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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to examine the relation between cardiac state and the capacity to excrete a water load, 10 normal subjects and 61 patients with heart disease were studied during water diuresis. Under these conditions, urine flow approximates to the rate of delivery of filtrate, and therefore of sodium, from the proximal tubule of the kidney to the loop of Henle, while free water clearance is a function of distal sodium reabsorption. In 12 patients with complete heart block, ventricular pacing was associated with increased urine flow and free water clearance. Oral propranolol in 3 normal subjects and in 9 patients with intact atrial septa caused a reduction, and oral practolol in 4 normal subjects and 8 patients caused no change. In 6 patients with atrial septal defect, propranolol was without effect. Maximum urine flow correlated with left ventricular end-diastolic pressure but not mean left atrial pressure in 16 patients with chronic rheumatic heart disease. In 7 patients with ischaemic heart disease, maximum urine flow was higher than in those with chronic rheumatic heart disease and similar increase in left ventricular end-diastolic pressure. These results reflect a close relation between proximal tubular sodium reabsorption and cardiac state, and suggest that inappropriate sodium reabsorption at this site may contribute to fluid retention in heart disease.
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PMID:Assessment of proximal tubular sodium reabsorption during water diuresis in patients with heart disease. 439 57

Exchangeable sodium and potassium, total body water, and sulphate space were measured in 42 patients with severe valvular heart disease who were free of oedema. Compared with normal subjects of the same height, no increase in exchangeable sodium was found but a mean potassium depletion of 27% was shown. This depletion was not related to diuretic therapy, and no relationship between the degree of depletion and postoperative arrhythmias was found. It is concluded that the major cause of the low exchangeable potassium is the reduction in cell mass that occurs in chronic heart disease, and that there is no significant fall in the intracellular potassium concentration.
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PMID:Potassium depletion in severe heart disease. 579 71

Previous studies have demonstrated that the anesthetic amine, chlorpromazine hydrochloride (CPZ), prevents cell necrosis in experimentally induced ischemic liver and heart disease and decreases the extent of galactosamine-induced cell death in the liver. The present model was designed to determine whether CPZ exerts a similar beneficial effect in kidney in a nephrotoxic model of acute renal failure in rats induced by the administration of mercuric chloride (2 mg/kg of body weight). The functional and structural changes in the kidney were evaluated and quantitated in animals pretreated with CPZ (40 mg/kg of body weight) or saline and then subjected to nephrotoxic injury. Compared to controls, the glomerular filtration rate was significantly lower (p less than 0.001) in saline- and CPZ-pretreated rats receiving mercuric chloride. Twenty-four hours after mercuric chloride administration the glomerular filtration rate was 446 +/- 38 microl/minute/gm of kidney weight, the fractional sodium excretion was 0.4 +/- 0.2%, and the urinary osmolality was 1440 +/- 193 mOsmoles/kg of H2O in the CPZ-treated animals compared to 26 +/- 18 microl/minute/gm of kidney weight (p less than 0.001), 10.1 +/- 9.8% (p less than 0.025), and 353 +/- 28 mOsmoles/kg of H2O (p less than 0.005), respectively, in the animals receiving mercuric chloride alone. The percentage of proximal tubule cell necrosis was 26.5 +/- 8.9% in the CPZ-pretreated group compared to 88.1 +/- 3.6% in the untreated group (p less than 0.001). Metabolic cage studies were performed to follow the time course of this model for 48, 72, and 96 hours after mercury injection. The serum creatinine values and fractional sodium excretions were significantly less in animals receiving CPZ compared to the untreated group at all time intervals examined. The serum urea nitrogen concentration and glomerular filtration rate were similar for the two groups after 48 hours, but the serum urea nitrogen level was significantly lower and the glomerular filtration rate higher after 72 and 96 hours in the animals pretreated with CPZ. In agreement with these findings were observations that animals pretreated with CPZ had significantly fewer necrotic cells 48 and 72 hours after mercury administration, and tubular regeneration appeared to be markedly accelerated. These results suggest that pretreatment with CPZ markedly lessens the degree of structural and functional impairment seen in mercuric chloride-induced acute renal failure in rats and increases the rate of recovery.
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PMID:Partial protection by chlorpromazine in mercuric chloride-induced acute renal failure in rats. 623 24

In this article we have briefly reviewed the role of Ca2+ in the excitation contraction coupling in the myocardium and have indicated that cardiac contraction and relaxation are initiated upon raising and lowering the intracellular concentration of free Ca2+, respectively. Different mechanisms for the entry of Ca2+ through sarcolemma as well as release of Ca2+ from sarcoplasmic reticulum and possibly mitochondria have been outlined for initiating cardiac contraction. Relaxation of the cardiac muscle appears to be intimately dependent upon efflux of Ca2+ through sarcolemma as well as sequestration of Ca2+ by the intracellular storage sites, particularly sarcoplasmic reticulum and possibly mitochondria. The actions of some pharmacological and pathophysiological interventions have been explained on the basis of changes in subcellular Ca2+ movements in myocardium. Quinidine, which produced an initial positive inotropic action on rat heart was also found to increase sarcolemmal Ca2+-ATPase activity without any changes in the Na+-K+ ATPase. Other antiarrhythmic agents, procainamide and lidocaine, also increased sarcolemmal Ca2+-ATPase activity without affecting the Na+-K+ ATPase. On the other hand, both Ca2+-ATPase and Na+-K+ ATPase activities were increased in heart sarcolemma obtained from cardiomyopathic hamsters. In this model the increased Ca2+-ATPase activity may promote the occurrence of intracellular Ca2+ overload in the cardiac cell whereas the increased Na+-K+ ATPase activity may increase Ca2+ efflux through Na+-Ca2+ exchange systems as an adaptive mechanism. It has been suggested that some caution should be exercised while interpreting the data from in vitro experiments in terms of functional changes in the myocardium. Furthermore, it has been proposed that the pathophysiology and pharmacology of Ca2+ movements at different membrane sites be understood fully in normal and diseased myocardium in order to improve the therapy of heart disease.
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PMID:Progress and problems in understanding the involvement of calcium in heart function. 623 64

The value of red blood cell (RBC) sodium/potassium ratio in diagnosing digitalis toxicity was studied in 60 adult patients. The normal ratio was established in 34 healthy volunteers and in 10 patients with heart disease not receiving digoxin (group I). During chronic digoxin therapy, RBC sodium/potassium (Na/K) ratio and plasma digoxin were measured in 50 nontoxic patients (group II), in 10 toxic patients (group III), and in 9 of these 10 toxic patients after resolution of digoxin toxicity. Red cell sodium and RBC Na/K ratio in nontoxic patients were significantly greater than in the control group. Red cell sodium and the RBC Na/K ratio in toxic patients were significantly greater than in nontoxic patients. Despite significant group differences in these variables, however, there was considerable overlap among the subjects studied. After resolution of toxicity, red cell sodium and the RBC Na/K ratio fell to values indistinguishable from those in the nontoxic group. Although there was a statistically significant positive correlation between RBC Na/K ratio and plasma digoxin level, the RBC Na/K ratio had weak predictive value (33%) in determining digoxin toxicity. Plasma digoxin was a better predictor of digoxin toxicity (60%). The combination of plasma digoxin concentration and of RBC Na/K ratio had a higher calculated predictive value (75%), and may be more useful as an indicator of digoxin intoxication.
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PMID:Changes in red blood cell electrolyte concentrations in digitalis intoxication. 630 32

To determine the hemodynamic and clinical effects of long-term positive inotropic stimulation on the myocardium, we treated 31 patients with severe chronic heart failure with oral amrinone (600 mg daily) and performed invasive hemodynamic studies during short- and long-term treatment with the drug. Stroke volume and stroke work indexes increased markedly during the first 48 hr of therapy (p less than .01) but returned to pretreatment values after 2 to 10 weeks; upon drug withdrawal, both variables deteriorated rapidly to values significantly lower than those observed before treatment with amrinone (p less than .01), despite similar values for left ventricular filling pressure, mean arterial pressure, and systemic vascular resistance. This pattern of response indicated that progression of the underlying heart disease had occurred during treatment with amrinone and contributed importantly to its failure to produce long-term benefits. Progression of left ventricular dysfunction was associated with a progressive increase in heart rate and plasma renin activity and a decline in serum sodium concentration. Clinically, amrinone therapy was complicated by sustained symptomatic ventricular tachycardia in four patients, worsening myocardial ischemia in four patients, and worsening congestive heart failure in eight patients, all of whom had been stable before entry into the study; only three of the 31 patients improved clinically. Ten patients died during the first 2 weeks of treatment, and 16 (52%) were dead within 3 months, a mortality rate twice as great as that seen during comparable trials with vasodilating drugs. Although noncardiac adverse effects were frequent, they were not the primary reason for drug failure. In conclusion, long-term therapy with amrinone may accelerate progression of left ventricular dysfunction, exacerbate myocardial ischemia, and provoke life-threatening ventricular tachyarrhythmias, thereby shortening survival in patients with severe chronic heart failure. Prolonged administration of inotropic drugs may achieve short-term gains at the expense of long-term detrimental effects on the myocardium.
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PMID:Hemodynamic and clinical limitations of long-term inotropic therapy with amrinone in patients with severe chronic heart failure. 638 99

The effects of lorcainide, a new antiarrhythmic drug, on serum electrolytes and osmolality are described in a series of 33 patients with organic heart disease and complex ventricular arrhythmias treated with lorcainide. In eight patients, a mean decrease in serum Na+ of 8.25 +/- 3.2 mEq/L was observed after a single 200 mg intravenous dose of lorcainide. Sixteen of 33 patients developed significant hyponatremia and hypoosmolality during oral treatment with lorcainide. In all except two patients, serum Na+ returned to normal values within 3 to 12 months of continued lorcainide therapy. Low serum Na+ and hypoosmolality in the absence of volume depletion, clinically manifest edema, and unaltered renal, adrenal, cardiac, or thyroid function suggest that this antiarrhythmic drug produced the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH appeared to be transient and asymptomatic in our patients. One patient developed severe hyponatremia with serum Na+ of 108 mEq/L when hydrochlorothiazide was given to control hypertension. It is concluded that SIADH is an important side effect of lorcainide therapy. We recommend that serum Na+ be carefully monitored in patients started on lorcainide therapy, and extreme caution should be exercised in prescribing diuretics to patients with persistent hyponatremia.
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PMID:Hyponatremia in patients treated with lorcainide, a new antiarrhythmic drug. 650 40

Endocarditis and unilateral endophthalmitis due to Actinobacillus actinomycetemcomitans heart disease. The ocular infection was notable for its localized presentation and slow evolution. Treatment with systemic, subconjunctival, and topical gentamicin sulfate and ampicillin sodium achieved 20/20 acuity with a residual chorioretinal scar in the nasal periphery. Intravitreal injection of the organism into a rabbit confirmed its minimal pathogenicity within the eye. This organism must now be considered in patients with differential diagnosis of endogenous endophthalmitis complicating endocarditis and septicemia.
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PMID:Actinobacillus actinomycetemcomitans endophthalmitis with subacute endocarditis. 660 7

The electrocardiographic changes induced during a rapid bolus intravenous injection of both a conventional ionic agent (sodium iothalamate) and a new, low-osmolality non-ionic agent (iohexol) have been studied. Multiple abnormalities were observed but in every category significantly less frequently, or not at all, with iohexol. The most common abnormality was an increase in sinus rate of 15 beats/min over the rate during needle insertion. Other abnormalities observed included T-wave flattening and premature atrial and ventricular contractions. Contrary to some previous studies, we did not find that age, known heart disease or an abnormal base-line ECG were statistically significant determinants of subsequent ECG changes on contrast administration. There was, however, a significant correlation between ECG changes and more severe subjective side-effects experienced after the contrast injection. This offers support for the theories suggesting a psychogenic basis for some contrast reactions, since low-osmolality contrast media are known to produce less marked subjective side-effects. The new agents are known to be less cardiotoxic and to produce less profound haemodynamic changes. These factors may also play a part in the observed reduction in ECG disturbance.
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PMID:Electrocardiographic changes during intravenous urography: a study with sodium iothalamate and iohexol. 669 54

The results of measurements of body sodium, chloride and potassium by isotope dilution or whole body counting in patients with heart disease are reviewed. In patients with cardiac oedema exchangeable sodium and chloride are increased while body potassium tends to be decreased or normal. The findings in normonatraemic hypochloraemia, hypokalaemia and metabolic alkalosis, in diuretic hyponatraemia and in dilutional hyponatraemia are reviewed and their possible consequences in terms of changes in electrolyte gradients are discussed. The limitations and usefulness of measurements of exchangeable electrolytes in heart disease are mentioned.
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PMID:Exchangeable electrolytes in heart disease. 702 Mar 48


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