Podrobný výpis o publikaci

NOGOVÁ, Kateřina a Marie NOVÁKOVÁ. Acute effects of sigma receptor ligand haloperidol on electrogram and coronary flow in rat isolated heart. 2008.

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TY  - CONF
ID  - 776883
AU  - Nogová, Kateřina - Nováková, Marie
PY  - 2008
TI  - Acute effects of sigma receptor ligand haloperidol on electrogram and coronary flow in rat isolated heart
KW  - rat heart;sigma receptor;haloperidol;arrhythmias
N2  - Mechanisms of life-threatening cardiovascular side effects of sigma receptor ligands (cardiac arrhythmias such as torsade de pointes, ventricular fibrillation or even cardiac arrest) are not fully elucidated yet. Therefore we examined the effects of their representative haloperidol on 3-D electrogram and mean coronary flow in isolated rat hearts. Eight adult male rats were sacrificed under deep ether anesthesia. The hearts were perfused according to Langendorff with Krebs-Henseleit solution (K-H) at constant pressure (85mmHg) and 37C (CaCl2, 1.2 mM). The experiment consists of four 30min periods: control, 10nM haloperidol, washout, 10nM haloperidol. Ten successive RR intervals were averaged at the end of control (steady state heart rate). This value was used for normalization of heart rate during the rest of experiment. In the same way, QT intervals were examined in order to determine L-QT. The incidence of arrhythmias was assessed according to Lambeth Conventions. Coronary flow was measured every 5th minute. Normalized spontaneous heart rate showed a clear tendency to decrease during both haloperidol applications and this effect was partially reversible. In all hearts, the QT intervals lengthened in the first haloperidol period, partially restored in washout and in the second haloperidol administration QT interval remained unchanged. No significant incidence of life-threatening arrhythmias was observed, except of premature ventricular complexes (occurring as singles, salvos or tachycardia). Three hearts were classified by number 3. The changes of coronary flow were inconsistent and insignificant. In conclusion, QT prolongation observed in our experimental model can explain the occurrence of arrhythmias. No change of QT interval in the second haloperidol application can be reasoned by down-regulation of cardiac sigma receptor.
ER  -

Základní údaje
Originální název	Acute effects of sigma receptor ligand haloperidol on electrogram and coronary flow in rat isolated heart
Název česky	Akutní účinky ligandu sigma receptorů haloperidolu na elektrogram a koronární průtok u isolovaného srdce potkana
Autoři	NOGOVÁ, Kateřina a Marie NOVÁKOVÁ.
Vydání	2008.

Další údaje
Originální jazyk	angličtina
Typ výsledku	Konferenční abstrakt
Obor	30105 Physiology
Stát vydavatele	Česká republika
Utajení	není předmětem státního či obchodního tajemství
Organizační jednotka	Lékařská fakulta
Klíčová slova anglicky	rat heart;sigma receptor;haloperidol;arrhythmias
Štítky	arrhythmias, haloperidol, rat heart, sigma receptor
Příznaky	Mezinárodní význam
Změnil	Změnila: prof. MUDr. Marie Nováková, Ph.D., učo 1188. Změněno: 18. 6. 2009 15:11.

Anotace
Mechanisms of life-threatening cardiovascular side effects of sigma receptor ligands (cardiac arrhythmias such as torsade de pointes, ventricular fibrillation or even cardiac arrest) are not fully elucidated yet. Therefore we examined the effects of their representative haloperidol on 3-D electrogram and mean coronary flow in isolated rat hearts. Eight adult male rats were sacrificed under deep ether anesthesia. The hearts were perfused according to Langendorff with Krebs-Henseleit solution (K-H) at constant pressure (85mmHg) and 37C (CaCl2, 1.2 mM). The experiment consists of four 30min periods: control, 10nM haloperidol, washout, 10nM haloperidol. Ten successive RR intervals were averaged at the end of control (steady state heart rate). This value was used for normalization of heart rate during the rest of experiment. In the same way, QT intervals were examined in order to determine L-QT. The incidence of arrhythmias was assessed according to Lambeth Conventions. Coronary flow was measured every 5th minute. Normalized spontaneous heart rate showed a clear tendency to decrease during both haloperidol applications and this effect was partially reversible. In all hearts, the QT intervals lengthened in the first haloperidol period, partially restored in washout and in the second haloperidol administration QT interval remained unchanged. No significant incidence of life-threatening arrhythmias was observed, except of premature ventricular complexes (occurring as singles, salvos or tachycardia). Three hearts were classified by number 3. The changes of coronary flow were inconsistent and insignificant. In conclusion, QT prolongation observed in our experimental model can explain the occurrence of arrhythmias. No change of QT interval in the second haloperidol application can be reasoned by down-regulation of cardiac sigma receptor.

Anotace

Mechanisms of life-threatening cardiovascular side effects of sigma receptor ligands (cardiac arrhythmias such as torsade de pointes, ventricular fibrillation or even cardiac arrest) are not fully elucidated yet. Therefore we examined the effects of their representative haloperidol on 3-D electrogram and mean coronary flow in isolated rat hearts. Eight adult male rats were sacrificed under deep ether anesthesia. The hearts were perfused according to Langendorff with Krebs-Henseleit solution (K-H) at constant pressure (85mmHg) and 37C (CaCl2, 1.2 mM). The experiment consists of four 30min periods: control, 10nM haloperidol, washout, 10nM haloperidol. Ten successive RR intervals were averaged at the end of control (steady state heart rate). This value was used for normalization of heart rate during the rest of experiment. In the same way, QT intervals were examined in order to determine L-QT. The incidence of arrhythmias was assessed according to Lambeth Conventions. Coronary flow was measured every 5th minute. Normalized spontaneous heart rate showed a clear tendency to decrease during both haloperidol applications and this effect was partially reversible. In all hearts, the QT intervals lengthened in the first haloperidol period, partially restored in washout and in the second haloperidol administration QT interval remained unchanged. No significant incidence of life-threatening arrhythmias was observed, except of premature ventricular complexes (occurring as singles, salvos or tachycardia). Three hearts were classified by number 3. The changes of coronary flow were inconsistent and insignificant. In conclusion, QT prolongation observed in our experimental model can explain the occurrence of arrhythmias. No change of QT interval in the second haloperidol application can be reasoned by down-regulation of cardiac sigma receptor.

Anotace česky
Mechanisms of life-threatening cardiovascular side effects of sigma receptor ligands (cardiac arrhythmias such as torsade de pointes, ventricular fibrillation or even cardiac arrest) are not fully elucidated yet. Therefore we examined the effects of their representative haloperidol on 3-D electrogram and mean coronary flow in isolated rat hearts. Eight adult male rats were sacrificed under deep ether anesthesia. The hearts were perfused according to Langendorff with Krebs-Henseleit solution (K-H) at constant pressure (85mmHg) and 37C (CaCl2, 1.2 mM). The experiment consists of four 30min periods: control, 10nM haloperidol, washout, 10nM haloperidol. Ten successive RR intervals were averaged at the end of control (steady state heart rate). This value was used for normalization of heart rate during the rest of experiment. In the same way, QT intervals were examined in order to determine L-QT. The incidence of arrhythmias was assessed according to Lambeth Conventions. Coronary flow was measured every 5th minute. Normalized spontaneous heart rate showed a clear tendency to decrease during both haloperidol applications and this effect was partially reversible. In all hearts, the QT intervals lengthened in the first haloperidol period, partially restored in washout and in the second haloperidol administration QT interval remained unchanged. No significant incidence of life-threatening arrhythmias was observed, except of premature ventricular complexes (occurring as singles, salvos or tachycardia). Three hearts were classified by number 3. The changes of coronary flow were inconsistent and insignificant. In conclusion, QT prolongation observed in our experimental model can explain the occurrence of arrhythmias. No change of QT interval in the second haloperidol application can be reasoned by down-regulation of cardiac sigma receptor.

Anotace česky

Návaznosti
GA102/07/1473, projekt VaV	Název: Optické metody registrace elektrických potenciálů a koncentrace vápníku v srdci s laserovou stabilizací
GA102/07/1473, projekt VaV	Investor: Grantová agentura ČR, Optické metody registrace elektrických potenciálů a koncentrace vápníku v srdci s laserovou stabilizací
MSM0021622402, záměr	Název: Časná diagnostika a léčba kardiovaskulárních chorob
MSM0021622402, záměr	Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Časná diagnostika a léčba kardiovaskulárních chorob