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

Left ventricular performance has been studied in 50 patients affected by primary polycythemia (P.V.) by determining systolic time intervals. 50 normal subjects were used as control group. All cases underwent a pharmacodynamic test with Amyl Nitrite. The results indicate that patients with P.V. present an abnormal behaviour of left ventricular performance after Amyl Nitrite; this alteration is more evident in patients with arterial hypertension. Amyl Nitrite, through its pharmacological action, causes changes in systolic time intervals and reveals a state of latent cardiac failure.
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PMID:[Study of left ventricular function using systolic time intervals in a group of patients with polycythemia vera (Vaquez-Osler disease)]. 615 Nov 50

Angiotensin II has been previously implicated as a mediator of vasoconstriction during the development of hypoxic pulmonary hypertension. The effect of angiotensin-converting enzyme inhibition with teprotide (SQ 20881) on development of pulmonary hypertension was determined by measurement of the drug's ability to modify hypertension-induced protein synthetic changes in the rat pulmonary trunk. Rats were injected with either SQ 20881 (2 mg/kg body wt every 8 hr) or saline vehicle during exposure to chronic hypoxia at 0.5 atm for either 3 or 7 days. Comparisons were made of tissue weight, absolute protein content, and in vitro synthesis of collagen and noncollagen protein of the pulmonary trunks of SQ-treated hypoxic, SQ-treated normoxic, saline-treated hypoxic, and saline-treated normoxic rats. Treatment of hypoxic rats with SQ 20881 was found to significantly decrease right ventricular pressure, tissue weight, absolute protein content, and in vitro protein synthesis after 7 days compared to saline-treated hypoxic rats. Neither right ventricular hypertrophy nor the development of polycythemia was decreased by SQ 20881 treatment.
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PMID:Reduction in hypertension-induced protein synthesis in the rat pulmonary trunk after treatment with teprotide (SQ 20881). 620 42

We studied the effect of continuous and intermittent normoxia for 6 and 20 wk on the muscularization of pulmonary arterioles in rats with chronic hypoxic hypertension. After 4 wk in a hypobaric chamber (380 mm Hg) the proportion of small pulmonary blood vessels with 2 elastic laminae (PVTEL) was 21.57 +/- 14.86% (SD) (n = 10) compared with 3.66 +/- 1.86% in 10 untreated control animals. Recovery using continuous normoxia and intermittent normoxia 16 h/day for 6 wk caused a reduction in PVTEL to 8.45 +/- 4.09% (n = 6) and 7.16 +/- 6.96% (n = 6), respectively. Right ventricular hypertrophy (RVH) was reversed by recovery using continuous normoxia for 6 wk but was unaffected by intermittent normoxia (16 h/day). Intermittent normoxia 8 h/day for 6 wk did not reduce the PVTEL or RVH. Continuous normoxia for 20 wk reversed the muscularization of small pulmonary vessels (PVTEL, 3.86 +/- 3.57%; n = 4) and RVH. Intermittent normoxia (16 h/day) for 20 wk significantly diminished the PVTEL to 7.39 +/- 3.73% (n = 5) but did not reduce RVH. Prolonged continuous normoxia slowly reversed the pulmonary hypertension, RVH, pulmonary vascular lesions, and polycythemia induced by chronic hypoxia. Intermittent normoxia (16 h/day) diminished the pulmonary vascular lesions but not the pulmonary hypertension, RVH, and polycythemia. Intermittent normoxia (8 h/day) was ineffective.
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PMID:Effect of intermittent normoxia on muscularization of pulmonary arterioles induced by chronic hypoxia in rats. 645 44

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

Report of a case of so called "benign" intracranial hypertension whose main characteristics are: the etiology attributed to a thrombosis of the venous transverse sinus in the course of a polycythemia; the clinical signs with a reinforcement during the course of the illness of a previous epilepsy; the prognosis with specially heavy visual impairment questioning the prefix "benign" applied to this condition.
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PMID:[Benign intracranial hypertension in polycythemia which had caused a lateral sinus thrombosis]. 671 20

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Patients with congenital cardiac shunts in whom marked functional disability, cyanosis and pulmonary arterial hypertension develop have been considered inoperable or at exceedingly high risk. Three adult patients, 2 with atrial septal defect (ASD) and 1 with patent ductus arteriosus (PDA), presented with New York Heart Association class IV symptoms, bidirectional shunting with cyanosis, polycythemia, severe pulmonary hypertension, and increased pulmonary vascular resistance. Pulmonary arterial pressure did not decrease in response to administration of 100% oxygen in any patient, and 2 had lung biopsy results showing advanced pulmonary vascular obstruction. While a right-to-left shunt caused cyanosis in all patients, the net shunt was left to right (Qp/Qs greater than 1) and the resistance ratio (Rp/Rs) less than 0.5. All 3 patients survived operation, became acyanotic with normal hematocrit, and are in functional class I or II a mean of 36 months postoperatively. At repeat cardiac catheterization, pulmonary arterial pressure and resistance had decreased substantially. This high-risk group of patients with bidirectional shunts, in whom cyanosis due to pulmonary vascular obstruction and polycythemia develop and who appear to be at very high operative risk, should still be considered for surgical correction if the usual criteria for operability exist: net left-to-right Qp/Qs and Rp/Rs less than 0.50.
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PMID:Management of adults with congenital bidirectional cardiac shunts, cyanosis, and pulmonary vascular obstruction: successful operative repair in 3 patients. 684 83

Oxygen therapy is justified both on theoretical grounds and by clinical studies. Chronic hypoxia bodes ill for the system and is a prognostic factor in pulmonary disease. Low flow oxygen therapy has not shown any risk of pulmonary toxicity from anatomical or physiological studies. Clinical studies have shown that the correction of hypoxaemia by long term oxygen therapy improves exercise tolerance, mental state, the general sense of well being, polycythaemia, pulmonary hypertension, the quality of sleep, and finally the prognosis. But long term oxygen therapy is costly and requires patient co-operation and close supervision. It should be reserved for hypoxic patients in a stable state: the exact degree of hypoxaemia at which oxygen therapy is permissible cannot be defined precisely and depends on other criteria (such as polycythaemia, pulmonary arterial hypertension, nocturnal desaturation). Account should be taken of the PaCO2 level and the cause of the disease in deciding the oxygen flow. Polycythaemia, pulmonary arterial hypertension, nocturnal desaturation despite a normal waking PaO2, may represent some indications for oxygen therapy but further studies are necessary.
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PMID:[Indications and decision criteria for supplemental oxygen therapy in chronic hypoxemia]. 687 56

All contributory factors to the unusual occurrence of stroke in young people were evaluated in patients under age 40 admitted to the Stroke Unit of the Austin Hospital in Melbourne, Australia. Over the August 1977 to December 1980 period there were 700 admissions. Of these 14 patients were under the age of 40. There were 7 males and 7 females whose ages ranged from 17-38 years. Each patient was screened for factors which might contribute to premature vascular disease including hypertension, diabetes, smoking, obesity, and hyperlipidemia. In addition, the following tests were performed to exclude an arteritic process: full blood examination; ESR; protein electrophoresis; syphilis serology; and the presence of antinuclear factor. Each of the 14 patients suffered cerebral infarction. A summary of each case is presented in a table. In 9 patients, infarction occurred in the carotid territory of supply. Large cortical infarcts with or without subcortical involvement occurred in cases 1-8, of whom 5 had major vessel occlusion demonstrated angiographically and another had stenosing and ulcerative atheromatous disease at the extracranial carotid bifurcation. In a further 4 patients, infarction occurred within the vertebrobasilar territory and was either confined to the brain stem, the occiptal cortex, or involved both. Angiograms were performed in 2 of these patients and showed irregular narrowing of the vertebral artery which was interpreted as spasm and segmentally narrowing of the basilar artery. The final patient had several ischemic events which included right sided amaurosis fugax, and left frontal, right parieto-occipital and left occipital infarctions. Angiography was normal. All patients survived the stroke and were able to go home. There may be an interrelationship between the pathological findings of Irey et al. (1978) and the effect oral contraceptives (OCs) has on migraine. This is relevant to Case 13. Sustained exposure to OCs may produce the pathological changes described (visible as segmental narrowing angiographically). In 2 patients cerebral infarction was caused by atheromatous or hypertensive occlusive vascular disease. In Case 3 an embolus occluded the middle cerebral artery. Infarction complicating migraine was diagnosed confidently in 4 patients on the basis of typical migrainous symptomatology in the past and accompanying the stroke. Of the 12 patients fully evaluated, there were no cases of polycythemia or thrombocytosis. There were no abnormalities of the clotting factors. Almost every patient had some form of emotional upset, and there were 7 who had significant psychiatric illness and emotional problems of extreme magnitide.
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PMID:Stroke syndromes in young people. 692 82

Polycythemia developed in 18 of 133 first kidney allograft recipients (13.5%) with onset from the third month to the fifth year posttransplantation. A group of matched nonpolycythemic patients were used as case controls to compare multiple variables in order to identify predisposing factors. In the polycythemia group, there were: (1) significantly more patients who had not undergone pretransplant nephrectomy; (2) significantly more patients who had glomerulonephritis as original disease; (3) significantly more patients who had received pretransplant transfusions; and (4) significantly more patients who were hypertensive posttransplant. Thus, the factors of the presence of native kidneys, original disease, pretransplant transfusions as well as hypertension posttransplant are factors associated with the presence of posttransplant polycythemia. This condition is usually self-limiting and benign.
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PMID:A matched-pair control study of postrenal transplant polycythemia. 704


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