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

In a decade from 1980, 11 children aged 3 to 11 years presented with Takayasu's arteritis (TA). All were severely hypertensive. Operative correction was offered to 10 of 11 children presenting with renovascular hypertension (RVH) including cardiac failure alone in 1 and both renal and cardiac failure in 8, a result of TA involving renal arteries by stenosis or occlusion. Nine patients had renal autotransplantation to an heterotopic site in the pelvis. Seven of 12 kidneys were salvaged by autotransplant with relief of RVH. Renal artery stenosis was successfully corrected by this procedure in 5 patients. Autotransplantation failed in 4 patients, 1 of whom subsequently had a successful allograft transplant. One patient was treated primarily by cadaver allograft transplantation. One patient whose autotransplant failed had a functioning contralateral kidney and is well with controlled RVH. One patient died prior to any treatment. Patient survival improved with the use of total lymphoid irradiation in the most recent 7 patients.
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PMID:Management of renal hypertension in children with Takayasu's arteritis using renal autografting or allograft transplantation in selected circumstances and total lymphoid irradiation. 135 25

A pathological study was conducted on 32 turkeys that died of sudden death with perirenal hemorrhage syndrome. Turkeys were selected from routine necropsy cases in a diagnostic laboratory. A higher incidence was observed in heavy tom turkeys. In addition to the characteristic gross lesions of perirenal hemorrhage, splenomegaly, and pulmonary congestion, turkeys in most cases had a hypertrophic cardiopathy. Microscopic lesions included moderate-to-marked acute passive congestion of all tissues examined (32/32), severe perirenal hemorrhage (32/32), and splenic lymphoid depletion (25/32). Changes in the thyroid follicular epithelium of most birds suggested an increased glandular activity. No lesions suggestive of arterial hypertension were observed. Adenoviral infection was detected in only four of 32 birds. Bacteriological cultures revealed no significant pathogen. Results suggest that sudden death in turkeys with perirenal hemorrhage is caused by an acute congestive heart failure consecutive to a hypertrophic cardiopathy. The perirenal hemorrhage would be a consequence of a severe passive congestion in kidneys.
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PMID:Sudden death in turkeys with perirenal hemorrhage: pathological observations and possible pathogenesis of the disease. 153 14

Immune dysfunction has been reported in spontaneously hypertensive rats (SHR), particularly in mature animals with established hypertension. The current study examined the time course of development of immune dysfunction and defined its cellular basis in male SHR and control normotensive Wistar-Kyoto rats (WKY). Mitogen-induced proliferative responses in lymphoid cells obtained from induced proliferative responses in lymphoid cells obtained from SHR thymus and spleen before (age 4 wk) and during the development of (ages 8 and 12 wk) hypertension and in age-matched normotensive WKY were monitored. A 50% reduction in concanavalin A (Con A)-induced proliferative responses was seen in SHR thymocytes compared with those of WKY at 12 wk only, suggesting differences in immature T-cell populations. Con A-induced T-cell proliferative responses in splenocytes also differed between strains: greatest (as much as 8-fold) decreases were found in 12-wk-old SHR. Similar findings were obtained in splenocytes stimulated with lipopolysaccharide (LPS), indicating differences in B-cell function. Mononuclear cells depleted of their adherent cell population were prepared from SHR and WKY at 12+ wk of age and assayed for their proliferative responses to LPS and Con A. The remaining nonadherent mononuclear cells of SHR had proliferative responses equal to or greater than those of WKY. Further, when SHR splenic mononuclear cells were allowed to adhere to plastic, and the adherent fraction was co-cultured with either SHR G-10 nonadherent or unfractionated SHR splenic mononuclear cells, proliferative responses were suppressed by as much as 88%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneously hypertensive rat: lymphoid depression is age dependent and mediated via a mononuclear cell subpopulation. 173 28

We report a case of primary malignant lymphoma of the central nervous system found in a 69-year old woman suffering from Parkinson's disease and hypertension. The CAT scan revealed an ill defined lesion in the left frontal lobe which at surgery appeared as a brownish-black friable neoformation. The histologic exam revealed a proliferation of voluminous round lymphoid cells with 2 or 3 nucleoli often apposed to the nuclear membrane. At the immunohistochemical investigation they were positive for LC and L26 monoclonal antibodies. Malignant centroblastic B-cell lymphoma was diagnosed. All post-surgery investigations excluded the presence of neoplasms in other sites.
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PMID:Primary malignant lymphoma of the central nervous system. Case report. 174 83

The involvement of an auto-immune mechanism has been suggested in the development and/or the maintenance of hypertension in male, genetically hypertensive rats of the Lyon strain (LH). The aim of this study was to determine whether hypertension may be transferred, by lymphoid cells, from hypertensive donors to male, normotensive rats of the Lyon strain (LN). Experiments designed to induce a resistance to hypertension in LH rats by transfer of lymphoid cells from LN animals were also performed. Since LH and LN are mismatched at the major histocompatibility complex, transfers of fetal liver cells (FLC) from fetuses of 13-14 days gestation were performed. These experiments demonstrate the ability of FLC to allow a prolonged survival (over 17 weeks) without graft versus host disease in the rat. As regards the blood pressure level, no LN recipient having received FLC from LH donor became hypertensive, thus showing that hypertension cannot be transferred by lymphoid cells in normotensive animals. Resistance to hypertension was so weakly transferred to hypertensive rats (results being significantly different only at 10 weeks post-grafting) that it may be considered doubtful.
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PMID:Fetal liver cell transplantation fails to transfer hypertension from genetically hypertensive rats to normotensive rats of the Lyon strain. 184 65

The pathological effects of focused electrohydraulic shock waves on renal parenchyma were studied using a porcine model. Testing was carried out using the Northgate SD-3 and Dornier HM-3 shock wave lithotripters. Pigs received 3,000, 5,000 or 6,000 shocks at energy levels equivalent to 18 to 20 KV on the Dornier HM-3. The animals were sacrificed one or four weeks post treatment and evaluated for renal injury. Kidneys were serially sectioned and injury volume calculations carried out. The predominant injury pattern was interstitial and perivascular fibrosis with chronic lymphoid infiltration. Dense areas of fibrosis ranged from less than 0.01% to 0.13% and from less than 0.01% to 1.04% of renal volume in those kidneys treated on the SD-3 and HM-3 respectively. Surrounding areas of perivascular and interstitial fibrosis intercalated with areas of normal appearing parenchyma were noted and were more extensive than the central scar. While the calculated volumes of parenchymal scarring are probably insignificant with respect to renal function, the surrounding areas of partial injury may be related to the development of hypertension.
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PMID:Electrohydraulic shock wave induced renal injury. 273 96

Induced systemic arterial hypotension by intravenous nitroprusside administration and by acute arterial occlusion in sheep have been found to reduce lymphocyte traffic as mirrored in the output of lymphocytes into the efferent lymph of peripheral lymph nodes. In the present series of experiments in sheep with chronically cannulated efferent lymphatics of peripheral lymph nodes, induced and monitored systemic arterial hypertension with intravenous pump infusions of phenylephrine or dopamine both produced sharp increases in the output of lymphocytes into efferent lymph in all of 27 studies. The increases in lymphocyte output with dopamine were more sustained and less associated with evidence of lymphoid tissue damage than with phenylephrine. Phenylephrine infusions were attended by a high incidence of gross bleeding into the efferent lymph, of increased coagulability of efferent lymph in the absence of gross bleeding and of prolonged depression of lymphocyte outputs after the cessation of intravenous infusion.
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PMID:Increased outputs of lymphocytes in lymph efferent from the lymph nodes of sheep during systemic arterial hypertension induced by phenylephrine or dopamine. 344 45

Among early life SLE mice, the male F1 hybrids of NZW X BXSB crosses are unique by their much earlier onset of glomerulonephritis (GN) (evident by 2 1/2 months of age), progressive hypertension, and high frequency of degenerative cardiovascular disease (CVD) with myocardial infarcts. In contrast, their female counterparts and the other kinds of SLE mice have later onset of GN, minimal hypertension, and lower incidence of CVD. The etiopathogenesis of these F1 males' disease was investigated by reciprocally transferring syngeneic lymphoid cells into lethally irradiated F1 male and female mice. As a result, female recipients of male lymphoid cells developed accelerated GN, hypertension, and severe CVD, but the male recipients of female lymphoid cells (at comparable ages) had delayed SLE, remained normotensive, and were spared coronary or myocardial damage. These findings strongly indicate that the hypertension and CVD of these F1 males originate from immunologic abnormalities rather than from other nonlymphoid factors.
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PMID:Transfer of renovascular hypertension and coronary heart disease by lymphoid cells from SLE-prone mice. 671 79

Alterations in the number and reactivity of thymic and splenic lymphocytes were studied during the development of experimental renal hypertension in Sprague-Dawley rats. The mitotic responses of thymocytes and splenic T and B lymphocytes were tested by the T cell mitogen concanavalin A and the B cell mitogen dextran sulfate 3, 8, 12, and 36 days after the initiation of hypertension. At 3 days, hypertensive rats showed a fourfold increase in plasma corticosteroid levels, marked thymic atrophy, and a 50% reduction in the total number of thymocytes. The mitotic reactivity of the cells remaining in the organ was depressed 60% when compared to sham-operated controls. At 8 days a similar reduction in thymus size was accompanied by similarly decreased lymphocyte populations. Twelve days after initiation of hypertension structural recovery of the gland, lymphoid proliferation, and slightly increased thymocyte populations were observed. Differences with sham-operated controls were, however, still remarkable. Hypertensive rats sacrificed at 36 days showed thymus hypertrophy, and the thymocyte populations were larger than those of sham-operated animals. Despite the fluctuations in the number of thymocytes registered during the development of renal hypertension, the impaired mitotic reactivity of these cells to concanavalin A was sustained throughout the 36 days of the experiment. A similar reduction in the total number of cells and a similar depression in T lymphocyte reactivity was observed in the spleen between 8 and 36 days of hypertension. In contrast, after an initial depressed response, splenic B lymphocytes showed a slight but sustained increase in reactivity throughout the entire experimental period. These results indicate that with evolving renal hypertension there is a reduction in the number of lymphocytes as well as a depression in the ability of the remaining T lymphocytes to react with concanavalin A. Since T lymphocytes are important regulators of immunological homeostasis, this reduction in T cell reactivity may suggest the existence of an immunological imbalance accompanying the development of experimental renal hypertension.
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PMID:Lymphoid alterations and impaired T lymphocyte reactivity in experimental renal hypertension. 698 32

Excessive salt intake is an important determinant of human essential hypertension. Hypertension resulting from genetically determined salt sensitivity can be studied by the used of the salt-sensitive (S) and -resistant (R) rat strains developed by Dahl. A longitudinal morphometric and ultrastructural study of S and R Dahl rats fed different amounts of salt (0.6%, 4.0%, and 8.0% NaCl) for 2-14 weeks was undertaken. Only S rats responded to high-salt (4.0% and 8.0%) diets with an increase in blood pressure, and the rate of hypertension development was proportional to the daily amount of salt consumed. Likewise, S but not R rats fed high-salt diets showed thickening of the aortic media which paralleled the rise of blood pressure. Intimal lesions were characterized by the accumulation of an amorphous, electron-dense substance in the subendothelial space (SES), adherence or penetration of lymphoid cells, and subendothelial fibrin deposition. The extent and severity of SES expansion correlated more closely with the duration of salt feeding than with the level of blood pressure. Fibrin deposition was noted only in severely hypertensive animals and was not related to the salt concentration in the diet. Morphologic abnormalities in endothelial cells were noted in hypertensive animals by transmission and scanning electron microscopy as well as by en face preparation, but endothelial denudation and junctional disruptions were notably absent. In contrast to the large numbers of lymphoid cells, neither platelets nor fibrin were seen adherent on the endothelium. These results, in conjunction with previous studies in other hypertensive models, indicate that the nature and extent of vascular lesions depend not only on the severity of hypertension but also on its rate of development, duration, and pathophysiologic characteristics.
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PMID:Aortic morphology in salt-dependent genetic hypertension. 708 90


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