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

We studied the changes in pulmonary hemodynamics and lung wet weight induced with opsonized zymosan (OZ) in isolated guinea pig lungs perfused with Ringer-albumin solution containing neutrophils (PMNs). Addition of OZ to the PMN-perfused lungs caused pulmonary vasoconstriction and weight gain; neither OZ nor PMNs added individually to the perfusate altered pulmonary vasomotor tone or wet weight. The steady gain in lung weight by 1,588 +/- 464 mg over the 45-minute study period was associated with pulmonary capillary hypertension and an increase in the capillary filtration coefficient, indicative of increased lung vascular permeability. These responses may not be due to generation of oxygen radicals, because the alterations in pulmonary hemodynamics and lung weight were not reduced by addition of superoxide dismutase, catalase, or superoxide dismutase plus catalase. We examined the basis of the PMN-mediated effects by layering PMNs on bovine pulmonary artery endothelial monolayers. Challenge with OZ resulted in increased endothelial permeability to 125I-albumin. The monoclonal antibody IB4 (directed against CD18, the common beta-subunit of structurally related adhesion receptors on phagocytes, LFA-1, Mac-1, and P150,95) prevented the OZ-mediated increase in PMN adherence to endothelial cells and the increase in endothelial permeability to 125I-albumin. IB4 also inhibited the lung weight gain mediated by the OZ-stimulated PMNs in intact lungs. The protective effect of IB4 could be ascribed neither to inhibition of uptake of OZ by PMNs nor to inhibition of release of oxygen radicals, myeloperoxidase, and elastase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary edema induced by phagocytosing neutrophils. Protective effect of monoclonal antibody against phagocyte CD18 integrin. 197 52

Previous evidence has shown that rats with spontaneous hypertension have on average about twice as many circulating leukocytes in comparison with their normotensive counterparts, the Wistar-Kyoto rats. Since such high levels of leukocytes may increase the risk for vascular complications for hypertensive animals, it is useful to ascertain whether a comparable derangement is present in other forms of hypertension. The present study deals with the properties of the circulating leukocytes in rats exhibiting another form of experimental hypertension; Dahl salt-sensitive (Dahl-S) hypertensive rats were compared with Dahl salt-resistant (Dahl-R) control rats. Measurements were performed to determine the following: circulating hematocrit levels, leukocyte counts, differential counts, number of activated leukocytes (by means of nitro blue tetrazolium [NBT] reduction), leukocyte adhesion in vitro and neutrophil CD-18 expression, alkaline phosphatase activity in individual neutrophils and in the plasma, and myeloperoxidase activity in neutrophils. The experimental cohort consisted of Dahl-S and Dahl-R rats maintained for a 6-week period on a 6% NaCl diet. The results show a highly significant elevation in the number of total leukocytes, neutrophil and monocyte counts, and NBT-positive neutrophils and monocytes in Dahl-S but not Dahl-R rats. There was a significant loss of alkaline phosphatase and myeloperoxidase activity in the neutrophils of the salt-treated Dahl-S rats but not in the neutrophils of the untreated Dahl-S or Dahl-R rats. No significant differences were found in neutrophil adhesion under in vitro test conditions between the two strains maintained on the salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating leukocyte counts, activation, and degranulation in Dahl hypertensive rats. 783 39

Protamine reversal of heparin anticoagulation can cause catastrophic pulmonary hypertension, systemic hypotension, and hypoxemia. This reaction is thought to be associated with pulmonary sequestration of activated neutrophils. To examine whether this reaction could be prevented by blocking neutrophil activation with NPC 15669 (N-(9H-(2,7-dimethylfluorenyl-9-methoxy)carbonyl)-L-leucine), an inhibitor of Mac-1 adhesion molecule up-regulation, we gave 12 piglets a heparin bolus (300 IU/kg i.v.) followed by protamine (3 mg/kg i.v. over 90 sec) 15 min later. Six of the piglets received NPC 15669 (10 mg/kg i.v. bolus, then 6 mg/kg/hr i.v. infusion) 15 min before the heparin bolus. Two minutes after protamine administration, CD18 (beta-subunit of Mac-1) expression measured by immunofluorescence flow cytometry increased 128 +/- 9% (mean +/- SEM) over preprotamine levels in control piglets but remained unchanged in NPC piglets (99 +/- 2%, P < 0.05). Fifteen minutes after protamine, lung myeloperoxidase activity, an index of neutrophil degranulation, was significantly lower in the NPC group (87.83 +/- 10.04 versus 57.23 +/- 2.59 mumol/10 mg; P < 0.005). NPC 15669 also prevented postreversal pulmonary artery hypertension (158 +/- 30, 150 +/- 20, and 140 +/- 13 versus 91 +/- 7, 91 +/- 18, and 85 +/- 9% preprotamine at Minutes 2, 5, and 10; P < 0.05). Systemic arterial pressure, cardiac output, and circulating neutrophil counts were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil activation mediates protamine-induced pulmonary hypertension. 810 32

Although the etiology of hypertension-related organ damage remains poorly understood, it has recently been proposed that activated and adherent leukocytes may contribute to the pathogenesis of progressive organ injury in hypertension. The objective of this study was to determine whether the adherence and emigration of leukocytes in microvessels differ between spontaneously hypertensive and normotensive rats. Leukocyte adherence, rolling, and emigration as well as vessel diameter and erythrocyte velocity were monitored in mesenteric venules of age-matched normotensive and hypertensive rats. Measurements were obtained under baseline conditions and during superfusion of the mesentery with either platelet activating factor, leukotriene B4, or NG-nitro-L-arginine-methyl ester, an inhibitor of nitric oxide synthesis. Tissue-associated myeloperoxidase activity, an index of the total tissue granulocyte population, was measured in various tissues of normotensive and hypertensive rats. Systemic arterial pressure and the circulating polymorphonuclear leukocyte count were elevated in hypertensive relative to normotensive rats. The number of adherent and emigrated leukocytes under baseline conditions did not differ between normotensive and hypertensive rats. Although the nitric oxide synthase inhibitor caused a similar rise in leukocyte adherence and emigration in both rat strains, the adhesive interactions elicited by either platelet activating factor or leukotriene B4 were significantly blunted in hypertensive relative to normotensive rats. Flow cytometric analysis of whole-blood samples revealed a lower surface expression of CD11b/CD18 on leukocytes from hypertensive rats under stimulated conditions. Myeloperoxidase activity in mesentery and small and large intestine was low, whereas lung, spleen, and stomach values were high in hypertensive compared with normotensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 May
PMID:Leukocyte-endothelial cell adhesion in spontaneously hypertensive and normotensive rats. 838 61

The factors responsible for predisposition to progressive organ injury and vascular complications in arterial hypertension are uncertain. Recent evidence shows that leukocytes participate in cardiovascular conditions for which hypertension is a risk factor. Therefore, there is a need to define the properties of circulating leukocytes in hypertensives. There are about twice as many circulating leukocytes in spontaneous hypertensive rats (SHRs) compared with their normotensive controls, the Wistar-Kyoto rats (WKYs). The SHR neutrophils are viscoelastic and similar to neutrophils in WKYs but exhibit lower deformability in short-term elastic deformation. Mature SHRs have elevated levels of spontaneous pseudopod formation. Mild stimulation with N-formyl-Met-Leu-Phe or platelet-activating factor (10(-8) M) results in a significantly enhanced level of neutrophil pseudopod formation in SHRs but not in WKYs. SHRs exhibit higher levels of spontaneous superoxide formation. Alkaline phosphatase content of individual circulating neutrophils in SHRs is on average lower while plasma levels of alkaline phosphatase in the same samples are elevated in the SHRs. Spontaneous degranulation of SHR neutrophils is also detectable with myeloperoxidase measurements. Such activity of circulating leukocytes poses a significant risk for vascular cytotoxicity in the hypertensive rats.
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PMID:Properties of circulating leukocytes in spontaneously hypertensive rats. 870 19

Intracerebroventricular injection of hypertonic saline induces experimental hypertension. To measure [Na] in the vicinity of osmosensitive sites, we continuously measured [Na] in cerebrospinal fluid ([Na]csf) in the lateral ventricle (LV, n = 6), in the third ventricle (V3, n = 6) and in the medial preoptic nucleus (MPO, n = 6) ([Na]MPO) with a Na-sensitive electrode together with mean arterial pressure (MAP) during infusion of hypertonic artificial cerebrospinal fluid (ACSF, [Na] = 1,000 meq/kg H2O) at 5 "mu"l/min for 3 min into the LV in urethane- anaesthetized rats. [Na]csf in the LV began to increase at the beginning of infusion, reaching a peak of 48 +/- 9 meq/kg H2O (mean +/- SE) around the end of infusion, then recovering to the pre-infusion level by 17 min. [Na]csf in V3 changed similarly to that in the LV without any delay, although the peak value was reduced (61% , P < 0.05). In the MPO, in contrast the increase in [Na]MPO was delayed (3 min, P < 0.002) and the peak reduced even further (to 37%, P < 0.01) compared with that in V3. Thereafter, it remained higher than the pre-infusion level until the end of recovery (P < 0.05). MAP began to increase at the onset of infusion (P < 0.05); the maximum increase of 16 +/- 2 mm Hg (n = 18) was reached at the end of infusion, whereafter this level was almost sustained until the end of the 22-min recovery period. To analyse quantitatively the relationship between MAP and [Na]csf, hypertonic ACSF was infused at 2.5 "mu"l/min into the LV. [Na]csf in the LV and MAP increased at half the rates seen with 5 "mu"l/min. These results suggest that the first increase in MAP after hypertonic infusion into the LV is due to the increase in [Na] in the LV and V3, and that the subsequent sustained increase in MAP is related to the delayed increase in [Na] in the periventricular tissues of the V3.
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PMID:Cerebrospinal fluid sodium concentration and osmosensitive sites related to arterial pressure in anaesthetized rats. 892 96

We report a case of a reversible posterior leukoencephalopathy syndrome (RPLS). A 57-year-old male had classical polyarteritis nodosa with mononeuritis multiplex, renal insufficiency, and a high titer of p-ANCA (MPO). He was normotensive. He was treated with high dose methylprednisolone and then with oral prednisolone and cyclophosphamide. Despite the treatment, his renal function rapidly deteriorated and hypertension progressed. He had two generalized seizures; at that time his blood pressure was 200/140 mmHg. CT scan revealed bilaterally symmetric hypodensities in the thalamus, the occipital white matter, and the brainstem. T2-weighted MRI showed increased signal intensities in the temporo-occipital white matter, the thalamus, the posterior limbs of the internal capsules, the external capsules, the midbrain, the pons, and the middle cerebellar peduncles. T1-weighted images showed hypointensities in these areas. Treatment with nifedipine improved his blood pressure; 5 days later he was only moderately disoriented. Follow-up CT demonstrated an ill-defined hypodense area only in the left parietal lobe. To our knowledge, there are only two reported cases of RPLS associated with systemic vasculitides. Interestingly, thalamic lesions are outstanding also in these cases. Under these circumstances, treatment of hypertension is of primary importance, and steroid therapy should not be withdrawn or reduced.
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PMID:[A reversible posterior leukoencephalopathy syndrome in a patient with classical polyarteritis nodosa]. 914 79

A 46-year-old woman was referred to our department in July 1996 with complaints of fever and myalgia in her calves. She had a 20-year history of purulent sputum; diffuse panbronchiolitis had been diagnosed in 1983. Physical examination revealed low-pithed rhonchi over the lung fieldis and hypesthesia of the right leg. She had a white blood cell count of 16,100/mm3, including 4% eosinophils, and a platelet count of 80.0 x 10(4)/mm3. The serum IgE level was 2,200 U/ml, and the cold hemagglutinin titer was high. Pulmonary-function tests showed mixed ventilatory dysfunction, and arterial blood gas analysis revealed a PaO2 of 55.8 Torr on room air. Pseudomonas aeruginosa was cultured from her sputum. A chest X-ray film and CT scan showed diffuse nodular shadows and bronchiectatic changes with mild hyperinflation. An infiltrative lesion in right S6 area could also be seen. Administration of broad-spectrum antibiotics did not alleviate her symptoms. The level of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA) in serum was 245 EU/ml, and 67Ga scintigraphy showed marked accumulation in the abdomen. Abdominal angiography demonstrated a bead-like appearance and irregularities in the peripheral branches of the hapatic artery, the splenic artery, the cystic artery, and the superior mesenteric artery. Because of the high MPO-ANCA level and the angiographic abnormalities, MPO-ANCA-related vasculitis was diagnosed. She was treated with 1 g of methylprednisolone daily for 3 days, followed by 60 mg of prednisolone and 50 mg of cyclophosphamide daily. Her condition improved dramatically, and the MPO-ANCA level became almost normal. During treatment, her blood pressure rose markedly with a normal serum creatinine level and normal urinalysis. Plasma renin activity was 13.3 ng/ml/hr. Renal angiography showed stenoses and irregularities in the peripheral branches of renal arteries bilaterally. These findings led to a diagnosis of renovascular hypertension due to vasculitis. Her blood pressure was controlled with an angiotensin-converting enzyme inhibitor and a calcium antagonist. Vasculitis associated with chronic supportive lung disease has occasionally been reported, which suggests a casual relation between chronic respiratory infection and ANCA-related vasculitis. Systemic vasculitis should be taken into account as a potential complication of chronic suppurative lung disease.
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PMID:[Diffuse panbronchiolitis with myeloperoxidase-specific antineutrophil cytoplasmic antibody-related vasculitis]. 974 63

An improved linkage map for rat Chromosome (Chr) 10 with two F2 populations was constructed. Thirty new microsatellite markers were generated from a Chr 10-specific, small-insert genomic library and mapped to rat Chr 10. Among them were the rat homologs for the mouse gene for light and heavy chains of myeloperoxidase and human neurofibromatosis 1. Eight newly generated markers (D10Mco62, D10Mco63, D10Mco64, D10Mco65, D10Mco67, D10Mco68, D10Mco70, and D10Mco74) were mapped to the region of the rat Chr 10 blood pressure QTL. The availability of such markers may be instrumental in the search for genes responsible for the hypertension.
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PMID:Improved linkage map and thirty new microsatellite markers for rat Chromosome 10. 989 28

Scleroderma renal crisis is characterized by intimal thickening of the afferent glomerular arterioles resulting in hypertension and fibrinoid necrosis of the capillary tuff. We report a 67-year-old man with long-standing systemic sclerosis who developed normotensive progressive renal failure, proteinuria, and a nephritic urinary sediment with serum myeloperoxidase-antineutrophil cytoplasmatic antibodies (MPO-ANCA). Renal biopsy showed pauci-immune crescentic glomerulonephritis but none of the typical vascular changes of scleroderma renal crisis. Because comparable cases have recently been reported from Japan, normotensive MPO-ANCA-positive crescentic glomerulonephritis may form an entity of progressive renal failure in scleroderma.
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PMID:MPO-ANCA-Positive crescentic glomerulonephritis: a distinct entity of scleroderma renal disease? 1019 34


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