Matsuoka Tadashi, Suzuki Masaru, Sano Motoaki, Hayashida Kei, Tamura Tomoyoshi, Homma Koichiro, Fukuda Keiichi, Sasaki Junichi
From the Department of Emergency and Critical Care Medicine (T.M., M.S., K.H., T.T., J.S.), Center for Medical Hydrogen Medicine (T.M., M.S., M.S., K.H., T.T., K.H.), Department of Cardiology (M.S., K.F.), School of Medicine, Keio University, Tokyo, Japan.
J Trauma Acute Care Surg. 2017 Sep;83(3):469-475. doi: 10.1097/TA.0000000000001620.
Mortality of hemorrhagic shock primarily depends on whether or not the patients can endure the loss of circulating volume until radical treatment is applied. We investigated whether hydrogen (H2) gas inhalation would influence the tolerance to hemorrhagic shock and improve survival.
Hemorrhagic shock was achieved by withdrawing blood until the mean arterial blood pressure reached 30-35 mm Hg. After 60 minutes of shock, the rats were resuscitated with a volume of normal saline equal to four times the volume of shed blood. The rats were assigned to either the H2 gas (1.3% H2, 26% O2, 72.7% N2)-treated group or the control gas (26% O2, 74% N2)-treated group. Inhalation of the specified gas mixture began at the initiation of blood withdrawal and continued for 2 hours after fluid resuscitation.
The survival rate at 6 hours after fluid resuscitation was 80% in H2 gas-treated rats and 30% in control gas-treated rats (p < 0.05). The volume of blood that was removed through a catheter to induce shock was significantly larger in the H2 gas-treated rats than in the control rats. Despite losing more blood, the increase in serum potassium levels was suppressed in the H2 gas-treated rats after 60 minutes of shock. Fluid resuscitation completely restored blood pressure in the H2 gas-treated rats, whereas it failed to fully restore the blood pressure in the control gas-treated rats. At 2 hours after fluid resuscitation, blood pressure remained in the normal range and metabolic acidosis was well compensated in the H2 gas-treated rats, whereas we observed decreased blood pressure and uncompensated metabolic acidosis and hyperkalemia in the surviving control gas-treated rats.
H2 gas inhalation delays the progression to irreversible shock. Clinically, H2 gas inhalation is expected to stabilize the subject until curative treatment can be performed, thereby increasing the probability of survival after hemorrhagic shock.
失血性休克的死亡率主要取决于患者在接受根治性治疗之前能否耐受循环血量的丧失。我们研究了吸入氢气（H₂）是否会影响对失血性休克的耐受性并提高生存率。
通过抽血使平均动脉血压达到30 - 35 mmHg来诱导失血性休克。休克60分钟后，用相当于失血量4倍体积的生理盐水对大鼠进行复苏。将大鼠分为氢气处理组（1.3% H₂、26% O₂、72.7% N₂）和对照气体处理组（26% O₂、74% N₂）。从抽血开始即进行指定气体混合物的吸入，并在液体复苏后持续2小时。
液体复苏后6小时，氢气处理组大鼠的生存率为80%，对照气体处理组为30%（p < 0.05）。通过导管抽取以诱导休克的血量，氢气处理组大鼠明显多于对照组大鼠。尽管失血更多，但休克60分钟后，氢气处理组大鼠血清钾水平的升高受到抑制。液体复苏使氢气处理组大鼠的血压完全恢复正常，而对照气体处理组大鼠的血压未能完全恢复。液体复苏后2小时，氢气处理组大鼠血压保持在正常范围内，代谢性酸中毒得到良好代偿，而在存活的对照气体处理组大鼠中，我们观察到血压下降、代谢性酸中毒未得到代偿以及高钾血症。
吸入氢气可延缓进展至不可逆休克。临床上，预计吸入氢气可使患者在进行根治性治疗之前保持稳定，从而提高失血性休克后的生存概率。
