PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	29-38	alpha-internexin	Cavia porcellus	73-76	
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	29-38	alpha-internexin	Cavia porcellus	330-333	
10320683-3	1999	RESULTS: Salicylate enhanced quinidine-induced tonic and phasic block of INa at a holding potential of -100 mV but not at a holding potential of -140 mV; this enhancement was accompanied by a shift of the hinfinity curve in the presence of quinidine in a further hyperpolarized direction, although salicylate alone did not affect INa.	Quinidine	240-249	alpha-internexin	Cavia porcellus	73-76	
1337728-3	1992	The channel state dependent blocking effects on cardiac sodium current (INa) of quinidine and disopyramide were studied under the whole cell variation of the patch clamp technique.	Quinidine	80-89	alpha-internexin	Cavia porcellus	72-75	
9592721-4	1998	Quinidine (30 microM) and verapamil (0.1 microM) produced use-dependent depression of INa and ICa, respectively.	Quinidine	0-9	alpha-internexin	Cavia porcellus	86-97	
1337728-10	1992	CONCLUSIONS: Quinidine produces more potent tonic and use dependent block of INa by binding to sodium channels at both rested and inactivated states, while disopyramide has a higher affinity for activated state.	Quinidine	13-22	alpha-internexin	Cavia porcellus	77-80	
1658339-1	1991	To determine if the fast sodium current inactivation process is necessary for sodium current (INa) blockade by quinidine, we studied the effects of quinidine on INa in guinea-pig ventricular myocytes treated with chloramine-T, which removes the fast inactivation process of INa.	Quinidine	111-120	alpha-internexin	Cavia porcellus	94-97	
1658339-3	1991	Quinidine (10 microM) produced resting block of INa of 36 +/- 2% (n = 5) at the peak potential of -30 mV in chloramine-T treated myocytes.	Quinidine	0-9	alpha-internexin	Cavia porcellus	48-51	
1658339-4	1991	Quinidine decreased INa in a dose-dependent manner.	Quinidine	0-9	alpha-internexin	Cavia porcellus	20-23	
1658339-7	1991	Even after removal of the fast inactivation process of INa, use-dependent block was observed in the presence of quinidine when various depolarizing pulse durations (5 ms approximately 200 ms) were applied repetitively at intervals of 300 ms approximately 2 s. Longer depolarizing pulses and higher frequency pulse trains produced greater use-dependent block.	Quinidine	112-121	alpha-internexin	Cavia porcellus	55-58