3-methylsulfonyl-4-piperidinobenzoyl guanidine

05/01/1996 - "Improved cardiac function after prolonged hypothermic ischemia with the Na+/H+ exchange inhibitor HOE 694."
02/01/1996 - "In contrast, HOE-694 improved the postischemic recovery of LVDP from 39 +/- 5% in control to 66 +/- 6% (P < 0.05) when given before ischemia and from 33 +/- 4% in control to 65 +/- 4% (P < 0.05) when given before ischemia plus during reperfusion. "
05/01/1996 - "This study shows a marked protective effect of the Na+/H+ exchange inhibitor HOE 694 in rabbit hearts subjected to 12 hours of hypothermic ischemia and strongly suggests that antiport inhibitors could play an effective role in myocardial preservation."
03/01/2010 - "We used a more potent and specific NHE1 inhibitor HOE 694 (HOE) to test whether inhibition of NHE1 during ischemia limits increases in Nai and [Ca]i in newborns. "
12/01/2003 - "HOE 694 also provided an almost complete recovery of LVDP (88 +/- 9% vs 30 +/- 7% in controls) when given before ischemia plus during reperfusion. "

06/01/1994 - "Experiments were carried out using the new Na(+)-H+ exchange inhibitor (3-methylsulfonyl-4-piperidinobenzoyl)guanidine methanesulfonate (HOE 694) to assess the role of Na(+)-H+ exchange in myocardial ischemic and reperfusion injury. "
06/01/1998 - "Extensive studies using NHE inhibitors such as amiloride or its analogs, or more specific compounds including 3-methylsulphonyl-4-piperidinoloenzoyl-guanidine methanesulphonate (HOE 694) or 4-isopropyl-3-methylsulphonylbenzcyl-guanidine methane sulphonate (HOE 642) have consistently shown protective effects against ischemic and reperfusion injury in a large variety of experimental models and animal species particularly in terms of attenuating contractile dysfunction. "
09/01/1993 - "In this study, we evaluated the effect of two Na+/H+ exchange inhibitors (dimethylamiloride and HOE694) and a Na+/Ca2+ exchange inhibitor (dichlorobenzamil) on pH-dependent reperfusion injury. "
10/01/1998 - "In an effort to alter these pathophysiologic events, a number of investigators have studied the ability of various NHE inhibitors, such as amiloride, analogues of amiloride, and other drugs (HOE 694, HOE 642), to prevent cardiac ischemic-reperfusion damage. "

06/01/1994 - "HOE 694 did not affect the time course of intracellular acidosis during ischemia but suppressed a small alkaline overshoot occurring early in reperfusion (pH 6.96 +/- 0.02 in HOE 694-pretreated hearts versus 7.14 +/- 0.05 in control hearts). "
12/15/2004 - "HOE694 induced a significant increase in bicarbonate excretion in mice given an acute bicarbonate load, but there was no effect during metabolic acidosis. "
09/30/2002 - "The possible underlying mechanism for H2O2-induced acidosis is likely due to its inhibition on the activity of NHE and other acid extruders, as the pHi changes after H2O2 exposure could be detected even though the activity of NHE was completely blocked by 30 mM Hoe 694."
09/30/2002 - "By continuously monitoring pHi changes in human atrial myocardium, we have found, for the first time, that (a) H2O2 (30 microM-3 mM) induced a significant dose-dependent intracellular acidosis, (b) N-MPG caused a significant block on the intracellular acidosis induced by 3 mM H2O2, whereas L-methionine did not, and (c) Hoe 694, a specific Na+/H+ exchanger (NHE) inhibitor, caused a similar extents like that induced by 3 mM H2O2. "
01/01/1998 - "Blockade of the Na+/H+ exchanger [NHE; with 5-(N-ethyl-N-isopropyl) amiloride (EIPA) or HOE-694] eliminated the attenuation of ischemic acidosis seen with PC stimuli (pH: CI + EIPA, 6.5 +/- 0.1; PE + EIPA, 6.46 +/- 0.2; PE + HOE-694, 6.26 +/- 0.15; not significantly different from control). "

02/01/1995 - "HOE694 (10 microM) was partially effective when infused during reperfusion alone (ventricular fibrillation incidence reduced from 83% to 42%). "
02/01/1995 - "The novel NHE-1 selective Na+/H+ exchange inhibitor HOE694 (10 microM), when infused into the left coronary bed before ischaemia (concomitantly with 10 microM phenylephrine) and throughout reperfusion, reduced the incidence of reperfusion induced ventricular fibrillation from 83% to 25%*. "
06/01/1993 - "In these animals, pretreatment with Hoe 694 caused a dose-dependent reduction of ventricular premature beats and ventricular tachycardia as well as a complete suppression of ventricular fibrillation down to doses of 0.1 mg kg-1, i.v. Blood pressure and heart rate remained unchanged. "
01/01/2001 - "Ischemic contracture, which typically develops during ventricular fibrillation, was ameliorated by HOE-694 when either a bicarbonate-buffered (20 +/- 7 mm Hg vs 15 +/- 5 mm Hg, P <.05) or a HEPES-buffered (14 +/- 5 mm Hg vs 10 +/- 3 mm Hg, P <.04) perfusate was used. "
01/01/2001 - "We used an isolated rat heart model to investigate whether inhibition of the sodium-hydrogen exchanger isoform-1 (with the benzoylguanidine derivatives HOE-694 and cariporide) with or without concomitant inhibition of the sodium-bicarbonate co-transporter (with perfusate buffered with N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid [HEPES]) during ischemia and ventricular fibrillation could ameliorate functional myocardial abnormalities presumed to limit cardiac resuscitability. "

12/01/1995 - "Treatment with HOE 694 leads to a significant reduction in infarct size, even when administered after the onset of ischaemia. "
12/01/1995 - "Treatment with HOE 694 prior to the ischaemic insult or upon reperfusion significantly reduced infarct size [4.1%(1.4%), P < 0.01 and 38.2%(5.8%), P < 0.05, respectively], compared with 77.7%(4.0%) in the control group. "
12/01/1995 - "We assessed whether HOE 694, a specific inhibitor of Na+/H+ exchange, is able to reduce infarct size in swine myocardium. "
08/15/1995 - "Treatment with Hoe 694 before ischemia decreased histochemical infarct size from 65 +/- 18% (control group) to 13 +/- 8% (P < .01) and histological infarct size from 49 +/- 20% (control group) to 14 +/- 4% (P < .01). "
01/01/1999 - "The infarct reducing effect of 2 min hyperosmotic pretreatment was not blunted by inhibition of protein kinase C (chelerytrine chloride), the Na+/H+-exchanger (HOE 694) or stretch-activated anion channels (gadolinium chloride). "