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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with insulin-dependent diabetes mellitus have an increased mortality and morbidity due to vascular complications. Nitric oxide from the vascular endothelium contributes to the control of normal vascular tone, and endothelial dysfunction has been implicated in the pathogenesis of diabetic vascular disease. In this study we have examined basal and stimulated nitric oxide-mediated vasodilatation in insulin-dependent diabetics and age- and sex-matched healthy controls. Drugs were infused locally into the brachial artery and forearm blood flow measured using venous occlusion plethysmography. Noradrenaline and NG-monomethyl-L-arginine produced similar reductions in resting forearm blood flow in healthy controls. However, in the diabetics, NG-monomethyl-L-arginine was significantly less effective than noradrenaline. Comparing between groups, the response to NG-monomethyl-L-arginine was also significantly less in the diabetics compared with the healthy controls. The response to sodium nitroprusside was significantly less in the diabetics compared with the healthy controls, whereas the responses to both acetylcholine and verapamil were the same in the two groups. The results provide evidence for an abnormality of basal nitric oxide-mediated dilatation in the forearm arterial bed of patients with insulin-dependent diabetes mellitus, and suggest that the vascular smooth muscle is less sensitive to nitric oxide.
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PMID:Inhibition and stimulation of nitric oxide synthesis in the human forearm arterial bed of patients with insulin-dependent diabetes. 146 3

Cocaine abuse and its association with vascular disease has become common in the medical literature. A variety of vascular problems have been described including neurovascular complications, cardiovascular complications, aortic dissection, venous thrombosis, mesenteric artery thrombosis, and renal infarction. The pathogenesis of these vascular complications has largely been related to increased adrenergic activity leading to vasospasm. Interaction of cocaine with the vascular endothelium resulting in thrombosis or vasculitis has also been suggested. We report a case of diffuse aneurysmal change of the aorta associated with an atypical inflammatory component consistent with possible cocaine induced vasculitis.
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PMID:Accelerated atherosclerosis, aneurysmal disease, and aortitis: possible pathogenetic association with cocaine abuse. 152 57

The pathophysiology of peripheral circulatory disturbance in patients presenting with vibration syndrome was studied from the viewpoint of blood coagulation. Plasma levels of fibronectin (FN), vitronectin (VN), thrombin-antithrombin III complex (TAT), and alpha 2-plasmin inhibitor-plasmin complex (PIC) were measured in 23 subjects who showed no evidence of vibration-induced white finger [VWF(-) group] and in 24 patients who presented with VWF [VWF(+) group]. In the VWF(-) group, plasma FN concentrations were elevated but plasma TAT and PIC levels were within the normal ranges. In the VWF(+) group, plasma FN concentrations were normal but plasma TAT and PIC levels were significantly elevated. In both groups, plasma VN concentrations were similar to those in normal controls. For purposes of comparison, 32 patients presenting with diabetes mellitus were also studied. They were divided into 2 groups, 13 subjects who showed no evidence of angiopathy [complication(-) group] and 19 patients who presented with angiopathy [complication(+) group]. In the complication(+) group, plasma TAT and PIC concentrations were significantly elevated, as in the VWF(+) group. These results suggest that in vibration syndrome, vibration, cold stimulus, or other factors first injure the vascular endothelium, resulting in a rise in plasma FN, and that in the VWF(+) group, augmentation of coagulation and fibrinolysis induces a state of compensated disseminated intravascular coagulation (DIC).
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PMID:Activation of blood coagulation and fibrinolysis in vibration syndrome. 172 Jul 65

Altered permeability of vascular endothelium to macromolecules may play a role in vascular disease as well as vascular homeostasis. Because the shear stress of flowing blood on the vascular wall is known to influence many endothelial cell properties, an in vitro system to measure transendothelial permeability (Pe) to fluorescein isothiocyanate conjugated bovine serum albumin under defined physiological levels of steady laminar shear stress was developed. Bovine aortic endothelial cells grown on polycarbonate filters pretreated with gelatin and fibronectin constituted the model system. Onset of 1 dyn/cm2 shear stress resulted in a Pe rise from 5.1 +/- 1.3 x 10(-6) cm/s to 21.9 +/- 4.6 X 10(-6) cm/s at 60 min (n = 6); while 10 dyn/cm2 shear stress increased Pe from 4.8 +/- 1.5 X 10(-6) cm/s to 50.2 +/- 6.8 X 10(-6) cm/s at 30 min and 49.6 +/- 8.9 X 10(-6) cm/s at 60 (n = 9). Pe returned to preshear values within 120 and 60 min after removal of 1 and 10 dyn/cm2 shear stress, respectively. The data show that endothelial cell Pe in vitro is acutely sensitive to shear stress.
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PMID:Endothelial albumin permeability is shear dependent, time dependent, and reversible. 190 93

Endothelium-derived relaxing factor (EDRF) is probably identical to nitric oxide (NO) and is released by the vascular endothelium both in the basal unstimulated state and in response to a wide range of physical and chemical stimuli. Since it was first described 10 years ago, evidence is accumulating that it is an important modulator of vascular smooth muscle tone. EDRF acts on the pulmonary vascular bed as on the systemic circulation. EDRF release to pharmacologic stimuli is impaired in pulmonary arteries from patients with chronic hypoxemia. This impairment is associated with severity of respiratory failure and of structural change of vessel walls. Disturbance of EDRF activity may be important in the pathophysiology of pulmonary vascular disease. This brief review describes the current status of experimental studies concerning the possible role of EDRF on the pulmonary circulation in normal conditions and in the pathogenesis of pulmonary hypertension.
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PMID:Endothelium-derived relaxing factor and the pulmonary circulation. 192 72

The nonhemodynamic actions of nifedipine and some other calcium antagonists are reviewed with regard to their relevance to the vasculoprotective and antiarteriosclerotic action of calcium antagonists. Nifedipine, and in order of declining potency, verapamil and diltiazem were shown to inhibit vascular myocyte proliferation and migration. Also, the incorporation of cholesteryl esters into macrophages or myocytes was inhibited by dihydropyridines and verapamil but not by diltiazem. The cholesterol and calcium contents were found to be lowered in the aortae of hypercholesterinemic rabbits treated chronically with dihydropyridine calcium antagonists. Replacement of damaged vascular endothelium and internal elastic lamina was seen in hypertensive Dahl-S rats after 6 weeks of antihypertensive treatment with nifedipine. In addition to their blood-pressure lowering action, these nonhemodynamic effects might be involved in the prevention and reversal of hypertensive vascular disease and neuropathologic symptoms observed after the treatment of hypertensive rats with nifedipine or other dihydropyridine calcium antagonists, since these therapeutic effects were also seen after blood-pressure neutral doses.
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PMID:Influence of nifedipine on experimental arteriosclerosis. 207 89

Prostacyclin and endothelium-derived relaxing factor (or nitric oxide) are unstable mediators produced by the vascular endothelium, that are important for local regulation of platelet behavior and blood flow. This review focuses on the basic biochemistry and pharmacology of prostacyclin, its interactions with nitric oxide and nitrovasodilator drugs, and the implications of disturbances in this system for vascular disease, particularly hypertension and atherosclerosis. Prostacyclin and its stable analogs are also finding limited therapeutic applications in preservation of platelet function, pulmonary hypertension, and investigation into the cytoprotective and antiatherosclerotic properties is continuing.
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PMID:Prostacyclin and vascular function: implications for hypertension and atherosclerosis. 208 4

Expression of major histocompatibility complex class II antigens was investigated in the normal lungs and in lung allografts of mongrel dogs after single-lung transplantation. Cryostat sections were stained with an indirect immunoperoxidase technique that used B1F6 and 7.5.10.1 as anti-MHC class II monoclonal antibodies. In the normal lungs and native lungs of the recipient dogs after single-lung transplantation, only some cells of lymphoid tissue and macrophages/dendritic cells were MHC class II-positive. During acute rejection, increased infiltration with MHC class II-positive cells in perivascular, peribronchial, and interstitial areas and intraalveolar spaces was found in lung allografts. In addition, expression of MHC class II antigens was induced on the bronchial epithelium and vascular endothelium. Induced expression of MHC class II antigens on the bronchial epithelium and vascular endothelium in rejecting lung allografts was found as early as two days after single-lung transplantation. The intensity of MHC class II antigen expression on bronchial epithelium and vascular endothelium in graft lungs increased with the progression of rejection response and directly correlated with the bronchoalveolar lavage fluid (BALF) levels of biochemical markers, as tumor necrosis factor alpha, gamma-interferon (IFN-gamma), interleukin 2 (IL-2) and soluble interleukin 2 receptor (SIL-2R). Abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium and abnormal elevation of BALF levels of the cytokines in lung allografts could be prevented by cyclosporine (CsA) treatment. Our results suggested that MHC class II antigen expression could be induced on the bronchial epithelium and vascular endothelium of canine lung allografts during acute rejection. This abnormal expression of MHC class II antigens on bronchial epithelium and vascular endothelium of graft lungs may serve as a specific index for diagnosis of lung allograft rejection when infection as an inducing factor can be excluded. Furthermore, bronchial epithelium and vascular endothelium of lung allografts have become MHC class II-positive, and are likely to be the targets for low-grade rejection, resulting in the development of bronchiolitis obliterans and occlusive vascular disease in lung allografts.
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PMID:Increased expression of MHC class II antigens in rejecting canine lung allografts. 211 27

A 45-year-old woman with a 4-year history of systemic lupus erythematosus (SLE) developed fever, decreased visual acuity and skin ulceration. A biopsy of a cutaneous ulcer demonstrated small vessel vasculitis with characteristic cytomegalovirus (CMV) inclusions in the vascular endothelium. The presence of CMV was confirmed by DNA hybridization immuno-histochemistry. Retinal artery vasculitis, previously associated with flares of her SLE, was also noted on ophthalmologic examination. Our case demonstrates that CMV infection can mimic the cutaneous manifestations of collagen vascular disease and that early identification can be made by biopsy of suspicious skin lesions.
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PMID:Systemic lupus erythematosus and concurrent cytomegalovirus vasculitis: diagnosis by antemortem skin biopsy. 254 61

We measured simultaneous plasma beta-thromboglobulin (BTG) and adhesion of 51Cr-labelled, washed platelets to confluent, bovine aortic endothelial monolayers in 50 insulin-dependent diabetic patients and 30 normal subjects (respective mean ages (+/- SD) = 45.1 +/- 16.4 and 45.8 +/- 17.2 years). Compared to normal subjects without arteriosclerotic complications, diabetic patients had higher plasma BTG (34.8 +/- 1.8 (SEM) vs. 21.3 +/- 1.8 ng/ml) and platelet adhesiveness to endothelium (PAE) (3240 +/- 170 vs. 2430 +/- 120 X 10(3) platelets per well) (p less than 0.0002, respectively). Results in diabetic patients did not correlate with plasma glucose, hemoglobin AIa-c, known duration of disease, or sex; plasma BTG correlated with age (r = +0.36), and PAE correlated with plasma creatinine (r = +0.39). Those with clinically evident vascular disease, who were also older (47.8 +/- 2.6 (SEM) vs. 37.3 +/- 4.5 years, p less than 0.05), showed trends to higher plasma BTG (36.7 +/- 2.2 (SEM) vs. 28.8 +/- 3.4 ng/ml, p = 0.06) and PAE (3400 +/- 200 vs. 2800 +/- 280 X 10(3) platelets per well, p = 0.09). A strong correlation was found between plasma BTG and PAE in diabetic patients (r = +0.62, p less than 0.0001) either with or without vascular disease, which remained strong after statistical correction (partial Pearson correlation) for age and plasma creatinine, but not in normal subjects (r = +0.08, p greater than 0.1). These studies demonstrate that platelets in some diabetic patients are excessively adhesive to vascular endothelium, and that plasma BTG and platelet adhesiveness are intercorrelated.
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PMID:Plasma beta-thromboglobulin is correlated with platelet adhesiveness to bovine endothelium in patients with diabetes mellitus. 257 51


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