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

The work is based on the results of operations on the cerebellar dentate nuclei in 92 patients. In 42 of them, combined manipulations were carried out on the cerebellar dentate nuclei and the diencephalic structures (relay nuclei, median centre, pulvinar and subthalamus). Analysis of the results showed that stereotaxic destruction of the ventrooral parts of the cerebellar dentate nucleus is a very effective surgical manipulation in various forms of spastic dyskinesia. A natural decrease in the spastic component of the muscular hypertonia is the principal clinical effect of dentatotomy. Its effect on the rigid component of muscular hypertension is negligible. Combined manipulations on the cerebellar dentate nuclei and diencephalic structures are indicated in cases with combined spastic conditions and hyperkinesia which cannot be corrected by dentatotomy. The analysis of the results of combined interventions on the nuclear structures of the thalamus shows that pulvinarotomy is most effective, it reduces or corrects hyperkinesia in infantile cerebral paralysis and, in addition, causes diminution of the general hypertonia, of the upper extremities before all else. Proper rehabilitation treatment is the decisive factor in the final outcomes of stereotaxic intervention on the cerebellar motor systems and on those of the diencephalon in spastic forms of hyperkinesia.
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PMID:[Stereotaxic combined dentate-thalamotomy in the treatment of spastic-hyperkinetic forms of subcortical dyskinesias]. 39 18

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

The examination of 68 patients with biliary dysfunction determined hypokinesia of the gallbladder in 40, sphincter of Oddi spasm in 15 and combination of the two conditions in 13 patients. Blood biochemical indices showed no differences in patients with biliary dyskinesia compared to normal subjects except for alkaline phosphatase levels elevated in 35.3% of patients. This suggests the development of biliary hypertension and cholestasis. All the patients demonstrated disturbed colloid stability of the bile, in those with combined dyskinesia it became lithogenic. Helium-neon and semiconductor laser radiation of biologically active points and the hepatic region, respectively, improved the patients' performance status. The pain and dyspepsia discontinued. The function of the gallbladder and sphincter of Oddi recovered. Positive changes occurred in the blood and bile biochemistry. Laser therapy promoted bilirubin and bile cholesterol decrease. Cholic acid concentration grew, lithogenic characteristics of the bile returned to normal. It is inferred that laser therapy of biliary dyskinesia proved effective.
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PMID:[Possibilities of the treatment of biliary dyskinesia by laser irradiation]. 239 9

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.
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PMID:Acute myocardial ischemia with prolonged left ventricular dyskinesia and mural thrombus formation in asymmetric septal hypertrophy. 334 53

Function of the hepatobiliary system was studied in 33 patients with thyroid diseases (11 with diffuse euthyroid goiter, 15 with diffuse toxic goiter, of them 7 with thyrotoxicosis of a mild degree and 8 with thyrotoxicosis of an average severity, and 7 patients with primary hypothyrosis) and in 14 healthy persons of the control group by a radionuclide method using a gamma-chamber and 99mTc-HIDA, a hepatotropic radiopharmaceutical. It was established that absorptive-excretory liver function and the concentration ability of the gall bladder decreased in noticeable thyrotoxicosis and moderate hypothyrosis. Hypermotor dyskinesia of the gall bladder and hypertension of the biliary tract sphincters were revealed in more than half of the patients. Similar changes though quantitatively less pronounced were noted in the patients with euthyroid goiter. Thyrotoxicosis of a mild degree was characterized by the affection of motor function of the gall bladder (hypermotor dyskinesia) and frequent hypertension of Oddi's sphincter. Possible mechanisms of the development of the above changes were discussed.
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PMID:[Functional state of the hepato-biliary system in patients with thyroid diseases studied with radiopharmaceuticals]. 382 18

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

L-DOPA is proposed to be a neurotransmitter and/or neuromodulator in CNS. It is released probably from neurons, which may contain L-DOPA as an end-product, and/or from some compartment other than catecholamine-containing vesicles. The L-DOPA itself produces presynaptic and postsynaptic responses. All are stereoselective and most are antagonized by competitive antagonist. In striatum, L-DOPA is neuromodulator, mother of catecholamines, not only a precursor for dopamine but also a potentiator of children for presynaptic beta-adrenoceptors to facilitate dopamine release and postsynaptic D2 receptors, and ACh release inhibitor. All may cooperate for Parkinson's disease. Meanwhile, supersensitization of increase in L-glutamate release to nanomolar levodopa was seen in Parkinson's model rats, which may relate to dyskinesia or "on-off" during chronic therapy. In lower brainstem, L-DOPA tonically activates postsynaptic depressor sites of NTS and CVLM and pressor sites of RVLM. L-DOPA is probably a neurotransmitter of primary baroreceptor afferents terminating in NTS. GABA, the inhibitory neuromodulator for baroreflex in NTS, tonically functions to inhibit, via GABAA receptors, L-DOPA release and depressor responses to levodopa. Levodopa inversely releases GABA. L-DOPAergic monosynaptic relay from NTS to CVLM and from PHN to RVLM is suggested. Tonic L-DOPAergic baroreceptor-aortic nerve-NTS-CVLM relay seems to carry baroreflex information. Disturbance of neuronal activity to release L-DOPA in NTS, loss of the activity in CVLM, enhancement of the activity with decreased decarboxylation and increase in sensitivity to levodopa in RVLM may be involved in maintenance of hypertension in SHR. This is a story of "L-DOPAergic receptors" with extremely high affinity and low density.
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PMID:Neurobiology of L-DOPAergic systems. 889 95

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

The paper presents the results obtained upon examination of inpatients with various types of biliary dyskinesia. The examination included: fraction chromatic duodenal intubation, stepwise manometry, cholecystography, ultrasound investigation of the liver, gall bladder, biochemical tests of the bile. Fraction duodenal intubation discovered gall bladder dysfunction. The manometry was necessary for diagnosis of duodenal hypertension. X-ray revealed primary defects in gall bladder motility. It is concluded that the diagnosis of functional disorders implies combined clinical and instrumental modalities.
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PMID:[The role of different investigations in diagnosis of functional disorders of the biliary system]. 912 Oct 86

The nigrostriatal dopaminergic system seems to be involved in both reserpine-induced orofacial dyskinesia in normal rats and in the pathogenesis of hypertension in spontaneously hypertensive rats. In the present study, repeated reserpine administration (1.0 mg/kg, s.c., every other day, for 3 days) increased tongue protrusion and vacuous chewing frequencies as well as the duration of facial twitching in Wistar normotensive but not in spontaneously hypertensive rats. These results suggest that genetic hypertension and drug-induced orofacial movements may be inversely modulated by similar mechanisms in the nigrostriatal dopaminergic system.
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PMID:Reserpine does not induce orofacial dyskinesia in spontaneously hypertensive rats. 977 39


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