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Effect of calcium antagonist, nicardipine, on cerebral blood flow in postasphyxial newborn piglets
Author(s) -
IMAI TADASHI,
KONDO MASATOSHI,
KUSAKA TAKASHI,
SUGIHARA SATORU,
ISOBE KENICHI,
ITOH SUSUMU,
ONISHI SHOJU
Publication year - 1995
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1995.tb03318.x
Subject(s) - nicardipine , medicine , antagonist , calcium , anesthesia , cerebral blood flow , pharmacology , receptor
An experiment was carried out in nine piglets within 24 h after birth (control group: four, nicardipine group: five) for the purpose of evaluating the effects of a calcium antagonist, nicardipine, on cerebral blood flow changes induced by asphyxia neonatorum. Under respiratory control with a mechanical ventilator, the animals were exposed to hypoxia. The inspiratory oxygen level was lowered at 15 min intervals from 0.08 to 0.06 and then to 0.05. When bradycardia (heart rate: 60/min or less) was observed, 100% oxygen, adrenaline, and sodium bicarbonate were administered for resuscitation. Nicardipine was administered at a dosage of 10μg/kg via bolus injection 30 min after the resuscitation. It was administered thereafter at a rate of 10μg/kg per h. The cerebral blood flow was measured using a laser Doppler velocimeter. The cerebral blood flow, electroencephalograph (EEG), blood pressure, and heart rate were continuously measured for 120min after the resuscitation. In the control group, the mean arterial pressure 35 min after the resuscitation was 60 mmHg or more. However, the cerebral blood flow was lower than the prehypoxia value in the animals with a mean arterial pressure of 75mmHg or less. In the nicardipine group, the mean arterial pressure was lower, but the cerebral blood flow was higher than the prehypoxia value and cerebral ischemia was not induced. The mean arterial pressure 120 min after the resuscitation was 72.0 ± 8.2 mmHg in the control group, while it was 56.7 ± 7.5 mmHg in the nicardipine group. It was significantly lower in the latter. The cerebral blood flow as compared to that before the initiation of exposure to hypoxia (this being considered 100) was 83.1 ± 22.0% in the control group, while it was 125.1 ± 26.2% in the nicardipine group. It was significantly higher in the latter. A suppression burst‐like abnormal EEG finding occurred in two of four animals from the control group and was noted in one of five animals from the nicardipine group. In the nicardipine group, the mean arterial pressure was lowered, but a decrease in the cerebral blood flow after asphyxia was totally prevented and the incidence of EEG abnormality was low. It seems possible that this drug protects the brain from asphyxia‐induced changes.