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

The synthesis and deposition of collagen and other proteins has been measured in the aorta of the rat by radiolabeling in short term organ culture. Under these conditions, the synthesis of collagen and other proteins is linear for at least five hours. Autoradiography demonstrates a labeling in all cell layers and protein deposition in the extracellular matrix. Hypertension was induced by renal ischemia using Goldblatt's technique. The synthesis and deposition of collagen was stimulated in aorta from the first week of hypertension and in pregnancy, and was even more increased in hypertensive pregnant animals. Reserpine suppresses the rise in blood pressure in operated animals and prevents these modifications.
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PMID:Aortic collagen biosynthesis during renal hypertension, pregnancy and hypertension during pregnancy in the rat. 36 58

End-stage kidneys in patients who are receiving long-term intermittent treatment with hemodialysis are metabolic structures that participate in many body processes and that themselves develop and change despite severe excretory deficiencies. Nephron loss is severe. Other lesions in such kidneys include the following: smooth muscle nodules that arise in necrotic arteries and arterioles; embryonal hyperplasia of Bowman's capsular epithelium; remodeling of the arteries and veins; tubular atrophy; dilation and cyst formation (acquired cystic disease); arteriolar granular cell hyperplasia and hypertension; deposits of oxalate, calcium, and immune complexes; interstitial fibrosis with collagen and smooth muscle; mucoid change; and cellular infiltration. This list does not include all pathologic conditions found in the end-stage--dialysis kidney. The necessity of and the criteria for an experimental model of human long-term intermittent hemodialysis for end-stage renal disease, presently lacking, are indicated.
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PMID:New therapies and new pathologies: end-stage--dialysis kidneys. 36 73

The main objective of this study was to produce primary acute ischemic injury to myocardium in a live animal. In vitro, guinea pig platelets were sensitive to perturbation and aggregation by a suspension of ultrafine fibrillary collagen material isolated from the aorta of an aged burro (Equus asinus). The platelets responded to the stimulatory action of this material down to 100 to 200 ng (dry weight) added to 0.45 ml of platelet-rich plasma, as determined by aggregometric technique. Aortic fibrillary collagen material injected IV into guinea pigs (350 to 1900 microgram protein/kg of weight) produced a transitory disappearance of virtually all circulating platelets within 5 minutes. In animals in which blood samples were taken 2.5 hours after injection, 50 to 75% of the average base-line platelets in the circulation of controls returned to the circulation. In other experiments, 3 anesthetized animals were injected by jugular vein with an amount of active fibrillary collagen material (300 microgram as protein/kg of animal weight) estimated to produce reversible platelet aggregation in vivo. Two control animals were injected with the same dose of the material that had been inactivated (15 minutes at 100 C) to abolish platelet aggregation. Treated and control animals were maintained under general anesthesia for 2.5 hours. Intraventricular pressures and electrocardiographs (ECG) were monitored continuously for the first 30 minutes. The injection of the active fibrillary collagen material caused a large ventricular pressure elevation (170/10, 180/10, and 150/10 mm of Hg) in approximately 40 s. Preinfusion ventricular pressures in the 3 animals were 65/0, 85/5, and 88/0 mm of Hg, respectively. Within 60 s, there was a reduction in the absolute platelet number in the peripheral circulation. The elevation of ventricular pressure persisted for approximately 5 minutes and was followed within 30 minutes by a set of ECG events suggestive of acute myocardial ischemic injury, which included premature ventricular contractions, transient S-T segment depression concurrent with ventricular hypertension, and S-T segment elevation with reversed tall upright T-waves in association with a decrease to the preinfusion ventricular base line. Other ECG changes included prolongation of the P-R segment, missed ventricular contractions, and arrhythmia. The ECG changes seemed to be subsequent to platelet microthrombus formation in the pulmonary arterial microcirculation. By 2.5 hours after the treatment, platelets "rebounded" into the circulation in 2 surviving guinea pigs, and left ventricular pressures and ECG profiles returned to the preinfusion base lines. Guinea pigs IV infused with similar amounts of inactivated (15 minutes at 100 C) fibrillary collagen material did not show changes.
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PMID:A proposed mechanism(s) of transitory ischemic injury to myocardium. 46 53

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Although glycosaminoglycans, particularly proteoglycans, have been characterized biochemically in normal and diseased arteries, little is known regarding their ultrastructural characteristics in human arteries. The observations reported here were made in renal arteries from nephrectomy specimens from patients with endstage kidney disease and hypertension. By light microscopy, the diffusely thick intima is characterized by small, slender smooth muscle cells embedded in a finely fibrillar, strongly alcian-blue positive, intercellular matrix. Ultrastructurally, there is a loose meshwork of collagen fibrils, elastic units and abundant fibrillogranular units staining strongly with ruthenium red and identified as proteoglycans. These consist of ovoid or diamond-shaped electron-dense granules about 300-500 A in diameter, having fine filamentous processes.
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PMID:Ultrastructure of proteoglycans in human renal arteries from end stage renal disease. 56 69

The static elastic properties and medial scleroprotein content of the aorta have been examined in spontaneously hypertensive rats (AS strain) aged 6 and 20 weeks (group SH). The results are compared with data from two previous studies on normal (group N) and induced hypertensive animals (group H). Spontaneous hypertension is associated with a relative increase in elastin and decrease in collagen when compared with the normal aorta. These changes are similar to, although smaller in magnitude than, those associated with induced hypertension. Elasticity measurements show that the functional stiffness (incremental strain) of the aorta in group SH is greater than normal. However, this difference diminishes with age, suggesting an adaptive response which tends to maintain the functional stiffness near to normal levels.
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PMID:Static mechanical properties and chemical composition of the aorta of spontaneously hypertensive rats: a comparison with the effects of induced hypertension. 69 88

The authors consider that attention should be paid to the arterial time in intravenous pyelography in all patients who undergo the examination. Manual injection or an injector containing 80 to 100 ml of 38% iodine contrast medium set at a speed of 20 ml/sec, on the one hand, and films taken during the arterial phase on the other hand, are the two conditions necessary to obtain a satisfactory arteriogram. Slight abdominal compression and subtraction improve the definition of the films. 600 cases have been collected so far, in the exploration of 105 patients with hypertension, 17 cysts, 7 malignant tumours, extra-renal pathology and various nephropathies in which no indication for arteriography existed. Thus pyelographic arteriography made it possible to avoid renal arteriograms in almost all our patients. Only one selective and one complete arteriogram were necessary. Unusual arterial lesions in nonsurgical renal conditions may be seen (glomerulonephritis, nephroangiosclerosis...) and unexpected images in abdominal conditions with renal manifestations or in association with nephropathies (aneurysms of digestive arteries and the aorta, collagen diseases etc.).
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PMID:[Arterial time of intravenous pyelography: initial results (author's transl)]. 79 61

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

One hundred and twenty patients with arterial hypertension and 3 cases of fibromuscular displasia of the renal arteries (FDRA) (group D) were studied; besides the usual arterial hypertension work up, a search of Ehlers-Danlos syndrome stigmata was carried out in all patients. The population of 120 hypertensive patients were classified in 3 groups: group A, fromed by 104 subjects without EDS stigmata; group B, constitued by 7 cases with hypermobility of one to three metar-carpophalangic joints and group C in which 9 subjects with hipermobility of more than 3 metacarpophalangic joints were included. Neither case of groups A and B showed arteriographic signs of FDRA. In 4 cases of group C there were arteriographic evidence of FDRA (3.3% of the whole population) and stigmata of SED (2 cases with skin biopsy positive for this entity). Two cases of group D showed stigmata of SED and a positive skin biopsy; the other case had a normal histology of skin and no clinical signs of SED. The presence of SED stigmata in a patient with arterial hypertension should alert the clinician in the diagnosis of FRDA; in such a case it is recommended that a renal arteriography be performed. In this paper similarities of SED of the arterial type and some cases of FDRA are remarked and it is proposed the both entities share the same or a very closed molecular collagen defect.
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PMID:[Further cases of Ehlers-Danlos syndrome of the renovascular dysplasic variety]. 93 46

Out of 136 placentas with vascular obliterations, 25 cases were placentas of children born alive, in 92 cases the placentas belonged to children born dead. In 19 cases we had no data on the baby. In placentas of babies born alive, the same vascular changes (subtotal and total obliterations, septal partitions of vascular lumina) were found as in those of dead-born children, although considerably less severe. Vascular obliterations should not be considered as post-mortal alterations of the placenta blood vessels, since only quantitative differences could be proved. Septum-like partitions are hardly ever found in placentas of babies born alive, in dead-born babies they are more frequent. They seem to present recanalizations, and are understood as a compensation mechanism for a placental insufficiency caused by vascular obliterations. The accentuated collagenization of the placental periphery, noticed in placentas of babies born alive, is being interpreted as the consequence of an impaired blood circulation, caused by partial and total vascular obliterations. The high collagen rate in the placental periphery in placentas of the dead-born is probably a reaction to the diminished fetal circulation. Endangitis obliterations in 73 placentas out of 4600 pregnancies of cases with late abortions, premature deliveries, perinatal death, underweigh and small for gestational age babies, impaired adaptation in newborns of mothers with proteinuria and hypertension speak strongly for assuming that endangitis obliterans presents a form of placental insufficiency. Endangitis obliterans of the placental blood-vessels has, however, been discovered frequently after Rubella infection in early pregnancy. The etiological factors of the endovascular process can be multiple, the morphological and the pathophysiological reactions are the same.
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PMID:[Obliterative angiopathy of placental stem villi (author's transl)]. 99 57


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