Inhibition of gasotransmitters production and calcium influx affect cardiodynamic variables and cardiac oxidative stress in propofol-anesthetized...
Djuric M., Nikolic T. T., Kostic S., Radonjic K., Jeremic J., Petkovic A., Bradic J., Milosavljevic I., Srejovic I., Zivkovic V., Djuric D., Yakovlevich V., Stevanovic P.
Canadian Journal of Physiology and Pharmacology
Vol.97, Issue9, P. 850-856
Опубликовано: 2019
Тип ресурса: Статья
DOI:10.1139/cjpp-2018-0719
Аннотация:
It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but
Ключевые слова:
Antioxidative enzymes; Cardiodynamics; DL-PAG; L-NAME; Oxidative stress; Propofol; Verapamil; ZnPPIX
anesthetic agent; calcium; cardiotonic agent; gasotransmitter; propofol; animal; biosynthesis; cardiac muscle; drug effect; heart; male; metabolism; oxidative stress; physiology; rat; transport at the cellular level; Wistar rat; Anesthetics; Animals; Biological Transport; Calcium; Cardiotonic Agents; Gasotransmitters; Heart; Male; Myocardium; Oxidative Stress; Propofol; Rats; Rats, Wistar
Язык текста: Английский
ISSN: 1205-7541
Djuric M.
Nikolic T. T. Turnic T.
Kostic S.
Radonjic K.
Jeremic J.
Petkovic A.
Bradic J.
Milosavljevic I.
Srejovic I.
Zivkovic V.
Djuric D.
Yakovlevich V. Vladimir 1971-
Stevanovic P.
Дйуриc М.
Николиc Т. Т. Тюрниc Т.
Костиc С.
Радонйиc К.
Йеремиc Й.
Петковиc А.
Брадиc Й.
Милосавлйевиc И.
Срейовиc И.
Зивковиc В.
Дйуриc Д.
Яковлевич В. Владимир 1971-
Стевановиc П.
Inhibition of gasotransmitters production and calcium influx affect cardiodynamic variables and cardiac oxidative stress in propofol-anesthetized male wistar rats
Inhibition of gasotransmitters production and calcium influx affect cardiodynamic variables and cardiac oxidative stress in propofol-anesthetized...
Текст визуальный непосредственный
Canadian Journal of Physiology and Pharmacology
NRC Research Press
Vol.97, Issue9 P. 850-856
2019
Статья
Antioxidative enzymes Cardiodynamics DL-PAG L-NAME Oxidative stress Propofol Verapamil ZnPPIX
anesthetic agent calcium cardiotonic agent gasotransmitter propofol animal biosynthesis cardiac muscle drug effect heart male metabolism oxidative stress physiology rat transport at the cellular level Wistar rat Anesthetics Animals Biological Transport Calcium Cardiotonic Agents Gasotransmitters Heart Male Myocardium Oxidative Stress Propofol Rats Rats, Wistar
It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but