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

Chronic psychosocial stress in male mice produces chronic interstitial nephropathy not explained by renal vascular disease or urinary infection. Four groups of male CBA mice were studied. Group 1 and group 2 were placed in Henry-Stephens complex population cages for 5 months. Group 2 had caffeine, 800 micrograms/ml, added to their drinking water. Control groups 3 and 4 were unstressed, but group 4 had 800 micrograms/ml of caffeine added to their water. Stressed animals developed chronic interstitial nephropathy which was more severe in animals drinking caffeinated water. In addition, the percent of cortex involved in interstitial fibrosis was higher in group 2, 18.0 +/- 1.4, than in group 1, 15.2 +/- 2.3 (p less than 0.05). Both groups had more fibrosis than unstressed animals (p less than 0.01). Blood urea nitrogen was more elevated in group 2, 47 +/- 13 mg/dl, than in group 1, 29 +/- 17 mg/dl (p less than 0.05). Again both values exceeded those in unstressed animals (p less than 0.01). It is concluded that prolonged environmental stress can lead to the renal morphologic changes of chronic interstitial nephritis. Both renal pathology and function are worse when there is concurrent high caffeine intake. The relevance of this model to human disease related to analgesic use or with affective illness requires further study.
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PMID:Chronic interstitial nephropathy in mice induced by psychosocial stress: potentiation by caffeine. 668 61

A new type of endovascular prosthesis has been developed using a unique metal alloy (nitinol) with a heat-sensitive memory. Nitinol wire coil grafts were straightened in ice water and passed into the canine aorta via catheter, where they reformed into their original shapes. Follow-up aortograms demonstrated long-term patency with minimal thrombus formation. Nitinol endovascular coil grafts may eventually be used in the nonsurgical treatment of several forms of vascular disease.
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PMID:Nonsurgical placement of arterial endoprostheses: a new technique using nitinol wire. 682 42

Single-breath carbon monoxide diffusing capacity (Dsb) was measured before and during immersion of one hand in ice water (cold pressor test) in the following three groups of subjects: (1) normal subjects; (2) patients with isolated Raynaud's disease; and (3) patients with Raynaud's phenomenon and progressive systemic sclerosis. No change in Dsb was found in normal subjects or patients with progressive systemic sclerosis. Patients with isolated Raynaud's disease showed a rise in Dsb during cold pressor testing, the mean increase being 8 percent. These results suggest that a rise in Dsb during exposure to cold is a response unique to patients with isolated Raynaud's disease or Raynaud's phenomenon without progressive systemic sclerosis, and not a normal physiologic response to cold. The lack of change in Dsb in response to cold in progressive systemic sclerosis, interpreted by other authors as an indicator of pulmonary vascular disease, resembles the normal response to a challenge with cold.
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PMID:Effect of the cold pressor test on diffusing capacity. Comparison of normal subjects and those with Raynaud's disease and progressive systemic sclerosis. 688

We report an autopsy case of granulomatous angiitis of the central nervous system (GANS) complicated by the syndrome of inappropriate antidiuretic hormone (SIADH). A 88-year old female was admitted because of progressive mental deterioration, fever, and vomiting. A computed tomogram disclosed bilateral periventricular lucency, and a low-density area in the right occipital lobe. Laboratory studies during her hospital stay, revealed hyponatremia, hypoalbuminemia, and increased antidiuretic hormone. Treatment with antibiotics, hypertonic saline solution, and steroids, and water restriction was ineffective, and the patient died six weeks after admission. Autopsy examination of the brain revealed slightly turbid meninges with multiple small infarctions in the corona raiata of both cerebral hemispheres. Microscopic study disclosed granulomatous inflammation with many giant cells in the walls of small and medium sized vessels, and the adventitia and media were more involved than the intima. Their lumens were narrowed, and many thrombi were observed. Extensive non-granulomatous inflammatory change was found mainly in the subarachnoid space. All of these findings were similar to the GANS firstly reported by Cravioto et al, in 1959. Since the blood vessels in the central nervous system play an important part in any inflammatory conditions and the blood vessels may be involved by bacterial, fungal, parasitic or viral meningitis, various microorganisms have been suspected as the cause of GANS, including mycoplasma, herpes zoster, herpes simplex viruses, cytomegalovirus, and human T-lymphotropic virus type III (HTLV-III). Some reported cases have been associated with Hodgkin's disease and cerebral amyloid angiopathy. We could not identify any cause in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Granulomatous angiitis of the central nervous system complicated by the syndrome of inappropriate antidiuretic hormone]. 760 90

To gain new insights into the pathogenesis of diabetic angiopathy, the influence of high glucose concentration on cation transport of vascular smooth muscle cell (VSMC) membrane was investigated by measuring Na, K and Ca transport in serially passaged cultured VSMC. (1) Na-K pump activity, described as ouabain sensitive 86Rb uptake, and Na-K cotransport, described as bumetanide sensitive 86Rb washout of VSMC, grown in high glucose concentration medium (460 mg/dl), was lower than that grown in normal glucose concentration medium (100 mg/dl). A smaller 5-N,N-hexamethylene amiloride (HMA) sensitive 22Na uptake (Na-H antiport) in high glucose concentration medium. accounted for this difference. (2) 45Ca uptake was also smaller in VSMC cultured in high glucose concentration medium. However, the washout rate constant for 45Ca was comparable between high and normal glucose cultured VSMC. (3) Both intracellular concentration of Na and cytosolic free Ca concentration concentration ([Ca]i) of high glucose cultured VSMC were greater than normal glucose cultured VSMC. (4) Intracellular water volume based on the equilibrium distribution of 3-O-methyl-[14C]glucose was not different between normal and high glucose cultured VSMC. It is concluded that VSMC grown in high glucose concentration milieu manifests a decreased Na-K, and Ca transport in conjunction with an increase in intracellular concentration of Na and [Ca]i. These results suggest that high glucose, per se, may alter membrane permeability to cations, possibly leading to changes in VSMC contractility and/or proliferation. This abnormality seen in the diabetic state may closely link to the pathogenesis of diabetic angiopathy, thus as a result risking hypertension and vascular disease.
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PMID:Differential regulation of cation transport of vascular smooth muscle cells in a high glucose concentration milieu. 795 12

(1) In Japan, atherosclerosis in the extracranial arteries has now been more or less prevailing. (2) Many devices are widely used to extra- and intracranial vascular disease. However, such a simple sign as an auscultation of the carotid bruit or aortic-arch calcification in the X-ray picture may give valuable information of extra- and intracranial atherosclerosis. (3) Anti-heat-shock protein 64 antibody has recently been presented as an independent risk factor of carotid atherosclerosis. (4) Clinical features of carotid occlusion or stenosis are markedly variable. PET study has revealed that a water-shed ischemic zone may be in a state of "misery perfusion". (5) Regression may occur in the cervical as well as cerebral atherosclerosis.
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PMID:[Cerebrovascular diseases due to extra- and intracranial atherosclerosis]. 841 81

Accelerated graft atherosclerosis is a major cause of death after cardiac transplantation. Although its detection currently requires surveillance angiography, loss of vasodilator responsivity may precede obstructive lesions and be detectable by noninvasive assessment of myocardial perfusion. Thirty-five allograft recipients were studied an average of 31 +/- 19 (mean +/- SD) months after transplantation. All were free from angiographically definable macrovascular obstructive coronary artery lesions. Nutritive myocardial perfusion at rest, estimated in absolute terms by positron emission tomography with oxygen-15 water averaged 1.63 +/- 0.51 ml/g/min in patients and was greater than that in 26 healthy volunteers (1.17 +/- 0.33 ml/g/min, p < 0.001). The increase correlated with increased cardiac work at rest in transplant recipients with arterial hypertension and tachycardia. Peak myocardial perfusion induced by intravenous administration of dipyridamole was normal in the transplant recipients (3.49 +/- 1.70 ml/g/min compared with 3.60 +/- 1.41 ml/g/min in volunteers). Because of the high flow at rest, myocardial perfusion reserve (the ratio of hyperemic flow to flow at rest) was diminished (2.3 +/- 1.2 compared with 3.3 +/- 1.5 in volunteers, p < 0.005). These results indicate that the responsivity to vasodilator stimulation is well preserved in transplant recipients devoid of macroscopic coronary arterial lesions obviating detection of early vascular dysfunction in individual subjects. Positron emission tomography may be useful, however, in quantifying the magnitude of the increase in flow at rest secondary to increased cardiac work--a potentially remedial cause of accelerated coronary vascular disease induced by high shear force activation of platelets in the coronary bed, and in detecting impaired perfusion once macrovascular vascular disease is extant.
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PMID:Persistence of coronary vasodilator responsivity after cardiac transplantation. 842 78

Hypertension is a common multifactorial vascular disorder of largely unknown cause. Recognition that hypertension is in part genetically determined has motivated studies to identify mutations that confer susceptibility. Thus far, mutations in at least 10 genes have been shown to alter blood pressure; most of these are rare mutations imparting large quantitative effects that either raise or lower blood pressure. These mutations alter blood pressure through a common pathway, changing salt and water reabsorption in the kidney. These findings demonstrate the utility of molecular genetic approaches to the understanding of blood pressure variation and may provide insight into the physiologic mechanisms underlying common forms of hypertension.
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PMID:Molecular genetics of human blood pressure variation. 861 26

The normal functional state of the vasculature and the events leading to the development of significant arterial disease involve the interaction of important vasoactive substances, which play important modulating or initiating roles in the development of hypertension and arteriosclerosis. Three endothelins have now been identified, of which ET-1 is the best characterized. ET-1 is produced by epithelial, mesangial, neuronal and glial, and liver cells, and is the most potent vasoconstrictor yet found. Each endothelin is derived from a different gene on separate chromosomes, and each binds to at least 2 types of receptor. The plasma half-life of ET-1 is about 7 min, and this provides a rapid mechanism for adjusting vascular resistance or blood pressure. The actions of endothelin are mediated through several pathways of postreceptor signaling, including activation of the mitogen-activated protein kinase cascade, which give rise to its growth-stimulating properties. Secretion of ET-1 from cultured endothelial cells is stimulated by a wide range of substances, and is inhibited by some prostaglandins. Endothelin in turn stimulates secretion of nitric oxide, arginine vasopressin and atrial natriuretic peptide, and participates in the hormonal control of salt and water balance. Hypoxia and ischemia augment ET-1 secretion, as does insulin, and this could play a role in the accelerated vascular disease of diabetes. ET-1 also causes bronchoconstriction and has been implicated in the development of acute asthma, primary pulmonary hypertension and pulmonary fibrosis. Its role in hypertension is still debatable, though most of the manifestations of congestive heart failure can theoretically be explained by the actions of ET-1. Endothelin also has extensive renovascular and parenchymal effects in the kidney. It is hoped that a fuller understanding of the role of endothelins in normal or pathologic vasculature will lead to effective therapy based on antagonism or augmentation of specific functions.
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PMID:Endothelins as cardiovascular peptides. 873 84

Apart from the initially described vasoconstriction, endothelins have been shown to cause a variety of biological activities in non-vascular tissues. A rapidly growing body of data supports the concept of endothelin as a paracrine acting hormone. In this review, we will discuss the impact of this local endothelin system for various cardiovascular pathophysiological states, especially atherosclerotic vascular disease, restenosis, myocardial infarction, congestive heart failure, and arterial hypertension. In addition, the endothelin system is a modulator of renal function via its binding to abundant receptors in renal tissue and by the ability of renal endothelial and epithelial cells to synthesize and release endothelin. In the kidney, endothelin may function as a paracrine/autocrine factor in the regulation of renal blood flow, glomerular haemodynamics, and sodium and water homeostasis. The renal endothelin system is involved in kidney diseases such as impaired renal function in liver cirrhosis, cyclosporin toxicity, acute renal failure and renal glomerular and interstitial fibrosis. Therapeutic approaches with new orally active endothelin receptor antagonists are also discussed.
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PMID:The paracrine endothelin system: pathophysiology and implications in clinical medicine. 929 57


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