Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous studies swimming training (ST) of spontaneously hypertensive rats (SHR) at 36 degrees water temperature (WT) led to a decrease in blood pressure (BP). A similar effect of ST has not been described in human hypertension. Our purpose was to investigate the influence of WT on this training effect, the influence of ST on LV hypertrophy and the involvement of adrenergic stimuli in the latter. Male SHR (20 weeks old) were divided randomly into 4 groups. 1) SHR sedentary 2) SHR ST 36 degrees 3) SHR ST 26 degrees 4) SHR ST 36 degrees + atenolol (50 mg/kg/die). ST was performed 2 X 90 min/day for 31 days and then reduced to 2 X 60 min/day. After 7 weeks of ST BP was lower in all ST groups compared with SHR sedentary (p less than 0.001). BP was higher in ST 26 degrees than in ST 36 degrees (p less than 0.05). No additional effect of atenolol on BP was observed. The increase in the degree of LV hypertrophy during ST (ST 36 degrees: +15%; ST 26 degrees: +26%) could be prevented by atenolol (ST 36 degrees + atenolol: -1.5%). ST 36 degrees led to improved ventricular and myocardial performance with decreased LV wall stress ("luxury hypertrophy"), while in ST 26 degrees ventricular dilatation occurred with increased systolic wall stress and elevated LVEDP. It was uncertain whether this should be interpreted as a state of LV pre-insufficiency in ST 26 degrees in spite of no indications of impaired myocardial contractile capability. Peripheral vascular resistance (PVR) was significantly reduced by ST. The reduction was more evident in ST 26 degrees, but was partially compensated for by an increased cardiac output. The weights of adrenal glands increased (p less than 0.001), most markedly for ST 26 degrees. The level of thyroid hormones (T3 and fT3) was increased in ST 26 degrees. In summary, ST proved to be effective in lowering BP of SHR. WT had great influence with respect to cardiovascular adaptation and mechanisms involved in ST of SHR. Cardioadrenergic drive was of great significance for the process of hypertrophy during ST in SHR.
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PMID:Significance of physical exercise in hypertension. Influence of water temperature and beta-blockade on blood pressure, degree of cardiac hypertrophy and cardiac function in swimming training of spontaneously hypertensive rats. 294 62

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary sinus blood flow (gas chromatic argon technique) was determined in patients with left ventricular hypertrophy, with or without dilatation, associated with entirely normal coronary arteriographic results: 12 patients with hypertrophic obstructive cardiomyopathy (left ventricular mass-to-volume ratio, 3.66 +/- 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (left ventricular mass-to-volume ratio, 2.12 +/- 0.26 g/ml), 18 patients with hypertensive dilatation (left ventricular mass-to-volume ratio, 1.6 +/- 0.48 g/ml), six patients with aortic stenosis (left ventricular mass-to-volume ratio, 1.99 +/- 0.41 g/ml), 12 patients with aortic incompetence, and 20 patients with normal heart function. Coronary sinus blood flow was determined as a control value and as the value following intravenous injection of dipyridamole (0.5 mg/kg of body weight). Coronary reserve was calculated as the ratio of coronary resistance before and after dipyridamole. Normal coronary reserve averaged 4.89 +/- 0.11. Similar values, despite marked left ventricular hypertrophy, were present for both hypertrophic obstructive cardiomyopathy (4.4 +/- 0.19) and aortic stenosis (4.66 +/- 0.12), whereas coronary reserve was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 +/- 0.19) (p less than 0.001). Moderate decrease in coronary reserve was found in aortic incompetence and in dilated essential hypertension. These results indicate that patients with nonhypertensive hypertrophy, despite left ventricular mass augmentation, may have normal coronary reserve, whereas at a comparable degree of left ventricular hypertrophy, patients with hypertensive hypertrophy have a specific reduction in coronary reserve. Independent from vascular effects, ventricular dilatation may result in deterioration of coronary reserve because of an abnormal component of coronary vascular resistance. These results were also verified in experimental hypertension. Moreover, prevention and/or regression of the impaired coronary circulation in experimental hypertensive heart disease, most probably due to the reduction of smooth muscle layers of the media of coronary resistance vessels, could be achieved by long-term vasodilator therapy.
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PMID:Coronary hemodynamics in hypertensive heart disease. Basic concepts, clinical consequences, and experimental analysis of regression of hypertensive microangiopathy. 297 65

Angiotensin converting enzyme (ACE) inhibitors are not known to have a direct effect on the myocardium. However, there is some evidence to suggest that they can play an important role in protecting the heart during the evolution of hypertensive and coronary arterial disease, both acutely and on a long term basis. Reduction of afterload by balanced arterial and venular dilatation has led to a sustained improvement of cardiac performance both in hypertension and heart failure. Reversal of cardiac hypertrophy has been shown to restore inotropic responsiveness to stimulators of the adenylate cyclase system. Following myocardial infarction, captopril has prevented undue ventricular dilatation and normalized left ventricular chamber stiffness; this prevented deterioration of cardiac function and improved long term survival after infarction. Control of secondary aldosteronism and prevention of hypokalaemia can play an important role in the prevention of cardiac arrhythmias. The lack of reflex sympathetic stimulation during long term captopril therapy can also play a favourable role in that respect. Although highly speculative, evidence is accumulating that ACE inhibition could have a cardioprotective effect in acute myocardial ischaemia. It is based on the demonstration that renin can be produced by myocardial cells, that angiotensin is liberated by the ischemic myocardium and that angiotensin in high renin conditions plays an active constrictor role in regulating the coronary circulation.
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PMID:Prospectives for angiotensin converting enzyme inhibition in heart diseases. 300 6

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

This paper investigates 21 patients (16 infants and 5 children) with Pneumococcal meningitis, 15 of which presented with a severe form. Intracranial pressure (IP) monitoring was performed in 7 patients who all had severe (4) or mild (3) intracranial hypertension (IH). Twelve children had a favourable outcome, 7 had sequelae (3 severe) and 2 died from coning, one before monitoring, the second after exhibiting the highest IP and the lowest cerebral perfusion pressure of the series. The 3 children with severe sequelae had a severe form (2) or a mild but prolonged form (1) of IH. The 4 patients who recovered with moderate sequelae presented severe (1), mild IH (1) or were not monitored (2). There were 14 cases with neurological complications. In 8 patients, this seemed to be related to cerebral oedema and IH; coning caused the death of 2 of them; the 6 others exhibited lesions of cerebral oedema on CT-scan, isolated or associated with cerebral infarction or subdural effusion. In the 6 others patients, IP monitoring was not performed; there was no evidence of cerebral oedema on CT-scan; 2 exhibited cerebral infarction and 3 a moderate ventricular dilatation; 2 had hemodynamic problems from acute pneumococcemia in one case and neurovegetative disturbances associated with cerebral infarction in the second. Pneumococcus meningitis remains a severe disease. The prognosis of severe forms can be improved by IP monitoring since IH seems to be the most frequent mechanism of complication.
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PMID:[Suppurated pneumococcal meningitis in infants and children: complications and prognostic factors]. 319 66

A seventeen year old boy sustained pelvic, femoral shaft and malleolar fractures in a road traffic accident. Six hours after admission, the patient became comatose (Glasgow coma score = 7); the coma worsened such that, 24 h later, the coma score was 4. Petechiae were present on the conjunctiva and anterior chest wall. Computed tomography revealed diffuse brain swelling. The diagnosis of cerebral fat embolism was made. There were multiple episodes of severe intracranial hypertension. After 23 days of traction, the femoral fracture was internally fixed. The patient returned home after five months of hospital, with just a few memory and writing problems. Ten months after the accident, magnetic resonance imaging showed a small ventricular dilatation due to subcortical atrophy. Residual ischaemic lesions and demyelination could be seen in the right centrum ovale and temporal lobe. The cerebral lesions contrast with the reversibility of the clinical state.
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PMID:[Post-traumatic cerebral fat embolism]. 320 32

There is increasing interest in the notion that some patients with hypertrophic cardiomyopathy (HCM) progress to morphological and functional manifestations similar to those of dilated cardiomyopathy (DCM). From 165 consecutive patients with HCM, 20 patients with left ventricular dilatation (left ventricular end-diastolic diameter greater than or equal to 50 mm) were selected and designated as dilated HCM. The diagnosis of HCM was established in these patients either by detection of the classical form of HCM in family members, with 2-dimensional echocardiographic evidence of asymmetric septal hypertrophy (ASH; septal thickness greater than or equal to 15 mm and a ratio of septal to posterior wall thickness greater than or equal to 1.3); or by demonstrating myocardial fiber disarray in autopsy or biopsy samples. The clinical manifestations of these patients with dilated HCM were then compared with those of other forms of HCM without left ventricular dilatation; 1) 40 patients with hypertrophic obstructive cardiomyopathy (HOCM) who had resting intraventricular pressure gradients of 20 mmHg or more, 2) 80 patients with non-obstructive HCM, each of whom had ASH of the entire ventricular septum (typical ASH), and 3) 25 non-obstructive patients whose hypertrophy was localized to the apical region of the ventricular septum (apical ASH). Patients having apical hypertrophy with a spade-like configuration on the left ventriculogram were excluded from the study. Compared with HOCM and typical ASH groups, the patients with dilated HCM had family histories of significantly more frequent HCM and less frequent hypertension. The patients with dilated HCM also had significantly less fractional shortening (FS), decreased interventricular septal thickness, greater left ventricular end-diastolic pressure (LVEDP), and left ventricular dilatation. During the follow-up period (average: 3.5 years), seven patients (35%) with dilated HCM died; five from congestive heart failure (CHF), one suddenly, and one three days following mitral valve replacement. The other five patients had CHF at the time of their follow-up examination. The patients with apical ASH had clinical features similar to those of dilated HCM; a higher familial frequency, less marked septal hypertrophy, and higher LVEDP. They tended to develop left ventricular dilatation, associated with reduced fractional shortening, although left ventricular diameter at end-diastole did not exceed 50 mm. These findings suggested that dilated HCM is not a rare condition. It is observed in 12% of consecutive patients with HCM.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Hypertrophic cardiomyopathy with left ventricular dilatation]. 324 61

A series of 23 patients with spontaneous cerebellar hematoma is analysed retrospectively. Several degrees of consciousness impairment, and headache occurred in all; 12 patients presented motor deficits among the more important clinical signs. Arterial hypertension (69.5%) and diabetes (34%) stand out in the pathological background, and their association was frequent (30%). Computerized tomography (CT) disclosing severe ventricular dilatation (69.5%) associated or not with intraventricular presence of blood is considered as an unsatisfactory prognosis sign, and indicative for emergency therapy. Emergency external ventricular draining is the best indication for the majority of these cases. Posterior fossa craniectomy for emptying the hematoma may be the indication in severe cases. Death and morbidity in this pathology are high as yet. However, CT contribution for diagnosis is quicker and better than benefits obtained through other methods. Results observed in the present series are illustrative on this statement, when compared to data of other series diagnosed through other methods.
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PMID:[Spontaneous cerebellar hematoma. Analysis of 23 cases]. 340 83

To investigate the pathogenesis and pathophysiology of dilated cardiomyopathy (DCM), we studied 28 patients with DCM by echocardiography and endomyocardial biopsy, and compared their findings with those of 34 patients including eight with myocarditis, seven with alcoholics, 12 with hypertensives and seven patients with hypertrophic cardiomyopathy. All 12 patients in the hypertensive group had congestive heart failure without accompanying high blood pressure, and prominent dilatation and uniform wall motion abnormality of the left ventricle observed echocardiographically on admission. After medical management, both heart failure and the echocardiographic abnormalities gradually resolved. Those in the alcoholic group had larger left ventricles and uniform wall motion abnormality compared to those in the other groups. The myocarditis and hypertrophic cardiomyopathy groups had smaller left ventricles, non-uniform wall motion and larger % myocardial fibrosis. Both ventricles in the hypertrophic cardiomyopathy group were thicker than those of the other three groups. Each patient with DCM had individual echocardiographic abnormalities, which could be categorized as two subsets depending on the degree of left ventricular dilatation and uniformity of the wall motion. The one was characterized by a prominently dilated left ventricle and uniform wall motion abnormality similar to the alcoholic group, and the other had less marked left ventricular dilatation and heterogeneous wall motion abnormality similar to the myocarditis group. From these findings, it was suggested that there are common factors to specific myocardial disease in the pathogenesis and pathophysiology of DCM, and thus, DCM might include many subsets of different etiologies.
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PMID:[Pathogenesis of dilated cardiomyopathy: a study based on comparison of the clinical features with other related conditions]. 342 22

We report the neurological, intellectual and visual outcome of 77 children with hydrocephalus of non tumoral origin. Neurological deficits and epilepsy were common, particularly in those with severe intellectual deficit and with acquired brain damages. Intellectual level prognosis was usually good, although lower than in a healthy population: 75% of children had full intellectual quotient (FIQ) higher than 70 but often, there was an heterogeneous pattern of the IQ with greater differences between verbal and performance results because of poor visual-spatial skills. Attention and syntax comprehension of language disabilities were also specifically encountered. Meningitis or toxoplasmosis secondary to hydrocephalus often resulted in a poor intelligence level but other causes did not influence intelligence level or pattern. Visual-spatial deficits, attention disorders and language disabilities did not seem related to the degree of hydrocephalus or the delay before shunting, but were especially encountered when ventricular dilatation persisted in spite of the operation. Functional amblyopias were frequent, certainly related to strabismus. Optic atrophy was rare and linked to direct compression of the optic nerves or to major and repeated episodes of intracranial hypertension.
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PMID:[What future is there for hydrocephalus children? Intellectual and visual neurological prognosis in series of 77 cases of non-tumor hydrocephalus]. 344 57


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