|1.||Tsai, Chien-Sung: 5 articles (08/2015 - 05/2002)|
|2.||Loh, Shih-Hurng: 5 articles (08/2015 - 05/2002)|
|3.||Chen, Wei-Hwa: 3 articles (09/2002 - 05/2002)|
|4.||Jin, Jong-Shiaw: 3 articles (09/2002 - 05/2002)|
|5.||Lee, Chung-Yi: 2 articles (08/2015 - 10/2014)|
|6.||Tsai, Yi-Ting: 2 articles (08/2015 - 10/2014)|
|7.||Chuang, Chao-Chin: 2 articles (08/2015 - 06/2002)|
|8.||Cheng, Tzu-Hurng: 2 articles (10/2014 - 05/2002)|
|9.||Chao, Chao-Ming: 2 articles (09/2002 - 06/2002)|
|10.||Tse, Chung M: 1 article (10/2015)|
12/01/2003 - "With bicarbonate-buffered medium, HOE 694 improved the post-ischemic recovery of left ventricular developed pressure (LVDP) when given before ischemia and before ischemia plus during reperfusion. "
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. "
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. "
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. "
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."
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). "
08/31/2015 - "In HEPES (nominally HCO₃⁻-free) Tyrode solution, a pHi recovery from induced intracellular acidosis could be blocked completely by 30 μM HOE 694, a specific NHE1 inhibitor, or by removing [Na⁺]₀. "
10/31/2014 - "In 3% CO₂/HCO₃⁻-buffered solution, HOE 694 slowed the pHi recovery from the induced intracellular acidosis only, while adding together with DIDS (a specific NBC inhibitor) or removal of [Na⁺]₀ entirely inhibited the acid extrusion. "
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. "
03/01/1996 - "Functional recovery in the high-glycogen hearts increased to 89% when reperfused before contracture and to 56% when reperfused in the presence of HOE 694. "
01/01/1996 - "Our findings demonstrate that HOE 694 prevents veratrine contractures at concentrations which presumably affect Na(+)-H+ exchange. "
01/01/1996 - "We examined the effects of the benzoylguanidine derivative HOE 694, an inhibitor of Na(+)-H+ exchange, against veratrine-induced diastolic contractures and action potentials recorded in rat isolated left atria. "
01/01/1996 - "HOE 694 affords protection versus veratrine contractures in rat atria by Na+ channel blockade."
01/01/1996 - "Concentration-dependent protective effects against veratrine-contractures, in the absence of negative inotropic responses, were observed with HOE 694 (IC50 = 20.1(7.6-27.0) microM, n = 24) and with the chemically related amiloride derivatives DMA, EIPA, HMA and MIA, but not with amiloride itself. "
|1.||Induced Heart Arrest (Cardioplegia)