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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male and female virgin rats and breeder rats with naturally-occurring diabetes, hypertension and arteriosclerosis, were made severely diabetic with a single, subcutaneous injection of alloxan (10 mg/100 g b.w.), after an 18 h fast. During five months of unrelenting diabetes, some animals became obese while others became emaciated. Only the emaciated animals survived but they were blind, their adrenal glands were hemorrhagic, hypertrophied and thrombosed, thymi involuted, kidneys swollen, hearts reduced in size while testes and ovaries were atrophic. Serum CPK, SGOT and SGPT were elevated concomitant with extensive cardiovascular damage, hepatic steatosis and generalized catabolism. Circulating triglycerides and free fatty acids were markedly elevated with total cholesterol only slightly increased. BUN and serum calcium levels were also greatly elevated. Sub-normal Cmpd. B levels indicated impaired adrenal steroidogenesis. Virgin rats developed arteriosclerosis and male and female breeder rats showed exacerbation of their pre-existing aortic sclerosis as well as P.A.N. lesions in their small-sized arteries. It is believed that severe diabetes causes exacerbation of the endogenous hormonal milieu resulting from abnormal hypothalamic-pituitary-adrenal function induced by repeated breeding, which conditions the connective tissue components of the arterial wall of rats toward accelerated degenerative changes.
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PMID:Polyarteritis nodosa induced in arteriosclerotic, male and female breeder rats by chronic alloxan diabetes. 1 32

The elevated blood pressure of spontaneously hypertensive rats (SHR) was further exacerbated by subjecting these animals to surgically induced adrenal-regeneration hypertension (ARH). When chronic abnormally high blood pressure had been in effect for 12 weeks, the animals were subjected to an acute and massive myocardial infarction with isoprenaline. Hypertensive but intact SHR survived better than ARH-treated animals. Circulating enzyme (CPK, SGOT, SGPT and LDH), lipid and glucose levels and BUN manifested much greater excursions commensurate with more extensive myocardial infarction in ARH-treated than in intact SHR. ARH-treated SHR displayed a high incidence of atrial and ventricular thrombi associated with frequent left ventricular aneurysm formation. It is suggested that the more extensive myocardial connective tissue and ground-substance degeneration in ARH-treated SHR is due to the impoverished steroidogenic capacity of their regenerated adrenal glands.
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PMID:Myocardial infarction in spontaneously hypertensive rats with superimposed adrenal-regeneration hypertension. 50 86

Male and female, 100 days old, spontaneously hypertensive rats (SHR) were divided into two major groups: intact and uninephrectomized, given either no treatment, 1p.100 saline drinking water, 1p.100 saline + Deoxycorticosterone (DOC), or DOC alone. The DOC (Percorten pivalate) was given subcutaneously 2 times weekly, at a dose level of 2 mg/rat for 8 weeks. At autopsy, the combination of DOC + saline caused: the greatest exacerbation of blood pressure, marked catabolism, adrenal hypertrophy and thymic involution, little increase in heart weight, but a marked increase in kidney weight, elevated triglyceride and free fatty acids, cerebral and myocardial necrosis, fibrinous hyalinization of the cerebral, coronary, mesenteric, renal, testicular and ovarian arteries, foci of aortic cartilaginous metaplasia, PAN, foci of hepatic necrosis, and extensive lipid depletion from the zonae glomerulosa. Circulating corticosterone levels were suppressed to below normal levels. Excursion of circulating CPK levels coincided with the finding of myocardial necrosis and cerebral damage. It is suggested that the genetically-mediated hypertension of SHR is programmed through abnormal activity of the hypothalamic-pituitary axis and the specific morphologic make-up of arterial lesions is dependent upon the variety of adrenal or gonadal steroids secreted and their conditioning effect on the arterial wall.
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PMID:Arterial lesions and hypertension induced by saline, unilateral nephrectomy, and deoxycorticosterone in spontaneously hypertensive SHR rats. 51 39

Repeatedly-bred, male and female Sprague-Dawley rats which develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously were killed at sequential time intervals, i.e., when the females had completed 1, 2, 3 and 4 pregnancies. The control breeders received no treatment; the experimental animals were given 113 mg of clofibrate/100 g of b.w., subcutaneously, daily, 5 times per week. Clofibrate-treated breeders manifested reduction in blood pressure and in the incidence and severity of arterial disease characteristic of repeatedly-bred rats. The aortic lesions of the clofibrate-treated breeders showed attenuation of the usual severe ground substance alterations, the degenerative changes in connective tissue elements, e.g., fibrosis and elastosis, and absence of calcification and cartilaginous metaplasia. Clofibrate-treated breeders did not show any unusual elevation in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, or significant reduction of their hyperlipidemia. They manifested a definite reduction in adrenocortical and medullary histopathology and their circulating corticosterone levels were subnormal compared to non-treated breeders. It is suggested that the protective effect of clofibrate was mediated through its ability to block normal adrenal steroidogenic pathways rather than through its antilipemic action.
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PMID:Clofibrate retardation of naturally-occurring arteriosclerosis in repeatedly-bred male and female rats. 66 83

Adrenal regeneration hypertension (ARH) was induced in virgin and breeder, spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. The blood pressure of the previously normotensive, virgin, SD rats and the SD breeder rats with preexistent mild hypertension became greatly elevated. ARH caused an increase in the preexisted severe hypertension in SHR virgin and breeder rats. Serum enzymes, e.g., CPK, SGOT and LDH, were greatly elevated concomitant with the finding of old and new foci of myocardial necrosis. ARH produced a dichotomous metabolic effect, i.e., elevated cholesterol, glucose, and corticosterone levels in SD rats but reduced levels in SHR rats. The zonae glomerulosae of the the regenerated adrenal glands of SD rats were devoid of lipid whereas the zonae glomerulosae of SHR rats were full of lipid. Intact SHR breeder rats develop arterial lesions confined to their reproductive organs but after ARH treatment, they were found to have aortic, coronary and renal arterial lesions which were similar to those which occur, spontaneously, in SD breeder rats. It is suggested that changes in the spectrum of adrenal steroids produced during ARH may contribute to the diverse metabolic changes and the alterations in the usual cardiovascular degenerative changes found in these two strains.
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PMID:Comparative effects of adrenal regeneration hypertension on non-arteriosclerotic and arteriosclerotic Sprague-Dawley vs spontaneously hypertensive rats. 83 44

Repeatedly bred male rats which develop arteriosclerosis spontaneously were subjected to unilateral nephrectomy, 1% saline drinking water, and 2 mg subcutaneous injections of deoxycorticosterone acetate per animal weekly for 7 weeks to induce severe hypertension (+/- 175 mmHg systolic). Acute cerebral ischemia was induced by ligating one carotid artery. Two days later, experimental animals were subjected to acute myocardial ischemia by injecting them subcutaneously with a single dose of isoproterenol (25 mg/100 g body weight). All of the experimental animals died within 4 hours of the injection of isoproterenol. During this same period, blood pressure, body weight, thymus, kidney, and testicular weights were reduced, whereas heart and adrenal gland weights increased markedly. Serum enzymes (CPK, SGOT, and LDH), lipids (triglycerides and free fatty acids), glucose, BUN, and corticosterone rose progressively. Fatty infiltration of the liver, adrenal hyperplasia, myocardial thrombi, renal degenerative changes, and cerebral edema became progressively more severe. A hypothalamic-pituitary-adrenal axis component may be involved in the reaction to the stress of acute cerebral or myocardial ischemia, which is intensified when the two ischemias are combined, and chronic hypertension may exacerbate both.
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PMID:Acute cerebrovascular and myocardial ischemia superimposed upon chronically hypertensive and arteriosclerotic male Sprague-Dawley rats. 90 14

Healthy virgin and breeder rats (Sprague-Dawley) with naturally occurring hypertension and arteriosclerosis were fed 5% oxonic acid and 1% uric acid added to their regular diet for 30 days. Although rats are able to convert uric acid into excretable allantoin, abnormal urinary and serum urate levels appeared. Males and females, virgins and breeders, differed in the severity of their increased urate levels. Animals with elevated urate levels developed hypertension, hyperglycemia, and hypertriglyceridemia, with only slight changes in cholesterol and free fatty acids. The kidneys were greatly enlarged and manifested medullary streaking indicative of urate deposits but were free of significant damage; BUN levels in these animals were abnormally high. Adrenal glands were reduced in size and depleted of lipid, circulating corticosterone levels were subnormal, and thymi were involuted. Serum enzymes CPK and LDH were greatly increased, whereas SGOT and SGPT levels were not elevated. The abnormal urate levels did not induce de novo arterial disease in the formerly healthy virgin rats and did not cause exacerbation of the pre-existing, naturally occurring arteriosclerosis characteristic of repeatedly bred rats. It is suggested that Sprague-Dawley rats are endowed with an especially efficient hepatic and renal capacity to metabolize uric acid. Increased urate levels in rats may have some direct metabolic relationship to the production of hypertension, hyperglycemia, and hypertriglyceridemia.
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PMID:Effect of increased serum urate levels on virgin rats with no arteriosclerosis versus breeder rats with preexistent arteriosclerosis. 92 65

For 30 months, from 1988, some risk factors and the satisfaction of basic needs, such as food, habitation, clothes, transport, health, security, family relation, possibility of affirmation, possibility of creation and cultural needs, were studied in 103 under 55-year-old patients with acute myocardial infarction and unstable angina pectoris. The control group matched the coronary group in age, sex, marital status, education, and working place. A cardiovascular clinical examination and ECG recording were performed in all subjects. In the coronary group also CPK and glucose in serum were recorded several times. Each person estimated the fulfillment of his basic needs from 1 to 5. The family history of coronary heart disease was positive in 43 (41.7%) coronary patients and in 12 (11.6%) control subjects (P less than 0.05). The prevalence of arterial hypertension in the coronary group was 46.6% and of diabetes mellitus 12.6%. In the coronary group 74.7% patients smoked and in the control group 47.5% (P less than 0.01). The mean body index in the coronary group was 27.5 +/- 0.36 and in the control group 27.9 +/- 0.36 (P less than 0.05). The basic needs (food, habitation, clothes, transport, and cultural needs) were given a significantly higher mark in the coronary than in the control group (P less than 0.05). The study has shown significant differences in the presence of classical risk factors between the group of 103 acute coronary patients and the control group. The socio-economic was higher in the coronary than in the control group.
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PMID:[Risk factors and satisfactory living circumstances in 103 patients with acute coronary disease under 50 years of age]. 172 14

In order to determine whether acute myocardial infarction (AMI) presents a circadian periodicity in its occurrence, the onset of AMI, evaluated by onset of clinical symptoms and pain, has been analysed in 520 patients with AMI. The definitive criteria of AMI were: typical chest pain, electrocardiographic findings, and plasma CPK-MB elevation. All cases of AMI were divided into subgroups according to sex (males = 369, females = 151), age (less than 60 years old = 254, more than 60 years old = 266), type of AMI (Q wave AMI = 407, non Q wave AMI = 113), previous pharmacological treatment (no treated = 373, treated = 147), history of arterial blood hypertension (normotensive = 403, hypertensive = 117). Cases of Q and non Q wave AMI were also subdivided according to treatment and hypertensive conditions. All AMI occurred outside hospital; silent AMI and reinfarctions were excluded by analyses. The data have been analysed by chronograms and by means of "single cosinor" method, both for total cases, and for each subgroup of AMI. The results show a diurnal variation in AMI occurrence regarding the whole group, with a peak from 4:00 am to noon and with a secondary small no-significant peak in the late evening, and the minimum in the afternoon. Rhythmometric analysis demonstrates a significant circadian rhythm (p less than 0.001) with acrophase at 7:52 am (from 6:08 am to 9:36 am). A statistically-significant circadian rhythm is demonstrated in each subgroup, except in hypertensive patients. Acrophases of males and females, and of patients aged over or under 60 years do not differ from that of the whole group, and between them (p greater than 0.05). The peak of non Q wave AMI occurs at 4:44 am, while the peak of Q wave AMI at 10:08 am: this difference is significant (p less than 0.001). There is also a significant difference between the acrophases of AMI in the treated and untreated groups (p less than 0.01), as well as between normotensive and hypertensive subjects (p less than 0.001). The previous treatment seems able to anticipate the maximum occurrence of AMI in the whole group and in the group of Q wave AMI. These results are very similar to previous observations and confirm the greater morning occurrence of AMI. The present data are discussed in respect with the literature observations, and the possible pathophysiological mechanisms that contribute and conditionate the morning increase and the different peaks in subgroups of AMI patients are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differentiated circadian chrono-risk of acute myocardial infarct]. 224 25

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct]. 239 9


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