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

Isometric contractions induced by noradrenaline (NA), 1.8 X 10(-5) M or by potassium (K+), 127 mM were studied in paired ring-preparations of the thoracic aortae from spontaneously hypertensive rats (SHR) and age-matched normotensive Kyoto-Wistar rats. In rats aged 8--16 weeks, NA-induced contractions were significantly more dependent on extracellular calcium in preparations from the SHR than from the NWR, whereas K+induced contractions showed no difference. Relaxation studies revealed differences between SHR and NWR also in K+-induced contractions. Comparison of responses in NWRs aged 3--4 months and 10--12 months showed a significant increment in Ca++-dependency with age. This age-related difference was less pronounced in SHRs, but the effect of blockade of Ca++-influx by nifedipine was significantly stronger in the old than in the young SHR-aorta. Treatment with propranolol or hydrochlorothiazide + timolol + minoxidil for 4--5 months caused no significant reduction of blood pressure and no change in Ca++-dependency. In contrast, treatment with verapamil (60 mg/kg/day) for 12 months resulted in a significantly lower blood pressure in the treated SHRs than in their controls. A trend towards "nomrlization" of the Ca++-dependency in verapamil treated rats was also observed. The results suggest that an increased Ca++-dependency in the SHR aortae is present already at the age of 8--16 weeks, but becomes more pronounced with age. As an age-related increment in Ca++-dependency is also found in NWRs, the results suggest that the SHR aortae are "functionally" older than the NWR vessels already in young animals. Calcium antagonists seem to be effective in lowering blood pressure in SHRs and represent a promising approach to the treatment of hypertensive vascular disease.
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PMID:Role of extracellular calcium in isometric contractions of the SHR aorta. Influence of age and antihypertensive treatment. 48 25

The angiotensin converting enzyme (ACE) inhibitors are a group of effective drugs with a unique mechanism of action. These drugs have proven to be useful for hypertension and congestive heart failure. Early clinical trials of captopril used doses that are now known to be inappropriately high, and dose-related adverse effects were observed frequently. The recognition that lower doses are effective has reduced the incidence of adverse reactions and resulted in improved patient tolerance. When patients are properly selected and correctable risk factors are removed, serious side effects are uncommon. Unfortunately, the early reputation of nephrotoxicity persists, as does the belief that significant blood dyscrasias, endocrine effects and rash are serious risks for the average patient. After wide use of captopril, enalapril and lisinopril, and investigational trials of nearly a dozen newer agents, a sufficiency of clinical observation, experimental evidence and accurate postmarketing recording of events is accumulating to allow insight into the major toxicities with regard to more intelligent patient selection, more rational dosing and proper identification of risk factors. The most common adverse reactions are cough and skin rash. It appears that the agents are generally not cross-reactive with regard to skin rash, although it is not clear whether this effect is drug-specific or class-specific with regard to cough. Statistically but not clinically significant lowering of haemoglobin and hematocrit is common; these effects are inconsequential in most patients. Neutropenia, once thought to be prevalent, now appears to be so only in patients with autoimmune or collagen-vascular disease; the majority of patients outside these groups are at low risk. Hyperkalaemia is a frequent occurrence. This should not be surprising in view of the effect of the ACE inhibitors on plasma aldosterone. When dietary potassium intake is regulated and sources of altered potassium excretion are identified, hyperkalaemia is seldom a serious problem. Identification of sodium and water deficits allows correction before the drugs are started, and the frequency of hypotension and hyperkalaemia caused by the drugs is quite low if these factors are properly managed. An unexpected finding emerging in recent years is the dry cough associated with ACE inhibitor therapy. Its mechanism is not definitely known. Nonsteroidal anti-inflammatory drugs may control this symptom in some patients. The frequent observation of proteinuria in patients taking ACE inhibitors has gained notice and sometimes caused undue alarm. It is difficult to separate disease effects in diabetes and hypertension from true drug effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse effects of angiotensin converting enzyme (ACE) inhibitors. An update. 153 95

The relationship between cerebral lesions such as amyloid angiopathy or senile plaques and amyloid deposition in the visceral organs were studied in 90 autopsy cases of dogs, 0 to 19-year-old. Cerebral amyloid angiopathy was detected in 28 aged dogs (mean age: 13.7-year-old) and was found mostly in or around the wall of cerebral meningeal arterioles and capillaries of the neocortex. That condition was often accompanied by cerebral hemorrhage in dogs more than 9 years of age. Senile plaques were detected in the neocortex of the brain of 12 dogs (mean age: 13.2-year-old) and classified into 3 subtypes, i.e., "diffuse plaque", "primitive plaque" and "classical plaque". Among those 3 subtypes of senile plaques, amyloid containing plaques were small in number. In the visceral organs of dogs with cerebral amyloid angiopathy, amyloid deposition was found in the vascular walls or connective tissues of small intestines at a high frequency and sometimes in the vascular walls of the heart, lung, liver and thyroid gland as well as in atrioventricular valves. Amyloid in both cerebral and visceral organs was congophilic and showed green birefringence under poralized light even after potassium permanganate oxidation.
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PMID:Pathological studies on cerebral amyloid angiopathy, senile plaques and amyloid deposition in visceral organs in aged dogs. 179 Feb 13

We report a case of intracerebral hemorrhages due to sporadic cerebral amyloid angiopathy in a 43-year-old male with a luxuriant giant cell reaction. The amyloid was resistant to potassium permanganate-sulfuric acid oxidation and reacted with an antiserum to synthetic beta-protein. The distribution and histologic characteristics of the multinucleated giant cell reaction suggest that it represents a foreign-body reaction rather than giant cell arteritis.
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PMID:Sporadic cerebral amyloid angiopathy with giant cell reaction. 208 98

Amyloid angiopathy with cerebral hemorrhage and senile plaques was found in the brain of aged dogs. In all 9 cases examined, 13 to 19 years old, 6 males and 3 females, amyloid deposits were observed mostly in the wall of cerebral arterioles and capillaries showed hyaline degeneration. The accumulation of amyloid fibrils measuring about 10 nm in diameter was seen in the cerebral vessel wall by electron microscopy. The cerebral hemorrhage was observed in 6 of 9 dogs and 2 of them showed massive hemorrhage. The hemorrhagic foci were sometimes closely contact with the vessels involved in amyloid angiopathy. In addition, senile plaques being classified into 2 types were found in the cerebral cortex of 3 dogs. The first type was characterized by the accumulation of degenerative neurites and often contained granular argyrophilic material. The second type had a well-defined amyloid core with neuritic halo. Amyloid deposits were also found in or around intestinal vessel walls of 3 dogs. The amyloid deposited in the cerebral vessels, senile plaques and intestinal vessels showed characteristic green birefringence under the polarized light even after potassium permanganate treatment.
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PMID:Amyloid angiopathy with cerebral hemorrhage and senile plaque in aged dogs. 238 40

Adverse drug reactions are more common in patients over sixty-five years of age. There is no significant change of absorption with aging but oxidations reactions are, usually, decreased. The most important change is in the renal elimination of drugs. The renal insufficiency related to the use of NSAIDs is prostaglandin dependent. It is characterized by a fall in urine output, body weight gain, rising of blood urea nitrogen, creatinine and, sometimes, potassium. This situation is usually rapidly reversible after discontinuation of the therapy but an acute renal failure may occur. Patients with atherosclerotic cardio-vascular disease and concurrent diuretic therapy have an increased risk of renal insufficiency. Liver damage induced by NSAIDs presents as an acute hepatitis with a greater or lesser degree of cholestasis. This picture is often indistinguishable from viral hepatitis and sometimes it may resemble chronic active hepatitis. Females with a concomitant impairment of renal function are specially at risk for liver damage and should be carefully followed on with a reduction of NSAIDs dosage.
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PMID:Renal and hepatic effects of NSAIDs in the elderly. 262 76

Diabetic patients who develop renal failure frequently have other serious manifestations of their disorder, including peripheral and central vascular disease, blindness, neuropathy and metabolic abnormalities which can include life-threatening loss of those mechanisms that normally control potassium homeostasis. In this report, the anaesthetic and metabolic management of five diabetic patients with end-stage renal failure undergoing combined pancreatic and renal transplantation, is presented and discussed.
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PMID:Anaesthesia for combined pancreatic and renal transplantation and potassium homeostasis. 305 68

Studies were conducted to determine whether experimental pulmonary hypertension is associated with alterations in pulmonary vascular smooth muscle responsiveness. Adult male rats were given a single s.c. injection of monocrotaline (105 mg/kg) or saline and were sacrificed 4, 7 or 14 days later. Segments of the main trunk and right extrapulmonary artery and an intrapulmonary artery were isolated for determination of vascular reactivity to contractile and relaxant agonists. Monocrotaline treatment caused changes in mechanical properties of pulmonary arteries in that vessels isolated from rats 14 days after monocrotaline administration required greater passive loads to achieve maximal active force development. Cumulative concentration-response curves were generated to potassium chloride, angiotensin II, norepinephrine, isoproterenol and acetylcholine. Vascular contractility was enhanced in main pulmonary artery 4 days after monocrotaline injection but no differences in responsiveness between control and monocrotaline exposed vessels were observed 7 days post-treatment. In contrast, significant decreases in contractility with a specific loss in the response to angiotensin II were observed in pulmonary arteries isolated from rats 14 days after monocrotaline administration. These vessels also were less responsive to the relaxant effects of isoproterenol and acetylcholine when compared to control vessels. These results demonstrate that changes in pulmonary vascular smooth muscle responsiveness occur during evolution of pulmonary hypertension induced by monocrotaline. Enhanced contractility may contribute to inappropriate vasoconstriction early in the development of hypertensive pulmonary vascular disease but does not appear to be involved in sustained elevations in pulmonary artery pressure. Diminished relaxation observed after pulmonary hypertension was well established may contribute to the loss in efficacy of vasodilators in the long-term management of pulmonary hypertension.
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PMID:Altered pulmonary vascular smooth muscle responsiveness in monocrotaline-induced pulmonary hypertension. 308 May 84

The impending release of erythropoietin (EPO) is expected to result in a dramatic increase in hematocrit (Hct) for most hemodialysis (HD) patients. Our studies indicate that as Hct rises, dialyzer mass transport for some clinically critical solutes will be adversely affected. When whole blood clearances are corrected for solute-specific blood-water flows (QBH2O), the effect on the surrogate molecule, urea, used in urea kinetic modeling (UKM) is deceptively minimal, because only urea can diffuse almost instantly from red cells into blood water. For the critical solutes, potassium and phosphate, QBH2O is reduced to Q (plasma water). With a KoA of 690 ml/min at QB = 300, clearance of potassium falls at least 19.3% as Hct rises from 20 to 40% so that steady-state predialysis potassium could rise from 6.0 to 6.95 mEq/L. Already inadequate phosphate clearance falls at least 10% and additional loss results from physical interference by RBCs with solute diffusion. Hcts are further increased with rapid weight losses during high-efficiency dialyses (0.15 per 5% weight loss in 3 hours, r = 0.82) resulting in blood-side pressures such that most dialysis machines cannot provide adequate dialysate pressures to maintain low ultrafiltration rates (UFRs) at the high QB levels. The combination of pre-existing diffuse vascular disease, postdialysis hypovolemia, hypotension, decreased cardiac output, and increased blood viscosity has and will produce disastrous syndromes of organ ischemia, thrombosis, and infarction. Predialysis hypertension can worsen. Extreme caution and adjustment of dialysis regimen is necessary as patient Hct rises above 36%.
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PMID:Erythropoietin alert: risks of high hematocrit hemodialysis. 319 6

Hypertension that is truly resistant to modern antihypertensive therapy is uncommon. In the majority of cases, apparent resistance is more likely associated with poor patient adherence, interacting drugs, drug interactions, and inappropriate drug dosages. Sodium and fluid volume play a major role in resistant hypertension. There is considerable evidence to support the role of dietary sodium restriction in successful nonpharmacological treatment of hypertension. Salt sensitivity in humans appears to represent at least one factor determining individual susceptibility to variable salt intakes. Sodium and water retention may lead to refractoriness to many antihypertensive agents, and there is evidence to suggest that extracellular fluid volume expansion also plays a role in many hypertensive patients. While retention of sodium and water is well established early in patients with renal parenchymal disease, hypertension associated with progression of renal parenchymal disease is complicated by other factors that include interactions between hemodynamic and humoral factors, functional changes in adrenergic responses, and structural vascular disease. The role of other cations such as potassium, calcium, and magnesium in resistant hypertension has yet to be established.
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PMID:The patient with resistant hypertension. Cations, volume, and renal factors. 328 Apr 98


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