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tvpjournal.com | January/February 2016 | Today's VeTerinary PracTice PracTicaL TecHniQUes FroM THe naVc insTiTUTe Peer reviewed 103 FIGURE 4. Diuresis occurs when urine levels of furosemide are within the therapeutic range. Urinary furosemide levels, of course, depend on the plasma concentration delivered to, and fltered by, the glomerulus, which, in turn, is affected by furosemide bioavailability. In this hypothetical example, diuresis begins by 1 hour and persists for 3 to 5 hours. This represents the ideal dosage for once-daily treatment, as corresponding plasma levels (refected in urinary concentration) are high enough to maximize time in the therapeutic range but not create a risk for ototoxicity. FIGURE 5. If resistance to furosemide results or other factors (eg, a high salt meal) dictate that more diuresis is needed, 1 of 2 strategies may be used: First is to administer a higher dosage, as shown with the red pharmacodynamic curve. The increase in dosage increases the urine level of the diuretic but provides only a small increase in time in the effective range, enhancing diuresis (red arrow) but increasing risk for toxicity. A better approach, although problematic in terms of owner compliance, is to administer multiple doses throughout the day. As shown in this fgure, administering the same dosage 3 times triples the time in the effective range and avoids the risk for toxicity. FIGURE 6. If resistance to furosemide results or other factors (eg, a high salt meal) dictate that more diuresis is needed, another approach (versus the 2 strategies demonstrated in Figure 5) would be to change to a longer- acting diuretic, such as torsemide (yellow curve). Note the higher peak urine level compared with furosemide at the original dosage, slight delay in peak diuresis, and prolonged period of time in the therapeutic range (dashed arrow; 10–12 H in this model). antialdosterone effects via Mr blockade, whereby high dosages of torsemide led to in vivo binding of the Mr in rat kidney cells. 16 a subsequent study, 17 however, demonstrated that torsemide does not bind the Mr in rat cardiomyocytes. This suggests that the increase in serum aldosterone seen in the study by Hori and colleagues 15 is not entirely the result of Mr blockade and likely represents raas activation from sodium depletion and diuresis. other antialdosterone and antifbrotic effects of torsemide are postulated, however, and warrant further study. 18-20 regardless of whether there is an Mr-blocking effect, it seems prudent to administer an ace inhibitor or spironolactone with torsemide due to the very high plasma aldosterone concentra - tions associated with its use (Figure 7 , page 104). Electrolyte Effects one study indicated that in experimental mitral insuffciency, there was less potassium loss with torsemide than with furosemide. 12 another study that compared normal dogs receiving an ace inhibitor alone or an ace inhibitor with torsemide (0.2 mg/kg for 28 days) showed no signifcant decrease in serum magnesium (Mg ++ ) and only a slight decrease in serum potassium (K + ), despite an increase in urine fractional excretion of both electrolytes. 21 These small studies could not prove whether