Hemodynamic Effects Of Furosemide Research Articles

Clenbuterol administration does not enhance the efficacy of furosemide in attenuating the exercise-induced pulmonary capillary hypertension in Thoroughbred horses.

The stimulation of pulmonary beta2-adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol-a beta2-adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise-induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre-exercise)-control, and furosemide (250 mg i.v., 4 h pre-exercise)+clenbuterol (0.8 microg/kg i.v., 11 min pre-exercise) experiments. The sequence of these treatments was randomized for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, pulmonary vascular pressures were determined at rest, sub-maximal exercise, and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate. In the control study, incremental exercise resulted in progressive significant (P<0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P<0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide-control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P<0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P<0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P<0.05), but these data were not different from the furosemide-control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood-gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.

Pulmonary vascular pressures of thoroughbred horses exercised 1, 2, 3 and 4 h after furosemide administration.

Furosemide premedication of horses 4 h prior to exercise significantly attenuates exercise-induced pulmonary capillary hypertension which may help diminish the severity of exercise-induced pulmonary haemorrhage. As pulmonary hemodynamic effects of furosemide may be mediated via a reduction in plasma volume (which is most pronounced 15-30 min postfurosemide administration, with plasma volume recovering thereafter), we hypothesized that administration of furosemide at intervals shorter than 4 h before exertion may be more effective in attenuating the exercise-induced rise in pulmonary capillary blood pressure. Thus, our objective was to determine whether furosemide-induced attenuation of exercise-induced pulmonary arterial, capillary and venous hypertension would be enhanced when the drug is administered at intervals shorter than 4 h before exercise. Using established techniques, right atrial, and pulmonary arterial, capillary and wedge (venous) pressures were ascertained in seven healthy, sound, exercise-trained Thoroughbred horses in a randomized split-plot experimental design. Measurements were made at rest and during exercise performed at maximal heart rate (217 +/- 3 beats/min) in the control (no medications) experiments and following furosemide administration (250 mg intravenously (i.v.)) at 1, 2, 3 and 4 h before exercise. Sequence of treatments was randomized and 7 days were allowed between experiments on each horse. Although furosemide administration in the four treatment groups caused only insignificant changes in the pulmonary arterial, capillary and wedge pressures of standing horses, furosemide-induced reduction in mean right atrial pressure achieved statistical significance in the 2 h postfurosemide experiments. In the control studies, exercise was attended by statistically significant increments in mean right atrial, as well as pulmonary arterial, capillary and wedge pressures. Although exercise in each of the four furosemide experiments was also attended by significant increments in right atrial as well as pulmonary vascular pressures, in the 1, 2 and 3 h postfurosemide experiments, mean right atrial pressure increased to a significantly lower value than in the control study. Exercise-induced changes in pulmonary vascular pressures in the 1 h postfurosemide experiments were not different from the pressures in the control study. There was a significant attenuation of exercise-induced pulmonary capillary and venous hypertension in the 2, 3 and 4 h postfurosemide experiments, but significant differences among these treatments were not found. Thus, these data did not support the contention that administration of furosemide at intervals shorter than 4 h before exercise is more effective in attenuating exercise-induced pulmonary capillary or venous hypertension in Thoroughbred horses.

Pharmacologic interaction of furosemide and phenylbutazone in horses

SUMMARY The effect of premedication with phenylbutazone on systemic hemodynamic and diuretic effects of furosemide was examined in 6 healthy, conscious, mares. Mares were instrumented for measurement of systemic hemodynamics, including cardiac output and pulmonary arterial, systemic arterial, and intracardiac pressures, and urine flow. Each of 3 treatments was administered in a randomized, blinded study; furosemide (1 mg/kg of body weight, iv) only, phenylbutazone (8.8 mg/kg, po, at 24 hours and 4.4 mg/kg, iv, 30 minutes before furosemide) and furosemide, or 0.9% NaCl. Phenylbutazone administration significantly attenuated, but did not abolish, the diuretic effect of furosemide. Phenylbutazone completely inhibited the immediate effect of furosemide on cardiac output, stroke volume, total peripheral resistance, and right ventricular peak pressure. Premedication with phenylbutazone did not inhibit equally the diuretic and hemodynamic effects of furosemide, indicating that some of furosemide's hemodynamic effects are mediated by an extrarenal activity of furosemide.

Hemodynamic effects of acute administration of furosemide in patients with cirrhosis receiving β-adrenergic antagonists

In patients with cirrhosis, both beta-blockers and diuretics decrease the degree of portal hypertension. Since their mechanisms of action differ, the combination of these two substances should induce a more pronounced effect on portal pressure than one of these substances alone. Thus, the hemodynamic effects of furosemide were evaluated in ten patients with cirrhosis receiving beta-blockers. One hour after furosemide (0.75 mg/kg intravenously) administration, cardiac output decreased significantly from 6.2 +/- 0.6 to 5.2 +/- 0.3 l/min and blood volume from 8.0 +/- 1.6 to 5.3 +/- 0.5 l. Mean arterial pressure was not affected. Wedged and free hepatic venous pressures did not change significantly; nor did the hepatic venous pressure gradient (19.6 +/- 1.7 to 18.6 +/- 1.5 mmHg). Azygos blood flow was not affected (0.46 +/- 0.05 to 0.50 +/- 0.07 l/min). In conclusion, this study did not demonstrate that the addition of furosemide to propranolol further decreased portal pressure in patients with cirrhosis. The long-term effects of this combination are unknown and should be tested.

The renal and hemodynamic effects of furosemide in acute myocardial infarction.

Renal and hemodynamic effects of furosemide were studied in 30 patients with acute myocardial infarction. When marked congestion of lungs was absent, the effects of furosemide were somewhat different from those of recent reports. The changes of pulmonary arterial pressure and wedge pressure were biphasic; there was first pressure rise in many occasions followed by reduced pressure; the latter is commonly believed to be the beneficial effect of furosemide. In these patients without marked congestion but in an acute state of myocardial infarction, within 5 min of furosemide administration, there was marked increase in urine volume, sodium and potassium excretion along with increases in creatinine clearance which is commonly found in the other conditions, but is in contrast to the recent reports on patients with acute myocardial complicated with pulmonary congestion.

Hemodynamic effects of furosemide in isolated perfused rat kidneys.

In anesthetized dogs, the diuretic furosemide has been shown to increase renal blood flow, an effect which can be blocked by the prostaglandin synthetase inhibitor, indomethacin (1, 2). Furosemide also caused an increase in PGE2 release into renal venous blood and this increase was inhibited by indomethacin (2). These data suggest a relationship between the hemodynamic effect of furosemide and the renal prostaglandins. PGE2 is a vasodilator in the dog kidney; however, Malik and MgGiff (3) demonstrated that this prostaglandin increases renal vascular resistance in the rat. This apparent species difference between the rat and other mammals (4) offers a potential tool for elucidating the relationship between furosemide and PGE2 on renal hemodynamics. If the action of furosemide to dilate the renal vasculature in dogs is dependent on release of PGE2, and if PGE2 is a vasoconstrictor in rats, then furosemide would be expected to decrease renal blood flow in the rat. Alternatively, if the primary effect of furosemide is to produce hemodynamic changes which secondarily influence prostaglandin synthesis, furosemide might increase renal blood flow in rats as it does in dogs. The purpose of this investigation was to determine the effect of furosemide on renal vascular resistance and to elucidate the interactions between this diuretic and PGE2 in isolated perfused rat kidneys. Since the renin-angiotensin system may also influence the renal vasculature, experiments were performed to evaluate interactions between this system and PGE2 and furosemide.

Renal and extrarenal hemodynamic effects of furosemide in congestive heart failure after acute myocardial infarction

Abstract Furosemide, 0.5 to 1.0 mg per kilogram intravenously, was given to 20 patients with left ventricular failure after acute myocardial infarction. Within five to 15 minutes, average left ventricular filling pressure fell from 20.4 to 14.8 mm Hg, accompanied by a 52 per cent increase in mean calf venous capacitance. During the same period there was no physiologically important change in either urine output or heart rate, blood pressure and cardiac output. Peak increase in urine flow (from mean of 0.82 to 4.0 ml per minute) occurred at 30 minutes, and peak natriuretic effect at 60 minutes. Thus, the action of furosemide in the treatment of pulmonary congestion is immediate and is not related to its diuretic properties. Rather, the prompt fall in left ventricular filling pressure probably is primarily vascular in origin, since marked changes in venous capacitance accompany this phenomenon, which is only later supplemented by the increase in urine output and electrolyte excretion. (N Engl J Med 288:1087...

Diuretic and hemodynamic effects of furosemide in the isolated dog kidney.

The effects of furosemide on the renal concentrating mechanism and on intrarenal hemodynamics were assessed in isolated blood-perfused dog kidneys. The natriuretic, diuretic and hemodynamic responses to furosemide were lesser in magnitude and shorter in duration than those seen in intact animals. Indocyanine green dye dilution curves were used to assess the intrarenal distribution of blood flow. The washout curve prior to furosemide was described by three components. After furosemide, the curve was described by four components. The greatest change in intrarenal distribution of blood flow after furosemide occurred in the noncortical compartments. The data suggest a disproportionately greater increase in medullary blood flow after furosemide. Blood flow through the slow-flow compartments increased 107% whereas flow through the fast-flow compartment increased only 7%. This is in agreement with our previous hypothesis that the increase in renal blood flow and, more importantly, the redistribution of blood flow, produced by furosemide can markedly enhance the effect of the drug, particularly on the concentrating mechanism.

Effect of ethacrynic acid and chlorothiazide on intrarenal hemodynamics in normal man.

ARTICLESEffect of ethacrynic acid and chlorothiazide on intrarenal hemodynamics in normal manM Epstein, NK Hollenberg, RD Guttmann, M Conroy, BI Basch, and JP MerrillM Epstein, NK Hollenberg, RD Guttmann, M Conroy, BI Basch, and JP MerrillPublished Online:01 Feb 1971https://doi.org/10.1152/ajplegacy.1971.220.2.482MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDiureticsDiuretic Use in Edema and the Problem of ResistanceRenal Blood Flow1 January 2011Effects of Diuretics on Renal Function1 January 2011Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascitesGastroenterology, Vol. 92, No. 6Acute Renal Failure30 August 2016 | Drug Intelligence & Clinical Pharmacy, Vol. 20, No. 6Insights into intrarenal sites and mechanisms of action of diuretic agentsAmerican Heart Journal, Vol. 106, No. 1Perinatal Nephrobiology: A Developmental PerspectiveClinics in Perinatology, Vol. 4, No. 2Fluid and electrolyte metabolism in the newborn infantClinics in Endocrinology and Metabolism, Vol. 5, No. 1Effect of intrarenal furosemide on renal function and intrarenal hemodynamics in acute renal failureThe American Journal of Medicine, Vol. 58, No. 4Renal function and diuretic therapy in infants and children. Part IThe Journal of Pediatrics, Vol. 86, No. 4Renal intracortical blood flow distribution, function, and sodium excretion in unanesthetized dogs following vena caval ligation.Circulation Research, Vol. 36, No. 1Diuretic and hemodynamic effects of furosemide in the isolated dog kidneyNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 277, No. 1Influence of volume expansion on proximal tubular sodium reabsorption in congestive heart failureAmerican Heart Journal, Vol. 85, No. 1 More from this issue > Volume 220Issue 2February 1971Pages 482-487 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.2.482PubMed5540902History Published online 1 February 1971 Published in print 1 February 1971 Metrics