Effects of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing newborn rats.
Effects of dexmedetomidine on cardiorespiratory regulation in spontaneously breathing newborn rats.
复制标题
右美托咪定对自主呼吸新生大鼠心肺调节的影响。
DOI:
10.1111/pan.12530
复制
发表时间:
2014
期刊:
影响因子:
--
通讯作者:
Saiki C.
中科院分区:
文献类型:
--
作者:
Tamiya J;Ide R;Takahashi M;Saiki C.
BackgroundDexmedetomidine, a selectiveα2‐adrenoceptor agonist, is a new sedative agent.ObjectiveTo examine the dexmedetomidine‐associated changes in cardiorespiratory indices in spontaneously breathing newborn rats.MethodsAn abdominal catheter to administer drugs and subcutaneous electrodes to record electrocardiographic data were inserted into 2‐ to 4‐day‐old rats under isoflurane anesthesia; the rats were then placed in individual chambers. After recovery from the anesthesia, the rats received intraperi‐toneal administrations of normal saline (NS, vehicle), dexmedetomidine (50 μg·kg−1), or dexmedetomidine (50 μg·kg−1) followed 5 min later with NS or the selectiveα2‐adrenoceptor antagonist atipamezole (1 mg·kg−1) (n= 10 in each group). Cardiorespiratory indices were recorded for each animal throughout the experiment.ResultsDexmedetomidine administration significantly decreased heart rate (HR) and minute ventilation (V′E) (P<0.05) compared with control, whereas NS administration did not. The decrease in HR andV′Eafter dexmedetomidine administration was significantly less in rats that received atipamezole (P<0.05) than in those that received NS after dexmedetomidine administration. The dexmedetomidine‐associatedV′Edepression was attributed to a significant decrease in respiratory frequency (fR) but not tidal volume (VT). The change infRwas reversed by atipamezole administration, which itself induced no significant changes in HR andfR.ConclusionIn spontaneously breathing immature rats, dexmedetomidine administration significantly reduced HR andV′E. Because atipamezole fully reversed decreases infRand thereforeV′E, dexmedetomidine‐related respiratory suppression occurs predominantly throughα2‐adrenoceptor‐related suppression offR.