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

1) It is generally accepted that the adequate environmental temperature to rear rats is about 23 degrees C, but the adequate temperature that directly contacts to the animal's skin seems to be about 30 degrees C. 2) The blood pressure increased on cold exposure or stimulation. There was a case that the blood pressure increased slightly on hot exposure. This suggests that it is necessary to pay close attention to the condition of warming-up at the indirect measurement of blood pressure. 3) Apoplexy seemed to occur earlier at the low environmental temperature, and the blood pressure seemed to increase also at the high temperature. However, these temperature effects on blood pressure and the incidence of stroke were not so obvious as observed in rearing SP with 0.9% salt solution for drinking.
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PMID:Blood pressure in stroke-prone SHR (SHRSP) exposed to unusual environmental temperature. 73 3

Heat tolerance was assessed by magnitude of strain induced in the body as a whole by heat load. The strain was represented by a combination of relative water loss, relative rise in rectal temperature and relative salt loss, using those critical values of the three factors which cause heat stroke (40.6 degrees C), water depletion heat exhaustion (7% of body weight) and salt depletion heat exhaustion (0.75 g per kg of body weight). As this numerical heat tolerance index is defined as the degree of disturbance induced by heat exposure concerning thermal regulation, water and electrolyte metabolism, the magnitude of the index is inversely proportional to that of heat tolerance. Our studies showed that adaptive changes in heat tolerance of unacclimatized subjects during short-term heat acclimatization could be followed up by this heat tolerance index and that superior heat tolerance of residents in subtropical zone and athletes could by reasonably evaluated by the index. Thus, it might be said that this numerical heat tolerance index is a reliable index for the assessment of heat tolerance.
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PMID:Index for the assessment of heat tolerance. 75 47

Hemodynamics and plasma renin activity were measured in 20 ambulatory hospital inpatients with untreated mild to moderate essential hypertension. The control measurements were made after a period of four to seven days just on a diet containing 10 mEq sodium per day. The measurements were repeated following a week of oral propranolol hydrochloride therapy plus the low salt diet. Heart rate (P less than .001), mean arterial pressure (P less than .001), cardiac output (P less than .05), and plasma renin activity (P less than .05) were reduced in the majority of these patients following propranolol therapy but stroke volume increased (P less than .05). Corrected ejection time and total peripheral resistance did not show significant change. The antihypertensive effect of propranolol could not be related to its hyporeninemic effect or to the fall in cardiac output. Under the experimental conditions of this study, no single parameter, either hemodynamic or plasma renin activity, was predictive of a definite antihypertensive response to propranolol therapy.
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PMID:Hemodynamic and plasma renin effects of propranolol in essential hypertension. 84 47

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

Four trained men worked 4 h/day at 40-50% of their maximum aerobic capacity first for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Between days 1 and 2 of heat exposure mean total circulating protein (TCP) and plasma volume (PV) increased 11.6% and 9%, respectively. Preexposure TCP and PV increased until day 6 of heat exposure. Of the protein fractions beta-globulins underwent the largest relative increase. During work movement of protein into and out of the vascular compartment was similar in control and acclimatizing subjects but the latter generally maintained a greater amount of protein and fluid within the vascular volume. There was no evidence of salt and water retention. The increase in vascualr volume was ascribed to transfer of interstitial protein and water to the vascular volume. Regression coefficients indicated significant correlations for changes in plasma volume versus heart rate, stroke volume, and cardiac output during acclimatization. It was concluded that the most critical event in heat acclimatization is the expansion of the plasma volume.
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PMID:Acclimatization in a hot, humid environment: body fluid adjustments. 93 7

The hemodynamic effect of fusaric acid calcium salt (calcium salt of 5-butylpicolinic acid), an inhibitor of dopamine beta-hydroxylase, was studied in long-term administration of this agent in 10 elderly hypertensive patients. The hemodynamic items were measured by dye-dilution method before and 3 months, 6 months and one year after administration of fusaric acid calcium salt. The main hemodynamic changes observed were as follows: 1) Heart rate did not show any consistent change. 2) Systolic, diastolic and mean blood pressure decreased. The mean values of these pressures after fusaric acid calcium salt administration were significantly lower than the mean values before administration of this agent. 3) Total peripheral vascular resistance index decreased. The mean values of this index at 3 months, 6 months and one year after fusic acid calcium salt administration were significantly lower than the mean value before administration of this agent. 4) Cardiac index showed various changes throughout administration of fusaric acid calcium salt. The changes in this index might be secondary following the changes in total peripheral vascular resistance index, an inverse correlation being existed between them. 5) Stroke volume index showed almost a similar pattern of change as observed in cardiac index. An inhibitory action of fusaric acid calcium salt on the inotropism of the heart could be hardly found. 6) Plasma volume showed no tangible changes after fusaric acid calcium salt administration throughout one year. It might be concluded that fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.
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PMID:The long-term hemodynamic effect of fusaric acid in elderly hypertensive patients. 99 14

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

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. beta-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13-14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.
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PMID:Vascular lesions in hypertensive rats under salt loading: kidney renin and lysosomal enzymes. 107 69

In isolated guinea pig hearts performing a defined stroke work, the influence of heart work and substrate uptake on the interconversion of pyruvate dehydrogenase (PDH) was studied. When hearts from fasted animals are perfused with a salt solution containing 10mM glucose, an increase in cardiac output and aortic pressure effects an increase in active PDH from 50 to 74% of total PDH activity and a decrease in tissue content of energy-rich phosphates. Pyruvate turnover calculated from oxygen consumption corresponds with PDH activity. Under these experimental conditions, PDH activity might either represent the rate limiting step of oxidative glucose breakdown, or it might be adjusted to a flux rate controlled by other factors. In fed animals, PDH activity exceeds the pyruvate turnover. However, an increase of heart work raises the active PDH from 76 to 95%. Addition of 10 mM acetate to the perfusion medium decreases PDH activity and glucose uptake. In fed animals, an increase of heart work raises the active PDH from 43 to 59% only, whereas in fasted animals this effect is abolished. The effect of changes in heart work on PDH interconversion might be explained by changes in energy-rich phosphate concentrations. However, substrate uptake and nutritional state may interfere or even abolish this effect.
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PMID:[Influence of heart work and substrate uptake on the regulation of pyruvate dehydrogenase activity in isolated guinea pig hearts (author's transl)]. 117 27

A new model for studies on atherogenesis in the cerebrovascular system was obtained by using recently established stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP on a hypercholesterolemic diet (20% suet, 5% cholesterol, and 2% cholic acid) had ring-like fat deposits in the circle of Willis, which were detected within a few weeks by new techniques for the macroscopical demonstration of fat deposits "as a whole" and were proved to be good quantitative indices for the initiation of atherogenesis. Experimental studies using more than 200 rats including SHRSP, experimental hypertensive rats (renal infarction hypertension) and WK rats, fed a hypercholesterolemic diet with 1% salt in the drinking water for 1 week, 2 weeks, 10 weeks and more than 10 weeks, revealed that the arterial fat deposition in the brain was affected by BP, serum cholesterol level, strain difference and age. High BP was confirmed to be more important than the other factors by the quantitative analysis of sudanophilic rings in relation to BP.
Stroke
PMID:Hypertension as an important factor for cerebrovascular atherogenesis in rats. 126 3


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