加和不加二氧化碳的高压氧对心血管的影响。

G W Bergo, I Tyssebotn
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引用次数: 29

摘要

人们普遍认为,在高压氧(HBO)治疗过程中,尽管呼吸气体中O2含量的增加引起血管收缩,但动脉血中O2承载能力的提高导致向组织输送的O2增加。本文描述的实验验证了这样一个假设,即如果通过向呼吸气体中添加二氧化碳来消除或减弱由升高的氧气引起的血管收缩,HBO治疗将更有效地向灌注不良的组织输送氧气。在暴露于300 kPa O2(1组)或300 kPa O2 + 2 kPa CO2(2组)之前、期间和之后,测量清醒、仪器化大鼠的器官血流量(QOBF)、全身血流动力学和动脉血气。在HBO暴露期间,呼吸频率(fb)下降(4次呼吸x min(-1) x 100 kPa O2(-1)),动脉CO2张力(PaCO2)无变化,但当添加CO2时,fb和PaCO2升高。左室压(LVP)和收缩压(SBP)升高。无论是否添加CO2, LVP的最大流速(+dP/dt)随LVP呈线性上升(r2分别= 0.72和0.75)。同样,心输出量(Qc)和心率(fc)下降,而搏量(SV)不变,与PaCO2无关。除中枢神经系统(CNS)、眼睛和呼吸肌外,两组大多数器官均有血管收缩。HBO使流向中枢神经系统的血流量减少了30%,但当加入二氧化碳时,这种血管收缩被减少或消除。2组CNS血流量随PaCO2升高、ph降低呈线性上升,减压后fc和收缩压保持高位,Qc通过降低SV恢复到控制值;第二组中枢神经系统血流量明显升高,而第一组则恢复到控制水平。我们得出结论,HBO诱导的fc、Qc、LVP、dP/dt、收缩压和大多数QOBF值的变化不受高碳酸血症的影响。在PaCO2不变的情况下,HBO治疗期间流向中枢神经系统的血流量减少。高碳酸血症阻止了这种衰退。PaCO2升高增加了向中枢神经系统和眼睛的O2输送,但增加了对O2中毒的易感性。在HBO暴露期间和在没有二氧化碳的情况下减压后的空气中,对中枢神经系统的氧气供应的长期抑制发生。这种抑制作用被向呼吸气体中加入二氧化碳所抵消。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide.

It is commonly believed that during hyperbaric oxygen (HBO) treatment, in spite of the vasoconstriction induced by the increased O2 content in the breathing gas, the elevated carrying capacity of O2 in the arterial blood results in augmented O2 delivery to tissues. The experiments described here tested the hypothesis that HBO treatment would be more efficient in delivering O2 to poorly perfused tissues if the vasoconstriction induced by elevated O2 could be abolished or attenuated by adding CO2 to the breathing gas. Organ blood flow (QOBF), systemic hemodynamics, and arterial blood gases were measured before, during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2), in awake, instrumented rats. During the HBO exposure the respiratory frequency (fb) fell (4 breaths x min(-1) x 100 kPa O2(-1)), with no changes in arterial CO2 tension (PaCO2), but when CO2 was added, fb and PaCO2 increased. The left ventricular pressure (LVP) and the systolic arterial pressure (SBP) increased. The maximum velocity of LVP (+dP/dt) rose linearly with LVP whether CO2 was added or not (r2 = 0.72 and 0.75 respectively). Similarly, the cardiac output (Qc) and heart rate (fc) fell, while the stroke volume (SV) was unaltered, independent of PaCO2. There was a general vasoconstriction in most organs in both groups, with the exception of the central nervous system (CNS), eyes, and respiratory muscles. HBO reduced the blood flow to the CNS by 30%, but this vasoconstriction was diminished or eliminated when CO2 was added. In group 2, the blood flow to the CNS rose linearly with increased PaCO2 and decreased pH. After decompression fc and SBP stayed high, while Qc returned to control values by reducing the SV; CNS blood flow remained markedly elevated in group 2, while in group 1, it returned to control levels. We conclude that the changes in fc, Qc, LVP, dP/dt, SBP and most QOBF values induced by HBO were not changed by hypercapnia. Blood flow to the CNS decreased during HBO treatment at a constant PaCO2. Hypercapnia prevented this decline. Elevated PaCO2 augmented O2 delivery to the CNS and eyes, but increased the susceptibility to O2 poisoning. A prolonged suppression of O2 supply to the CNS occurred during the HBO exposure and in air following the decompression in the absence of CO2. This suppression was offset by the addition of CO2 to the breathing gas.

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