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

Thoracic aortic aneurysms were detected in 72 residents (44 women and 28 men) in a stable midwestern community over a 30-year period, for an age- and sex-adjusted incidence of 5.9 new aneurysms per 100,000 person-years. The incidence was equal in both sexes and decreased slightly over the 30 years. Ages ranged from 47 to 93 years (median 65 years for men and 77 years for women). The ascending aorta was involved in 37 patients, the aortic arch in 8, and the descending aorta in 27. Pathologic examination was performed in 51 patients. The cause was aortic dissection in 27 patients (53%), atherosclerosis in 15 (29%), aortitis in 4 (8%), cystic medial necrosis in 3 (6%), and syphilis in 2 (4%). All autopsied patients had pathologic evidence of significant hypertension. Eleven patients (25%) had concomitant abdominal aortic aneurysms. Rupture occurred in 53 patients (74%) and 50 died. Thirty-seven of these patients had no prior diagnosis of aneurysm. The median interval between diagnosis and rupture in the 16 remaining patients was 2 years (range 1 month to 16 years). Ninety-five percent of aortic dissections ruptured and 51% of nondissecting aneurysms ruptured. The actuarial 5-year survival for all 72 patients was 13%; for patients with aortic dissection, 7% and for patients without dissection, 19.2%.
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PMID:Thoracic aortic aneurysms: a population-based study. 714 88

54 patients with an abdominal aortic aneurysm were hospitalized between 1969 and 1980 in the Clinic of Cardiovascular and Thoracic Surgery at Rennes (Pr. Y. Logeais): 35 were ruptured aneurysms, 19 non-ruptured. The average age of the patients was 70.6 years. 48% of patients showed signs of atheroma in at least one other site. 24% had arterial hypertension. Arteriography was carried out in 51.5% of the non-ruptured aneurysm cases and in 26% of the ruptured cases. Both ultrasound and tomography are regarded presently as very useful tests. The intervention carried out in 41 patients always involved the insertion of a by-pass graft (aortic only in 7 cases; aorto-biiliac in 19 cases; aorto-bifemoral in 15 cases). Mortality was 7.7% for the non-ruptured aneurysms. 59% for the ruptured aneurysms, the deaths above all being related to the degree of visceral ischaemia. Secondary mortality was comparable for all the aneurysms operated on. More than 80% of patients were surviving 5 years after surgery.
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PMID:[Surgery of aneurysms of the abdominal aorta. Clinical study and surgical results. Apropos of a series of 54 cases]. 716 75

Replication-deficient recombinant adenovirus vectors have been used to transfer foreign genes effectively to a wide variety of cell types in vivo and in vitro. We have now used adenovirus containing either the Escherichia coli beta-galactosidase (beta-gal) gene (AdHCMVsp1LacZ) or the firefly luciferase gene (Ad5-luc3) to test the hypothesis that efficiencies of adenovirus-mediated gene delivery into organ cultures of smooth muscle differ according to the anatomic origin of the muscle. Thoracic aorta and renal artery were isolated from 9-week-old male Sprague-Dawley rats and exposed to adenovirus after 16 hours of incubation with serum-free medium (Dulbecco's modified Eagle's medium). With the use of histochemical methods, beta-gal staining was noted in both endothelial and adventitial cells but not in the muscular media of thoracic aorta and renal artery exposed to AdHCMVsp1LacZ. The efficiency of the transfection, assessed either by counting of beta-gal-stained cells in intact vessels or by measurement of beta-gal activity in tissue extracts, was higher in renal artery than thoracic aorta (P < .05). Consistent with this result, luciferase activity in renal artery exposed to Ad5-luc3 (15.9 +/- 2.1 x 10(6) relative light units per milligram protein) was higher than that in thoracic aorta (8.3 +/- 2.0 x 10(6), P < .05). To determine whether increased efficiency of adenovirus-mediated gene transfer into renal artery is a function of the replication status of vessels, we assessed [3H]thymidine incorporation. [3H]Thymidine uptake by thoracic aorta was only 63% of that in renal artery (P < .05), indicating that more proliferating cells are present in renal artery. We conclude that the efficiency of adenovirus-mediated gene transfer into cultured renal artery is enhanced compared with that into thoracic aorta and propose that the increase in efficiency is related to the higher proliferative activity of renal artery.
Hypertension 1995 Dec
PMID:Heterogeneity of adenovirus-mediated gene transfer in cultured thoracic aorta and renal artery of rats. 749 65

Studies have shown that angiotensin-converting enzyme (ACE) inhibitor treatment in young genetically hypertensive rats prevents the full expression of blood pressure and vascular abnormalities in the adult. This model provides unique conditions with which to study the pathogenesis of altered Ca++ regulation. Normotensive (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) received at 6 to 10 weeks of age either ACE inhibitor (ramipril), hydralazine/hydrochlorothiazide or no treatment. At 17 weeks of age, rats were anesthetized, and vascular tissue was excised. Thoracic aorta challenged with 20 mM caffeine in Ca(++)-free buffer produced a phasic contractile response. The magnitude of this phasic response was used as a measure of Ca++ released from intracellular stores; a direct correlation between this phasic response and systolic blood pressure was observed. A concentration-response curve to Bay K8644 was performed on carotid arteries; a direct correlation of force development to Bay K8644 and systolic blood pressure was observed. All WKY groups showed lower blood pressure and force development in response to Bay K8644 than did SHRSP. Treatment with ramipril reduced blood pressure and force development in response to Bay K8644 in adult SHRSP, although not to levels of WKY rats, whereas WKY rats were unaffected by treatment. These data support the hypothesis that contractile responses to Bay K8644 in carotid arteries and caffeine in aorta parallel changes in systolic blood pressure. We conclude that alteration of Ca++ regulation in hypertension is directly related to elevated blood pressure and mediated by an angiotensin II-sensitive mechanism during development.
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PMID:Angiotensin-converting enzyme inhibition during development alters calcium regulation in adult hypertensive rats. 750 33

This study examined whether vascular contractions related to the extracellular or intracellular pools of calcium activated by serotonin are altered by high arterial pressure in chronic hypertension. Coarctation hypertensive (CH), sham normotensive control (C), and one-kidney, one-clip hypertensive rats (1K1C) were used. Tail systolic, carotid, and femoral arterial pressures were measured. Thoracic aortas from 1K1C and CH rats, as well as abdominal aortas from 1K1C rats, but not abdominal aortas from CH rats were exposed chronically to elevated arterial pressure. Isolated rings of thoracic and abdominal aortas from all groups were suspended in muscle baths for isometric force recordings. After cellular calcium depletion, dose-response curves to extracellular calcium, in the presence of 10(-5) mol/L serotonin, were unchanged in thoracic or abdominal aortas among the three groups. In the presence of submaximum levels of serotonin (2 x 10(-6) mol/L), thoracic and abdominal rings without endothelium and abdominal rings with endothelium from the three groups showed similar responses to extracellular calcium. Such responses were significantly depressed in thoracic rings with endothelium from CH and 1K1C rats. Transient contractions attributable to release of an intracellular calcium pool by 10(-5) mol/L serotonin were enhanced significantly in hypertensive thoracic and abdominal aortas from 1K1C rats, when the pool was loaded with 0.25, 0.5, 1.0, 2.0, or 4.0 mmol/L CaCl2, as well as in hypertensive thoracic aortas from CH rats when the pool was loaded with 1.0, 2.0, or 4.0 mmol/L CaCl2, but not in normotensive abdominal aortas from CH rats at any calcium-loading concentration. Similar results were observed in aortas from C, CH, and 1K1C rats loaded with 1.0 or 2.0 mmol/L CaCl2 and stimulated with 2 x 10(-6) mol/L serotonin. Endothelial removal had no effect on these calcium-release contractions in abdominal aortas from any group, but enhanced contractions in thoracic aortas of 1K1C rats. In rings loaded with 2.0 mmol/L CaCl2, 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate inhibited contractions attributable to release of cellular calcium stores to a similar extent in C, CH, and 1K1C rats. This study suggests that serotonin-stimulated intracellular calcium-dependent aortic contractions are enhanced by elevated pressure in renal hypertensive rats.
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PMID:Effect of chronic high pressure on transient and tonic vascular contractions to serotonin in hypertension. 761 49

Late survival rates were compared and analysed for 1070 patients undergoing repair of ruptured infrarenal abdominal aortic aneurysm (RAAA, n = 364, mean age 70.0 years, male:female ratio 5.6:1) and non-ruptured abdominal aortic aneurysm (AAA, n = 706, mean age 66.6 years, male: female ratio 5.4:1) between January 1970 and July 1992 at the Department of Thoracic and Cardiovascular Surgery of Helsinki University Central Hospital, Finland. There was a statistically significant difference in survival rates between the RAAA and AAA groups during the first three months after repair of abdominal aortic aneurysm. Operative mortality rates were 7.4% for electively repaired abdominal aortic aneurysms and 48.7% for ruptured abdominal aortic aneurysms. For 3-month postoperative survivors there existed no statistically significant difference in late survival rates, nor did these rates differ from those of an age- and sex-matched population. Five-year survival rates for 3-month postoperative survivors were 60% in the RAAA group and 67% in the AAA group. Median survival time was 5.7 years and 7.5 years, respectively. Coronary artery disease, hypertension, chronic obstructive pulmonary disease and renal insufficiency statistically significantly reduced late survival rates after 3 months post-surgery for non-ruptured abdominal aortic aneurysm, whereas these risk factors did not alter late prognosis after successful repair of ruptured abdominal aortic aneurysm. Cerebrovascular disease reduced late survival rates both in AAA (median survival time 6.3 years) and RAAA group (median survival time 4.9 years). Of late deaths 41% were caused by coronary artery disease in the AAA group and 38% in the RAAA group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of long-term survival after repair of ruptured and non-ruptured abdominal aortic aneurysm. 772 78

We delineate the current role of extra-anatomical revascularization techniques in the treatment of patients with atherosclerotic renal artery stenosis. There are 2 components to this study. In part 1 all abdominal aortograms performed between 1989 and 1993 were reviewed to document the presence of significant abdominal aortic and visceral arterial atherosclerosis in patients with atherosclerotic renal artery stenosis. A total of 254 patients with atherosclerotic renal artery stenosis was identified. Among 44 patients with severe unilateral disease the incidence of significant abdominal aortic atherosclerosis was 75%. The incidence of significant (greater than 50%) stenosis of the celiac, right common iliac and left common iliac arteries was 52%, 32% and 27%, respectively. In 129 patients with severe atherosclerotic renal artery stenosis bilaterally or in a solitary kidney the incidence of significant abdominal aortic atherosclerosis was 81%, and the incidence of significant (greater than 50%) stenosis of the celiac, right common iliac and left common iliac arteries was 59%, 57% and 59%, respectively. These data indicate that hepatorenal, splenorenal and iliorenal bypass cannot be performed in many patients with atherosclerotic renal artery stenosis due to significant disease involving the donor vessels for these operations. In part 2, all patients undergoing surgical renal revascularization with an extra-anatomical bypass operation between 1980 and 1992 were reviewed. A total of 175 operations was done in 171 patients, including hepatorenal bypass in 59, splenorenal bypass in 54, iliorenal bypass in 37, thoracic aortorenal bypass in 23, renal autotransplantation in 1 and superior mesentero-renal bypass in 1. There were 5 operative deaths (2.9%) and 7 cases of postoperative graft thrombosis (4%). All patients with poorly controlled hypertension were cured or improved postoperatively. Among patients with ischemic nephropathy, postoperative renal function improved in 35%, remained stable in 47% and deteriorated in 18%. Extra-anatomical techniques remain an important component of the surgical armamentarium for atherosclerotic renal artery stenosis. Thoracic aortorenal bypass is a useful new approach in patients with significant celiac and iliac occlusive disease.
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PMID:The contemporary role of extra-anatomical surgical renal revascularization in patients with atherosclerotic renal artery disease. 775 20

Coronary heart disease (CHD) is the leading cause of mortality in the United States. The present cohort study was conducted to determine whether rate of FEV1 loss independently predicts CHD mortality in apparently healthy men. White male Baltimore Longitudinal Study of Aging (BLSA) participants without CHD underwent clinical evaluation at 2-yr intervals; 883 had satisfactory pulmonary and lipid studies and returned for a least one visit. Cases were BLSA subjects without CHD on entry who died a "coronary death" (death from acute myocardial infarction, sudden death, or congestive heart failure in the presence of coronary artery disease). Forced expiratory maneuvers followed American Thoracic Society guidelines. Serum cholesterol, blood pressure, cigarette smoking, and body mass index were obtained from the BLSA database. There were 79 CHD deaths and 804 survivors during an average follow-up of 17.4 yr. After adjustment for age, initial FEV1% predicted, smoking status, hypertension, and cholesterol, a time-dependent proportional hazards model showed that cardiac mortality, but not all causes of mortality, generally increased with increasing quintile of FEV1 decline for the entire cohort (relative risk [RR] 2.92-5.13) and separately for the subset of never-smokers. Thus, excess CHD mortality follows a large decline in FEV1, independent of the initial FEV1% predicted, cigarette smoking, and other common CHD risk factors.
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PMID:Rapid decline in FEV1. A new risk factor for coronary heart disease mortality. 784 97

Tachycardia and hypertension may cause myocardial ischaemia in patients with coronary heart disease going through major surgery. Thoracic epidural analgesia (TEA) has been reported to be beneficial in this situation. The haemodynamic effects of TEA in aortocoronary bypass surgery were investigated in 30 male patients < 65 years old and with ejection fraction > 0.5. They were randomized into 3 groups: the high dose fentanyl (HF) group receiving high-dose fentanyl (55 micrograms.kg-1) anaesthesia, the HF+TEA group receiving the same fentanyl dose+TEA with 10 ml bupivacaine 5 mg.ml-1 followed by 4 ml every hour, and the low dose fentanyl (LF) + TEA group receiving low-dose fentanyl (15 micrograms.kg-1) anaesthesia+TEA. Haemodynamic parameters, the use of vasoactive and inotropic drugs and fluid balance were followed during the operation and for 20 h postoperatively. Before bypass the only significant difference between groups was a higher mean pulmonary arterial pressure in the HF+TEA group and a lower systemic vascular resistance (SVR) in the LF+TEA group, both compared to the HF group. 89% of epidural group patients needed small doses of ephedrine whereas more HF group patients were given nitroglycerine. During bypass SVR and mean arterial pressure (MAP) were significantly higher and pump flow lower in the HF group compared to the LF+TEA group. More ketanserin to HF group patients and methoxamine to epidural group patients were given. After bypass heart rate increased in all groups. Lower MAP 0.5 h after bypass and higher filling pressures in the early post bypass period in the epidural groups, most pronounced in the HF+TEA group, were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thoracic epidural analgesia in aortocoronary bypass surgery. I: Haemodynamic effects. 788 6

The endothelins are a recently discovered family of potent contractile peptides produced by endothelial cells. These peptides have been suggested to play an important role in the pathogenesis of hypertension, myocardial infarction, cardiogenic shock, and so on. The aim of our study was to compare the responses to endothelin-1 (ET-1) with those to L-noradrenaline (NA) in aortic rings from rats of different strains and ages. Thoracic aorta rings from spontaneously hypertensive (SHR), Wistar Kyoto (WKY), Brown Norway (BN) and spontaneously hyperlipemic (Yoshida, YOS) rats 2-4 (young), 6-8 (adult) and 20-25 (old) months old were used. There were no changes in the pD2 values for ET-1 and NA between WKY and SHR rats at the ages studied. The ET-1 and NA Emax in adult SHR rats was significantly lower than in the age-matched WKY animals. Old age reduced the ET-1 and NA Emax in both SHR and WKY rats abolishing the difference observed at 6-8 months in the same groups. The reactivity to ET-1 and NA of BN and YOS rats was modified only in young rats. In YOS strain aging did not modify the ET-1 and NA responses as the pD2 and Emax values remained unchanged. Our findings demonstrate that ET-1 is a more potent vasoconstrictor than NA and that this potency remains unchanged throughout the ages and the pathologies studied. In contrast, the pD2 of NA decreases with old age in SHR and WKY rats. We conclude that rat strain but not hypertension or hyperlipemia can modify the response to ET-1 or NA in old age. We suppose that this functional change may involve alterations in the responsiveness of vascular smooth muscle.
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PMID:Aging and in vitro vascular responses to endothelin-1 in several rat strains. 810 9


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