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Results for “DIURESIS AND DIURETICS”

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At least 919 records · Page 51Linked to original sources
PubMed1957

The antidiuretic action of 5-hydroxytryptamine in cats in relation to the production of certain chemoreflexes.

In cats lightly anaesthetized with cnloralose, small (5 to 50 mug./kg.) intravenous doses of 5-hydroxytryptamine temporarily reduced the flow of urine into the bladder in addition to causing reflex falls of blood pressure and heart rate and temporary arrest of breathing. Doses of phenyl diguanide and other aryl diguanides, the reflex effects of which on blood pressure and respiratory movement approximately matched those of 5-hydroxytryptamine, had comparatively little antidiuretic effect. Phenyl diguanide, unlike 5-hydroxytryptamine (tested previously under similar conditions), did not have an antidiuretic effect in hydrated mice in doses of 0.05, 1, and 2.5 mg./kg. subcutaneously. It is concluded that the reflex depressor action of 5-hydroxytryptamine plays little part in reducing urinary output.

Animals↗
PubMed1963

METABOLIC STUDIES WITH DI(AZIRIDIN-1-YL) SULPHOXIDE (DIETHYLENEIMINOSULPHOXIDE).

The work described was undertaken after the observation that the diuresis induced by several derivatives of ethyleneimine could be correlated with their content of ethyleneimine. The preparation of (35)S-labelled di(aziridin-1-yl) sulphoxide (diethyleneiminosulphoxide) is described together with its metabolism in rat, mouse, rabbit and dog. The drug was completely metabolized in all species and, with the exception of the dog, most of the activity was excreted in the urine within 3 days. The main radioactive metabolite in all species was sulphate. In vitro studies demonstrated that the compound was slowly broken down to sulphite and free ethyleneimine; this hydrolysis was greatly accelerated in the presence of phosphate.

Animals↗
PubMedDate not supplied

ECG changes in response to diuresis in an ambulatory patient with congestive heart failure.

This case report describes an ambulatory patient with congestive heart failure and peripheral edema who lost 18 lb in response to enhanced diuresis over the course of 1 week. The ECG showed increases in the amplitude of P waves, QRS complexes, and T waves; the duration of P waves, QRS complexes, and QT intervals; and the dispersion of P and QT. The clinical implications of these ECG changes are discussed.

Ambulatory Care↗
PubMed2002

Determinants of serum creatinine trajectory in acute contrast nephropathy.

The aim of this study was to describe the trajectory of creatinine (Cr) rise and its determinants after exposure to radiocontrast media. Included were 98 subjects who underwent cardiac catheterization and were randomized to forced diuresis with i.v. crystalloid, furosemide, mannitol (if pulmonary capillary wedge pressure was < 20 mmHg), and low dose dopamine versus intravenous crystalloid and matching placebos. Baseline and postcatheterization serum Cr levels were analyzed in a longitudinal fashion, allowing for differences in the time between blood draws, to determine the different critical trajectories of serum Cr. The mean age, baseline serum Cr, and Cr clearance (CrCl) were 69.3 +/- 10.8 years, 2.5 +/- 0.9 mg/dL, and 31.4 +/- 12.1 mL/min, respectively. The clinically driven postprocedural observation time was 5.5 +/- 5.1 days (range 19 hours and one Cr value to 25.7 days and 18 values). The mean maximum Cr was 3.3 +/- 1.4, range 1.7-8.7 mg/dL). Longitudinal models support baseline Cr clearance predictions for the change in Cr at 24 hours, time as the determinant of Cr trajectory, and requisite monitoring. For any given individual, a rise in Cr of < or = 0.5 mg/dL in the first 24 hours after contrast exposure predicted a favorable outcome. Baseline renal function is the major determinant of the rate of rise, height, and duration of Cr trajectory after contrast exposure. Length of observation and frequency of laboratory measures can be anticipated from these models.

Acute Kidney Injury↗
PubMed1976

Renal cortical blood redistribution after bumetanide related to heterogenicity of cortical prostaglandin metabolism in dogs.

Bumetanide is shown to increase renal blood flow and to augment the proportion of the cortical blood flow to middle cortex. This redistribution still takes place even when renal blood flow is maintained constant by renal artery clamping. Indomethacin pretreatment inhibits the increase of renal blood flow as well as the cortical blood redistribution. In vitro examinations of canine kidney tissue slices suggest that outer cortex and papillar are sites of prostaglandin synthesis. No differences in prostaglandin E degradation are observed within the cortex. This suggests a relative autonomy for prostaglandins in the outer cortex, whilst inner cortical areas are dependent on medullary/papillary prostaglandin E supply. The renal hemodynamic effect of bumetanide is therefore thought to be a result of a stimulation of mainly medullary/papillary prostaglandin synthesis.

Animals↗
PubMed1993

Renal effects of urodilatin and atrial natriuretic peptide in volume expanded conscious dogs.

The renal effects of urodilatin and atrial natriuretic peptide (ANP) were examined in conscious dogs during acute volume expansion maintained through independent infusions of water and NaCl. Peptide was infused in a step-up fashion, in 40-min periods at rates of 2.5, 12.5 and 50.0 ng kg-1 min-1 (ANP, urodilatin) or 0.5, 2.5 and 10.0 ng kg-1 min-1 (second series of urodilatin). ANP immunoreactivity (ANPir) in plasma was measured with an antibody showing 100% cross-reactivity with urodilatin. At 50 ng kg-1 min-1, ANP increased plasma ANPir some 10-fold (64 +/- 6 pg ml-1 to 728 +/- 82 pg ml-1) while urodilatin elicited a 25-fold increase in ANPir (78 +/- 13 pg ml-1 to 1645 +/- 204 pg ml-1). ANP doubled sodium excretion (61 +/- 12 to 124 +/- 30 mumol min-1, P < 0.05) while urodilatin increased sodium excretion to 269 +/- 45 mumol min-1. Both peptides approximately doubled urine flow. Urodilatin at 10 ng kg-1 min-1 increased sodium excretion from 57 +/- 17 mumol min-1 to 106 +/- 25 mumol min-1, i.e. similar to the response ANP elicited at 50 ng kg-1 min-1. In the time control series a significant fall in sodium excretion was observed, despite the continuous replacement of sodium and water. The results demonstrate that in identical, relatively high doses, the changes in sodium excretion, diuresis, heart rate (HR) and arterial pressures elicited by urodilatin are more pronounced than those of ANP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Liver and gastrointestinal first-pass effects of azosemide in rats.

Since considerable first-pass effects of azosemide have been reported after oral administration of the drug to rats and man, first-pass effects of azosemide were evaluated after intravenous, intraportal and oral administration, and intraduodenal instillation of the drug, to rats. The total body clearances of azosemide after intravenous (5 mg kg-1) and intraportal (5 and 10 mg kg-1) administration of the drug to rats were considerably smaller than the cardiac output of rats suggesting that the lung or heart first-pass effect (or both) of azosemide after oral administration of the drug to rats was negligible. The total area under the plasma concentration-time curve from time zero to time infinity (AUC) after intraportal administration (5 mg kg-1) of the drug was significantly lower than that after intravenous administration (5 mg kg-1) of the drug (1000 vs 1270 micrograms min mL-1) suggesting that the liver first-pass effect of azosemide was approximately 20% in rats. The AUC from time 0 to 8 h (AUC0-8 h) after oral administration (5 mg kg-1) of the drug was considerably smaller than that after intraportal administration (5 mg kg-1) of the drug (27.1 vs 1580 micrograms min mL-1) suggesting that there are considerable gastrointestinal first-pass effects of azosemide after oral administration of azosemide to rats. Although the AUC0-8 h after oral administration (5 mg kg-1) of azosemide was approximately 15% lower than that after intraduodenal instillation (5 mg kg-1) of the drug (27.1 vs 32.0 micrograms min mL-1), the difference was not significant, suggesting that the gastric first-pass effect of azosemide was not considerable in rats. Azosemide was stable in human gastric juices and pH solutions ranging from 2 to 13. Almost complete absorption of azosemide from whole gastrointestinal tract was observed after oral administration of the drug to rats. The above data indicated that most of the orally administered azosemide disappeared (mainly due to metabolism) following intestinal first-pass in rats.

Administration, Oral↗