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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in myocardial water content, left ventricular diastolic stiffness, cardiac performance, coronary blood flow, myocardial contractile force, rate of change of myocardial force, and peak acceleration of the aortic volume flow were examined in twenty-five dogs during glucose-induced hyperosmolality before and after pancreatectomy, the latter with and without insulin treatment. Glucose-induced hyperosmolality accounted for myocardial dehydration, increased diastolic stiffness and consequent decrease of left ventricular performance only in the absence of insulin, while coronary blood flow, myocardial contractile force, rate of change of myocardial force and peak acceleration of the aortic volume flow increased independently from the presence or absence of insulin during the glucose-induced hyperosmolality. These findings suggest that the frequent development of heart failure in hyperosmolar diabetic coma could partly be explained by myocardial dehydration and by the consequent decrease in left ventricular compliance and performance.
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PMID:Effect of hyperglycaemia-induced hyperosmolality on heart function in the dog. 11 46

Patients in the coronary care unit with acute pulmonary edema, heart failure, and other organic heart disease were studied. Blood and urine samples were taken on admission prior to any treatment and later at prescribed intervals. All the patients with APE were found to have elevated plasma osmolalities and hyperglycemia on admission which decreased with treatment. This was in contrast to the other two groups excluding those factors such as ethyl alcohol and diabetes which can raise plasma osmolality or blood glucose. A discussion of this mild hyperosmolal state in APE follows including possible causes as well as cellular effects of hyperosmolality on humans.
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PMID:Acute pulmonary edema and hyperosmolality: a clinical study. 106 77

Patients with congestive heart failure (CHF) have impaired peripheral vasodilation during exercise. Hyperosmolality is one local stimulus that produces vasodilation during exercise in normal subjects. This study addressed the hypothesis that vasodilation to hyperosmolal stimuli is impaired in patients with CHF. Forearm blood flow responses to intrabrachial artery infusions of isoosmolar (280 mosm/kg) and hyperosmolal (480 and 660 mosm/kg) solutions of saline and glucose were compared in 9 patients with CHF and 13 normal subjects. Forearm blood flow was measured by strain gauge plethysmography. In the normal subjects, hyperosmolal infusions of 480 and 660 mosm/kg increased forearm blood flow by 3.12 +/- 0.40 and 6.80 +/- 0.67 ml/min/100 ml forearm volume, respectively (both p < 0.001 compared with isoosmolal infusions). In contrast, in the patients with CHF, these infusions increased forearm blood flow by 2.19 +/- 0.44 and 4.06 +/- 0.92 ml/min/100 ml forearm volume (p < 0.05 normal vs CHF). The impaired forearm blood flow responses in heart failure occurred despite significantly greater (p < 0.05, normal vs CHF) increases in venous osmolality (17.3 +/- 6.5 vs 9.6 +/- 1.3 mosm/kg for the 660 mosm/kg infusion). There were no differences between groups in forearm venous hematocrit, calcium, and sodium or potassium changes during hyperosmolal infusions. It is concluded that peripheral vasodilation to hyperosmolal stimuli is impaired in patients with CHF.
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PMID:Impaired forearm vasodilation to hyperosmolal stimuli in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy. 144 84

1. This author believes that the present evidence (water shifts and vasodilatation) strongly indicates that low osmolality is probably the main advantage of the new contrast media. 2. Arteriographic adverse reactions (pain, vasodilatation) are less marked with the contrast medium of the lowest osmolality--i.e. ionic ioxaglate salts. 3. Minor adverse reactions (nausea and vomiting) are less marked with some non-ionic media (e.g. iohexol, iopamidol) than with ioxaglate but there are no data concerning the relative incidence of severe reactions or fatalities. 4. Dr. Lasser's suggestion in 1987, that 12 hours of corticosteroid prophylaxis reduces the adverse reaction rate of intravenous HOCM to the rate of LOCM reactions, awaits confirmation. However, corticosteroid prophylaxis will not reduce the side effects due to hyperosmolality, e.g. vasodilation, hypervolemia, and pain (on arterial injection). 5. Unless and until the necessary finances are available, I suggest LOCM (costing 12 times the price of HOCM in Canada and America) be used on a selective and discriminatory basis in three groups of patients: those undergoing painful procedures (e.g. peripheral arteriography), those undergoing potentially dangerous procedures (e.g. spinal angiography, coronary angioplasty) for patients considered on account of their previous medical history (e.g. asthma, allergy, previous adverse reactions, cardiac failure) to be at greater risk than the normal population.
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PMID:Radiological contrast media. 292 86

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39