Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many authors have postulated that angulation of the carotid artery is a cause of stroke and recommend corrective operation. Symptoms attributed to such lesions are often nebulous and unrelieved by the operation, and proof is lacking that unselected patients who have this condition have a risk of stroke exceeding operative risk. A review of 282 cerebral angiograms showed an incidence of elongation and potential angulation of 43 percent in children and 20 percent in adults. Acutal angulation was not found in children, however, and no child was suspected of having cerebral ischemia. Of 47 adults with potential angulation, 17 were suspected of having cerebral ischemia, the remainder having a variety of other lesions, such as tumors, aneurysm, and intracranial hemorrhage. Of the 17 having suspected cerebral ischemia, all had alternative explanations for their symptoms (hypertension, intracranial atherosclerosis), except one whose symptoms were completely inappropriate to the carotid distribution. A single patient had a completed stroke, demonstrable angulation, and only mild hypertension. Elongation and potential angulation of the carotid artery is common but usually coexists with other lesions. If the finding is postulated as the cause for neurologic morbidity the surgeon must be assured that symptoms are clearly neurologic, that no other cause exists, that angulation reduces the carotid lumen significantly and reproduces symptoms, and that the risk of operation is less than the expected risk of stroke in untreated patients.
 ...
PMID:The significance of elongation and angulation of the carotid artery: a negative view. 16 14

Four theories of atherogenesis are briefly reviewed and criticized: the degenerative, the thrombogenic, the platelet aggregation and the insudative theory. Evidence is presented in detail to suggest that a modified form of the insudative theory (1) accounts more satisfactorily than the other theories for the known association of risk factors with atherosclerosis and (2) allows one to understand how some of the more important risk factors operate at the level of the arterial wall. It is proposed that atherosclerotic plaques, and also certain extravascular lesions broadly associated with atherosclerosis (corneal arcus, xanthomas), arise because altered endothelial permeability allows certain reactive macromolecular plasma proteins (the plasma low density and very low density lipoproteins and fibrinogen, which are normally largely confined to the circulation) to permeate endothelium and interact with charged components of the connective tissue gel of the arterial wall or other tissues. The effect of hyperlipidemia, hypertension, arterial disease or injury upon this process, and the manner in which these factors interact, is examined in relation to experimental findings and clinical observations.
 ...
PMID:Pathogenetic mechanisms in atherosclerosis. 16 10

This report enumerates and analyzes the complications of percutaneous transaxillary catheterization encountered in 200 consecutive patients undergoing diagnostic arteriography, and 20 consecutive patients who had catheter placement for selective chemotherapy. Diagnostic arteriography led to minor complications in eleven percent and major complications in two percent. Risk correlated with the type of procedure, number of catheter exchanges and particularly, the presence of arteriographic risk factors, such as hypertension, bleeding tendencies, and advanced atherosclerosis. Therapeutic catheter placements had a 15 percent incidence of minor and a 20 percent incidence of major complications. Here, also, complications were more likely in the presence of the arteriographic risk factors. Suggested means for decreasing the hazards of the transaxillary catheterization include: exclusion of high risk patients, use of a proper puncture site, careful catheter manipulation, the fewest possible catheter exchanges, correct manual hemostatis following catheter withdrawal, and close observation of the patient after the procedure. Early surgical intervention is indicated in the presence of a progressively developing neural defect.
 ...
PMID:Complications of percutaneous transaxillary catheterization for arteriography and selective chemotherapy. 17 8

The entry of [125I]-labelled low density lipoprotein (LDL) into different regions of the aortic intima has been studied over a 6 hour period in both normotensive and renal hypertensive rabbits fed a normal diet. Studies have also been carried out in previously hypertensive rabbits in which the blood pressure was normalized with parenteral hydralazine during the six hour period, in which entry was studied. In the normotensive rabbits entry into the aortic intima was less than 1 mug of LDL protein/100 mg dry defatted weight over the 6 hour period with greatest entry into aortic arch intima and significantly less into both the thoracic and abdominal aortic intimae. Hypertension increased the entry into the arch and into aortic arch intimae. Hypertension increased the entry into the arch and into the thoracic and abdominal segments but this was only statistically significant for the aortic arch. The entry of [125I] LDL into the intima in those rabbits in which the hypertension had been normalized was similar to that for the hypertensive rabbits. The results suggest that hypertension in the normal fed rabbit increases lipoprotein entry into the arterial wall by an effect on vessel wall permeability rather than by a direct effect of filtration pressure.
Atherosclerosis
PMID:Effect of hypertension on the entry of 125 I-labelled low density lipoprotein into the aortic intima in normal-fed rabbits. 18 87

Entry of 125I-labelled low density lipoprotein ([125I]LDL) into the aortic intima was studied over 6 hours in normotenisve and hypertensive rabbits fed a 1% cholesterol diet for 9 and 4 weeks respectively. Studies were also made in hypertensive and normotensive cholesterol-fed rabbits in which blood pressure was reduced acutely with parenteral hydralazine. In all groups the entry of E1125I]LDL was greatest in the aortic arch and significantly less in both the descending thoracic and abdominal regions. Lipoprotein entry into the aorta of cholesterol-fed rabbits was increased some 10-fold over the corresponding value previously found in rabbits fed a normal diet [1]. This increase was due to increased vascular permeability as well as to increased plasma LDL concentration. The hypertensive cholesterol-fed rabbits did not show significantly greater entry of [125I]LDL than the normotensive cholesterol-fed rabbits. Comparison of the rate of LDL entry over 6 house and the quanitity of cholesterol accumulated in the aortic segments over the period of cholesterol feeding indicated that lipoprotein fractions other than LDL must contribute singificant amounts of cholesterol to the developing lesion. The finding that LDL entry paralledled accumulation during cholesterol feeding, together with the finding that acute reversal of hypertension did not reduce the entry of [125I] LDL suggest that mechanisms other than increased filtration of plasma low density lipoprotein contribute significantly to the accelerated development of atherosclerosis in hypertension.
Atherosclerosis 1977 May
PMID:Hypertension-accelerated atherogenesis in cholesterol-fed rabbits. 19 28

Cholesterol, triglycerides, and Lp(a)/pre-beta1 lipoprotein were analyzed in 153 patients typed for liproprotien patterns. Coronary atherosclerosis was determined by selective coronary angiography and graded by a system taking into account proximal, middle and distal segments. Smoking habits, family history and hypertension were also recorded. Normal coronary arteries were encountered in 45, moderate coronary atherosclerosis (less than median score) in 50, and severe changes (greater than median score) in 58 patients. Cholesterol (P less than 0.05), positivity of Lp (a)/pre-beta1 lipoprotein (P less than 0.01), a family history of coronary heart disease (P less than 0.05), and smoking (P less than 0.01) differed between the group of normal arteries and the whole group of luminal obstructions. Serum triglycerides were not associated with coronary atherosclerosis. Cholesterol, positivity of the Lp(a)/pre-beta1 lipoprotein and a family history of coronary heart disease were also associated with the severity of the disease. Smoking was less prevalent in the group with severe changes.
 ...
PMID:Serum lipids in angiographically assessed coronary atherosclerosis. 20 36

Cardiovascular diseases are the leading cause of death in Western countries, with an enormous increase in death rate and involvement of younger age groups during the last decades. This applies especially to coronary heart disease and is mainly caused by first-degree risk factors: hypertension, hyperlipoproteinemia, cigarette smoking, gout, obesity, polycythemia, lack of physical activity, and stress. These risk factors are discussed with special reference to overnutrition and increased cholesterol levels. Recent resuults of research concerning lipids and their relation to atherosclerosis are reviewed.
 ...
PMID:[Etiology and pathogenesis of arteriosclerosis]. 20 5

The aim of the present study was to determine whether skin fibroblasts derived from patients with ischemic heart disease (IHD), which could not be related to accepted risk factors, would show a metabolic abnormality with respect to lipid or lipoprotein metabolism. Male patients 30-52 years old suffering from IHD were subdivided into two groups: those in whom IHD was not associated with risk factors such as hypertension, hyperlipoproteinemia, diabetes or smoking (group I); and those in whom heavy smoking was the only major risk factor recognized (group II). The controls were patients with angiographically normal coronary arteries (group III). Skin fibroblasts obtained from these patients were cultured and investigated with respect to metabolism of low density lipoprotein (LDL), synthesis of cellular lipids and induction of cholesterol ester accumulation in the presence of chloroquine, an inhibitor of lysosomal hydrolases. After 24 h incubation, the uptake and degradation of LDL protein in cells from patients of group II was significantly higher than in the controls, group III, but not different from those of group I. Hydrolysis of [3H] cholesterol linoleate, and incorporation of [3H] oleic acid into total lipids and into cholesterol esters was similar in cell cultures of the 3 groups studied. After exposure to chloroquine and LDL, the cells from the different donors accumulated cholesterol ester to a similar extent. Thus, whereas no significant difference was encountered in the lipid and lipoprotein metabolism in cells of patients with IHD without risk factors and controls, some increase in LDL metabolism was seen in cells from patients with IHD and with a history of smoking. It remains to be determined whether this increase was causally related to smoking.
Atherosclerosis 1978 Jul
PMID:Study of cultured skin fibroblasts from patients with and without ischemic heart disease. Metabolism of low density lipoprotein and cholesterol ester, synthesis of cellular lipids and effect of chloroquine on accumulation of cholesterol ester. 20 2

An analysis was made of correlative factors which might be related to the angiographically measured extent of coronary artery disease in 140 patients. All patients presented with clinically important chest pain. Thirty-three had a normal coronary arteriogram. The extent of the atheromatous process was measured precisely at angiography by three different techniques. A coronary score, based on the percentage of luminal narrowing, was found to be best suited for the analysis. The most important contributory factors to the severity of atherosclerosis was duration of clinical history, number of previous myocardial infarctions, and male sex, but more specifically elevation of serum cholesterol and diabetes mellitus. Cigarette smoking, obesity, hypertension, a family history of atherosclerosis, and elevated serum triglycerides had a positive influence but this was not statistically significant.
 ...
PMID:Relationship between extent of coronary artery disease and correlative risk factors. 22 61

The proliferation of aortic smooth muscle cells (ASMC) of Wistar rats, impaired by risk factors such as arterial hypertension, diabetes mellitus, atherogenic diet and staphylolysin injections and of normal Wistar rats treated with antirheumatic drugs such as prednisolone and acetylsalicylic acid was investigated. The cells of these animals were cultivated, subcultivated, and in the 2nd subcultures the cell numbers/5 ml medium were counted by means of Coulter Counter, and the cells were incubated with [3H]thymidine and the percentage of labelling in 100 or 1000 counted cells was stated. The effect of risk factors such as LDL and staphylolysin and of antirheumatic drugs such as prednisolone, acetylsalicylic acid, D-penicillamine and chloroquine added to the 2nd subcultures of cultivated ASMC of normal minipigs was investigated by the same method. The proliferation of cultivated ASMC of rats impaired by risk factors was accelerated. The proliferation of cultivated ASMC of rats treated with antirheumatic drugs was inhibited. The proliferation of ASMC of minipigs in the 2nd subcultures was activated by addition of risk factors and inhibited by addition of antirheumatic drugs. Antirheumatic drugs given to the rats and added to the medium of the 2nd subcultures of ASMC of normal minipigs inhibit the acceleration of ASMC proliferation induced by simultaneously given risk factors. The proposal to augment up our arsenal of the hitherto existing preventive and therapeutical measures by the application of antirheumatic drugs based on the experimental models referred to is supported by the result of a limited prospective double-blind-study of a sample of 133 male patients after myocardial infarction. The most remarkable result that the acceleration of the ASMC proliferation, the real pathologic process of arteriosclerosis, is inhibited by the application of antirheumatic drugs, at exactly the same time as the acceleration of the fibroblast proliferation, the real pathologic process in rheumatic diseases--ASMC and fibroblast, both being mesenchymal cells--recommends the use of these drugs in the prevention and therapy of human arteriosclerosis. The surprising result of our in-vivo experiments, that the acceleration of the growth of the ASMC induced by risk factors and the inhibition of the growth induced by antirheumatic drugs persist in the subcultures, is explained by the "selection theory" that there are dissimilar kinds of ASMC in normal arteries and that they react differently.
Atherosclerosis 1979 Oct
PMID:Effect of risk factors and antirheumatic drugs on the proliferation of aortic wall cells. 22 70


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>