Blood Volume Following Diuresis Induced by Furosemide

Schuster, C. J.; Weil, Max Harry; Besso, Jose; Carpio, Moises; Henning, Robert J.

doi:10.1097/00132586-198502000-00011

Cited by 4 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of note, the stability of the effective circulating volume also is related to the refill rate from the interstitial space and the dynamics of the venous capacitance (see below). A study in heart failure patients demonstrated a net refill volume (and perhaps also venous-toarterial fluid redistribution volume) exceeding the diuresis induced by furosemide (140). Refill rate cannot be easily assessed, although a methodology has been developed to measure refill rate in hemodialysis (24).…”

Section: F961mentioning

confidence: 99%

“…Remarkably, in both groups, there was a decrease in colloid osmotic pressure and a decrease in central venous pressure. This could be explained if furosemide increased venous capacitance, decreased venous pressure, thereby facilitating fluid reabsorption from the interstitial space and subsequent decreases in plasma oncotic pressure (140). Others have reported such an acute increase in venous capacitance upon furosemide (38).…”

Section: F962mentioning

confidence: 99%

See 1 more Smart Citation

Everything we always wanted to know about furosemide but were afraid to ask

Huang

Mees

Vos

et al. 2016

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Huang X, Dorhout Mees E, Vos P, Hamza S, Braam B. Everything we always wanted to know about furosemide but were afraid to ask. Am J Physiol Renal Physiol 310: F958 -F971, 2016. First published February 24, 2016 doi:10.1152/ajprenal.00476.2015.-Furosemide is a widely used, potent natriuretic drug, which inhibits the Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC)-2 in the ascending limb of the loop of Henle applied to reduce extracellular fluid volume expansion in heart and kidney disease. Undesirable consequences of furosemide, such as worsening of kidney function and unpredictable effects on sodium balance, led to this critical evaluation of how inhibition of NKCC affects renal and cardiovascular physiology. This evaluation reveals important knowledge gaps, involving furosemide as a drug, the function of NKCC2 (and NKCC1), and renal and systemic indirect effects of NKCC inhibition. Regarding renal effects, renal blood flow and glomerular filtration rate could become compromised by activation of tubuloglomerular feedback or by renin release, particularly if renal function is already compromised. Modulation of the intrarenal renin angiotensin system, however, is ill-defined. Regarding systemic effects, vasodilation followed by nonspecific NKCC inhibition and changes in venous compliance are not well understood. Repetitive administration of furosemide induces short-term (braking phenomenon, acute diuretic resistance) and long-term (chronic diuretic resistance) adaptations, of which the mechanisms are not well known. Modulation of NKCC2 expression and activity in kidney and heart failure is ill-defined. Lastly, furosemide's effects on cutaneous sodium stores and on uric acid levels could be beneficial or detrimental. Concluding, a considerable knowledge gap is identified regarding a potent drug with a relatively specific renal target, NKCC2, and renal and systemic actions. Resolving these questions would increase the understanding of NKCCs and their actions and improve rational use of furosemide in pathophysiology of fluid volume expansion. extracellular fluid volume; natriuresis; renal function; chronic kidney disease; heart failure DIURETICS BLOCKING THE Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC) have an important place in the treatment of fluid overload, specifically in the context of kidney disease and heart failure (64). Of the drugs that inhibit the NKCC2 in the loop of Henle (furosemide, bumetanide, torsemide, ethacrynic acid), furosemide is most commonly applied (66) and Ͼ40 million prescriptions are dispensed every year in the USA (66a). However, many uncertainties remain about intrarenal and systemic actions of furosemide, including its two main targets NKCC1 and NKCC2.Clinically, there are a number of undesirable consequences of the use of furosemide, of which the pathophysiological mechanisms have not been sufficiently investigated. Furosemide has been associated with worsening of kidney function in patients treated for volume overload admitted for acute heart failure (104) and even glomerular filtration rate (GFR) ...

show abstract

Section: F961mentioning

confidence: 99%

Section: F962mentioning

confidence: 99%

Everything we always wanted to know about furosemide but were afraid to ask

Huang

Mees

Vos

et al. 2016

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…24 In addition, Na + -K + -Cl" cotransport appears to be very active in vascular endothelial cells. 23 Clinical studies of the cardiovascular actions of intravenously administered loop diuretics have revealed a prominent central venodilator activity, 26 an extrarenal pharmacodynamic effect that may represent cotransport inhibition.…”

Section: Summary Red Blood Cell LImentioning

confidence: 99%

“…We interpret the RBC cotransport findings as a clue that the decrease in venous distensibility may not be due only to structural adaptations. Venodilation is known to follow intravenous administration of furosemide, 26 and although experimental evidence supports roles for prostaglandins 52 and angiotensin 53 in this effect, the possibility that venous smooth muscle tone is chronically dependent on loop diuretic-sensitive cotransport activity has not been excluded. A circulating factor with activity shared with the loop diuretics, earlier termed the chloriuretic hormone* and now tentatively linked to atrial natriuretic factor, 55 '" is affecting both RBC and venous smooth muscle cotransports, could potentially explain the relationships demonstrated in the current study.…”

Section: Rbc Na + -K + Cotransport and Venous Compliancementioning

confidence: 99%

Red blood cell Li+-Na+ countertransport, Na+-K+ cotransport, and the hemodynamics of hypertension.

Weder¹,

Fitzpatrick

Torretti

et al. 1987

Hypertension

View full text Add to dashboard Cite

SUMMARY Red blood cell Li+ -Na + countertransport and Na + -K + cotransport activities, home blood pressure, invasive systemic hemodynamics, and limb venous compliance were measured in 65 white men (23 normotensive, 22 borderline hypertensive, and 20 mild essential hypertensive subjects). Li + -Na + countertransport activity was positively and significantly correlated with subject-determined home systolic blood pressure (r = 0.31, p < 0.02) and with directly measured systolic (r = 0.29, p<0.02) and diastolic (r=0.27, p<0.03) blood pressures in the hemodynamic laboratory, independent of potential confounding variables. Analysis of the hemodynamic determinants of blood pressure revealed a significant positive correlation of countertransport with vascular resistance (r=0.30, p<0.02) but not with cardiac output or cardiac index. High red blood cell Na + -K + cotransport activity was not independently associated with hypertension or with a characteristic hemodynamic pattern but was related to decreased venous compliance. Red blood cell Li + -Na + countertransport deserves further study as a marker for the genetic substrate of human essential hypertension. Red cell Na + -K + cotransport may be altered secondarily by factors related to high blood pressure and seems to be a valid marker for abnormalities of the venous system in hypertension. (Hypertension 9: 459-466, 1987) KEY WORDS • lithium-sodium countertransport • sodium-potassium cotransport bumetanide • vascular resistance • venous compliance I NCREASED systemic vascular resistance is the hemodynamic hallmark of established human essential hypertension. Borderline hypertension results from elevated cardiac output in about a third of patients, but even in such "hyperkinetic" hypertensive patients, vascular resistance is considered to be inappropriately elevated for the prevailing cardiac output.' Although structural changes may reinforce and amplify the development of elevated vascular resistance, 2 the events initiating hypertension can more plausibly

show abstract

“…When gross hematuria is present, treatment may be needed; one of the conservative approaches (renal pelvis irrigation with sodium oxychlorosene, silver nitrate, or aminocaproic acid; urinary alkalinization, exchange transfusion, or administration of urea, diuretics or epi nephrine) should be preferred to unilateral renal emboli zation or nephrectomy [2][3][4][5], The NS secondary to, or present with SCD-SCT, should be treated symptomati cally and as cautiously as possible, since measures used to induce diuresis have been associated with dehydra tion, thrombosis, and infections in the general NS popu lation; furosemide may be helpful if it is confirmed as a vasodilator agent [29]. Hypertension should be treated following general and specific approaches; beta blockers may have some beneficial side effects [4], Finally, dialysis (at least hemo) and renal transplantation should be rou tinely available to these patients, with the realization that they have special physical and emotional needs and no unusual responses to these modes of therapy except for an apparent increase in sickle cell crises [4].…”

Section: Therapeutic Maneuversmentioning

confidence: 99%