| Hemodynamic Effect of Nitric Oxide Inhalation in the Acute Hypoxic Pulmonary Hypertension Induced Newborn Piglet |
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Yun Cil Chang1, Won Soon Park1, Jung-Hwan Choi2, Chong Ku Yun2 |
1Department of Pediatrics, Samsung Medical Center, Sung Kyun Kwan University College of Medicine, Seoul, Korea
2Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea |
| 급성 저산소성 폐동맥 고혈압증이 유도된 신생 자돈에서 Nitric Oxide 흡입의 혈역학적 효과 |
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장윤실1, 박원순1, 최중환2, 윤종구2 |
1성균관대학교 의과대학 삼성서울병원 소아과,
2서울대학교 의과대학 소아과학교실 |
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| Abstract |
Purpose
s : Nitric oxide(NO) is classified as toxic gas in native states, but in most biologic
systems NO acts as a messenger molecule. NO is known as endothelium derived relaxing factor
that modulates tone of vascular smooth muscle. Inhaled NO has been reported to act as a selective
pulmonary vasodilator and we expect that NO inhalation can be used as a successful treatment
modality in the management of persistent pulmonary hypertension of the newborn. We used the
newborn piglet to create acute hypoxic pulmonary hypertension and examined the hemodynamic
effect of inhlaled NO and dose-response characteristics in different concentrations of NO in this
model. The aims of this study were to investigate the feasibility and safety of administering NO to
a neonatal model and to get a useful informations about clinical applications of administering NO.
Methods
: Nine 2- to 9-d-old piglets with an average weight of 3.1¡¾0.86kg were anesthetized,
intubated and instrumented in order to measure the hemodynamic variables. NO in nitrogen in a
concentration of 800 ppm in 47 liter sylinder was obtained and injected into the inspiratory line of
a time-cycled pressure-limited neonatal ventilator after reducing of pressure using 3 staged
regulator. Gas mixture in downstream of the injection site was analyzed for NO and NO2 using
electrochemical analyzer. Statistical analyses were done using with SAS software ver. 6.04.
Results
: Baseline hemodynamic parameters in normoxic breathing such as mean systemic arterial
pressure, mean pulmonary arterial pressure, systemic vascular resistance, pulmonary vascular
resistance and cardiac index were 79¡¾18mmHg, 16¡¾4mmHg, 0.20¡¾0.09mmHg․mL-1․min․kg,
0.04¡¾0.02mmHg․mL-1․min․kg, and 399¡¾201mL/min/kg respectively. Inhaling 20 and 80 ppm NO
during ventilation at FIO2 0.21 did not produce any significant changes in hemodynamic indices.
Pulmonary hypertension was induced by reducing the fraction of inspired oxygen to 0.10 to 0.15 and
arterial oxygen saturation between 35 and 45%. The hypoxic challenge caused a significant increase
in pulmonary arterial pressure, pulmonary vascular resistance and the ratio of pulmonary to systemic
vascular resistance of 105%(P < 0.001), 92%(P < 0.02), 72%(P < 0.01) respectively. Systemic arterial
pressure increased by 20%(P < 0.05), but systemic vascular resistance and cardiac index were not
changed significantly. Inhaled NO was then administered in concentrations of 10, 20, 40, 80, and 100
parts per million in random order. All concentrations of NO were associated with a rapid decrease in
pulmonary arterial pressure and pulmonary vascular resistance (P < 0.02, P < 0.001). The ratios of
pulmonary to systemic vascular resistance decreased with all levels of inhaled NO (P < 0.05). There
was no significant difference between the different doses of NO in their effects. There was no
significant increase in circulating methemoglobin, and the NO2 levels in the inspiratory limb of
ventilator never exceeded 1.5 ppm. Plasma nitrite and nitrate increased in a dose-dependent
manner(P < 0.05).
Conclusions
: In acute hypoxic pulmonary hypertension induced newborn piglets NO inhalation with
all the varying concentrations led to reduction of pulmonary arterial pressure promptly and safely
without significant increase of methemoglobin and NO2 levels. |
| Key Words:
Nitirc oxide, Hypoxic pulmonary hypertension, Newborn, Animal |
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