 13.5 ml/hr before to 58.2 ml/hr after dopamine (p less than 0.005). After 24 and 48 hr of dopamine, in addition to the above hemodynamic changes, PA pressure fell from 38 +/- 4 to 33 +/- 3 and 28 +/- 2, and PCW from 30 +/- 2 to 24 +/- 3 and 18 +/- 3 (p less than 0.05). Compared with nonsurvivors, survivors had significant decreases in PA and PCW pressures, PAR, and TPVR and an increase in SWI. These data indicate that dopamine is effective in some patients with refractive congestive heart failure associated with acute oliguric renal failure and that the prognosis may be improved.
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PMID:Hemodynamic effects of dopamine in patients with resistant congestive heart failure. 35 38

The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
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PMID:The toxicity of salt. 35 85

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.
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PMID:Renin-angiotensin system in stroke-prone spontaneously hypertensive rats. 42 75

Rapid administration of intravascular volume expanders is often necessary during anesthesia. Significant controversy still exists on the relative values of different volume expanders. Fifteen hypoxemic patients (Pao2 less than 70 torr on room air) were studied preoperatively. They were randomized into three groups. One group received 1.5 ml/kg of 25% salt-poor human albumin, a second group, 7 ml/kg of fresh frozen plasma; a third group, 7 ml/kg of 0.9% NaCl in water (normal saline). The infusions were given intravenously and completed in 20 minutes. Changes in hemodynamic pressures and flows, blood chemistries, and oxygen uptake and transport variables were studied. It was concluded that fresh frozen plasma afforded the greatest increase in cardiac output and oxygen availability with the least increase in left ventricular stroke work. Colloid osmotic pressure was more significantly increased by fresh frozen plasma than by salt-poor human albumin. Normal saline caused both a decrease in oxygen availability and colloid osmotic pressure. Pulmonary venous admixture increased to some extent in all patients receiving fresh frozen plasma or normal saline. In three patients, this increase was very marked and accompanied by severe arterial hypoxemia.
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PMID:Rapid volume expansion in patients with interstitial lung diseases. 57 Dec 16

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.
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PMID:What makes the renin-angiotensin system a pathogenic factor? 69 4

1. Liver nuclei from estrogenized chickens contain high-affinity low-capacity estrogen-binding sites, which are in part salt-extractable (60--70%) and in part tightly sticking to the nuclear residue (30--40%). During the preparation of chromatin with low salt buffers part of the salt-extractable nuclear-binding sites remains together with the non-extractable sites on the chromatin. Extractable and non-extractable sites can be separated by agarose as well as hydroxyapatite chromatography. 2. The extrogen-binding protein extracted from crude nuclei was characterized as follows: sedimentation coefficient of 3.9 S, Strokes' radius (a) of 3.3 nm, molecular weight (Mr) of 56,000 and frictional ratio (f/fo) of 1.20. Trypsination results in a globular receptor fragment (Mr = 41,000), which has lost a small asymmetric portion of the receptor molecule but still binds estradiol. 3. In contrast to the binding protein from crude nuclei the estrogen-binding protein extracted from purified nuclei at pH 7.4 is found mainly in an aggregated form. Dissociation of the aggregates is achieved in high salt/urea resulting in a receptor molecule with an apparent molecular weight of 130,000. Aggregation of the binding sites can be prevented to some extent by raising the pH of the extraction medium. At pH 8.7 the non-aggregated part of the binding protein from pure nuclei could be characterized as follows: 4.4 S, a = 4.3nm, Mr = 80,000 (apparent molecular weight of 150,000), f/fo = 1.40. 4. Mixing experiments indicate that an extranuclear protease present in a crude nuclear preparation converts the large receptor (the binding protein from pure nuclei) to the smaller one (the binding protein from crude nuclei) by digesting off an asymmetric portion of the molecule. This portion seems to be responsible for the strong tendency of the binding protein from pure nuclei to associate with other nuclear components.
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PMID:Estrogen-binding sites of chicken liver. Preliminary characterization of nuclear components. 72 Mar 32


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