ABSTRACT
Background: The mechanism of hypoxic pulmonary vasoconstriction [HPV] is still debatable. It has been proposed that reactive oxygen species [ROS] might be involved in HPV. However, there is no special transporter for superoxide anion in the cell membrane and it may release from the cells via anion exchanger. Therefore, the aim of this study was to investigate the interaction of ROS and anion exchanger in acute HPV
Methods: The present study was performed in the isolated rabbit lung. After preparation, the lungs were divided into four hypoxic groups of control, Trolox [antioxidant]-treated, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid [DIDS, anion exchanger inhibitor]-treated, and Trolox+DIDS-treated. Pulmonary artery pressure, left atrial pressure, and lung weight were continuously registered and PVR was then calculated. PO[2], PCO[2], HCO[3] -, pH, and NO metabolites of the perfusate were measured during steady-state and at the end of experiments [30 minutes]. All data were compared with ANOVA and t-test and significance was considered when P<0.05
Results: Ventilation of the lungs with hypoxic gas induced HPV in the control group. DIDS did not have a further effect on HPV compared with the control group. The combination of Trolox and DIDS decreased HPV rather than Trolox per se at 5 minutes. Furthermore, HPV was abolished in both the Trolox and Trolox+DIDS groups at 30 minutes. Concentrations of NO metabolites in the Trolox+DIDS group were more than other groups
Conclusion: The present study indicates a possible interaction between ROS and anion exchanger in acute HPV. It also suggests the modulatory effect of NO at above condition
ABSTRACT
The effect of severe soft tissue injury on the severity of hemorrhagic shock is still unknown. Therefore, the present study was aimed to determine hemodynamic and metabolic changes in traumatic/hemorrhagic shock in an animal model. Forty male rats were randomly divided into 4 equal groups including sham, hemorrhagic shock, soft tissue injury, and hemorrhagic shock + soft tissue injury groups. The changes in blood pressure, central venous pressure [CVP] level, acidity [pH], and base excess were dynamically monitored and com-paredsented. Mean arterial blood pressure decreased significantly in hemorrhagic shock [df: 12; F=10.9; p<0.001] and severe soft tissue injury + hemorrhagic shock [df: 12; F=11.7; p<0.001] groups 15 minutes and 5 minutes after injury, respectively. A similar trend was observed in CVP in severe soft tissue injury + hemorrhagic shock group [df: 12; F=8.9; p<0.001]. After 40 minutes, pH was significantly lower in hemorrhagic shock [df: 12; F=6.8; p=0.009] and severe soft tissue injury + hemorrhagic shock [df: 12; F=7.9; p=0.003] groups. Base excess changes during follow ups have a similar trend. [df: 12; F=11.3; p<0.001]. The results of this study have shown that the effect of hemorrhage on the decrease of mean arterial blood pressure, CVP, pH, and base excess is the same in the presence or absence of soft tissue injury
ABSTRACT
Background: Alveolar hypoxia induces monophasic pulmonary vasoconstriction in vivo, biphasic vasoconstriction in the isolated pulmonary artery, and controversial responses in the isolated perfused lung. Pulmonary vascular responses to sustained alveolar hypoxia have not been addressed in the isolated perfused rat lung. In this study, we investigated the effect of sustained hypoxic ventilation on pulmonary artery pressure in the present of phenylephrine, an alpha[1]-receptor agonist, under the above condition
Methods: We performed this study in the isolated perfused rat lung. After preparation, the lungs were divided randomly into five groups of normoxic-normocapnia, hypoxic-normocapnia, phenylephrine pre- or post-treated hypoxic-normocapnia and phenylephrine pre-treated normoxic-normocapnia. Pulmonary hemodynamic, airway pressure and lung weight were measured during 60 min of the experiment for each group
Results: In the phenylephrine-pre-treated hypoxic-normocapnia group we observed a gradual increase in pulmonary artery pressure which approximated the results seen in the phenylephrine-pre-treated normoxic-normocapnia group. In contrast, in the phenylephrine-post-treated hypoxic-normcapnic group, pulmonary artery pressure did not change during the first 3 min of hypoxic-normocapnia. However at 1.5 min after administration of phenylephrine, this pressure began to increase sharply and continued until the end of the experiment. This response was biphasic [0-10 min: acute phase, 10-60 min: sustained phase] with significantly higher pulmonary artery pressure compared to the other groups
Conclusion: This study, for the first time, showed biphasic hypoxic pulmonary vasoconstriction in the isolated perfused rat lung with the sole administration of phenylephrine after but not before hypoxic gas ventilation. This finding suggested a facilitative role of alveolar hypoxia on pulmonary vasoconstriction induced by an alpha[1]-receptor agonist