Changes in lung liquid dynamics induced by prolonged fetal hypoxemia

Our aim was to determine the effect of prolonged fetal hypoxemia, induced by reduced maternal uterine blood flow (RUBF), on fetal lung liquid secretion, flow, and volume. In chronically catheterized fetal sheep, lung liquid volume (VL) and the secretion rate of lung liquid (Vs) were measured before and after a 24-h period of either RUBF or normoxemia. Tracheal fluid flow and the incidence of fetal breathing movements (FBM) were measured before, during, and after the 24-h period. In normoxic control fetuses Vs was not significantly altered. After 24 h of RUBF, Vs was significantly (P less than 0.005) reduced compared with pre-RUBF values. During 24 h of RUBF the incidence of FBM declined initially but returned to control values after 12-16 h. In seven of eight fetuses, over the 12- to 24-h period of RUBF, large amounts of liquid (22.7-62.6 ml) were drawn into the lungs during FBM, resulting in a net movement of amniotic fluid into the lungs. During the 18- to 24-h period of RUBF, changes in the incidence of FBM were found to be significantly and positively correlated (r = 0.86, P less than 0.005) with the changes in VL that occurred over the 24-h period. Thus, prolonged RUBF can result in the inhalation of large volumes of amniotic fluid by the fetus, which could be a cause of in utero meconium aspiration.     

低氧反应和屏气反应在急性高原反应预测中的作用

目的:探讨低氧反应和屏气反应在急性高原反应预测中的作用.方法:在平原观察113名入藏人员吸入10%低氧气体10 min和屏气过程中的血氧饱和度、心率和血压变化;进入高原后进行急性高原反应(AMS)症状评分;两组数据进行相关分析,并对急性高原反应者和基本无反应者数据进行分析.结果:吸入10%低氧气体过程中,动脉血氧饱和度进行性下降,心率迅速升高,血压普遍呈现先升高后降低的变化趋势.急性高原反应者吸入低氧气体1min时的心率明显慢于基本无反应者.所观测指标均存在着较大的个体差异,但相关分析表明,AMS评分仅与吸入低氧气体7 min时的心率呈显著负相关,相关系数r为-0.176.结论:在平原单纯用低氧和屏气反应来预测3 658 m高原地区的AMS发病情况意义可能有限.     

Voluntary breath holding in the obese

Alveolar gas tensions and arterial O2 saturation (Sao2) during a voluntary breath hold at functional residual capacity (FRC) were examined in 13 healthy seated subjects. An excellent correlation (r = 0.80) was found between the fall of alveolar O2 tensions (delta PETo2) and body weight, expressed as the ratio of weight to height (wt/ht, kg/cm). An even greater correlation (r = 0.89) was found between delta PETo2 and the ratio of breath-hold time X O2 consumption/FRC. Alveolar Po2 decreased to 70 mmHg in the obese group after just 15 s of apnea, whereas this degree of hypoxia did not occur in the nonobese until the breath hold was sustained for 30 s. This variable rate of fall of alveolar Po2 during a breath hold can be ascribed to the changes of O2 consumption (Vo2) and FRC associated with changing body weight. In the obese, Vo2/FRC was twice as large as in the nonobese, thus accounting for the differences of breath-hold time needed to obtain the same alveolar Po2. Sao2 measured at the end of the breath hold was the same as that value predicted from the reduction of PETo2. This suggests that the fall of alveolar Po2 can entirely account for the observed fall of O2 saturation and that venous admixture had not increased during the 15-s apnea. In patients with sleep apnea, the ratio of Vo2/(initial lung volume) may also be an important determinant of the severity of hypoxemia observed.     

Cardiac performance in humans during breath holding

The effects on cardiac performance of high and low intrathoracic pressures induced by breath holding at large and small lung volumes have been investigated. Cardiac index and systolic time intervals were recorded from six resting subjects with impedance cardiography in both the nonimmersed and immersed condition. A thermoneutral environment (air 28 degrees C, water 35 degrees C) was used to eliminate the cold-induced circulatory component of the diving response. Cardiac performance was enhanced during immersion compared with nonimmersion, whereas it was depressed by breath holding at large lung volume. The depressed performance was apparent from the decrease in cardiac index (24.1% in the immersed and 20.9% in the nonimmersed condition) and from changes in systolic time intervals, e.g., shortening of left ventricular ejection time coupled with lengthening of preejection period. In the absence of the cold water component of the diving response, breath holding at the large lung volume used by breath-hold divers tends to reduce cardiac performance presumably by impeding venous return.     

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo

In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of the heart and brain. Peripheral vasoconstriction contributes to this response and is partly mediated by the release of catecholamines. Two mechanisms of catecholamine release in the fetus are reported: 1) neurogenic sympathetic stimulation and 2) a nonneurogenic mechanism via a direct effect of hypoxemia on chromaffin tissues. In the present study, the effects of sympathetic blockade on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia were studied in the chick embryo at different stages of incubation. Only at the end of the incubation period, sympathetic blockade markedly attenuated the increase in plasma catecholamine concentrations and resulted in a greater fraction of the cardiac output distributed to the carcass. However, these effects did not prevent a significant increase in cardiac output to the brain and heart during acute hypoxemia. These data imply that in the chick embryo the contribution of neurogenic mechanisms to the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period.     

Behavioral activity during prolonged hypoxemia in fetal sheep

Experiments were conducted in unanesthetized, chronically catheterized pregnant sheep to determine the fetal behavioral response to prolonged hypoxemia produced by restricting uterine blood flow. Uterine blood flow was reduced by adjusting a vascular occluder placed around the maternal common internal iliac artery to decrease fetal arterial O2 content from 6.1 +/- 0.3 to 4.1 +/- 0.3 ml/dl for 48 h. Associated with the decrease in fetal O2 content, there was a slight increase in fetal arterial PCO2 and decrease in pH, which were both transient. There was an initial inhibition of both fetal breathing movements and eye movements but no change in the pattern of electrocortical activity. After this initial inhibition there was a return to normal incidence of both fetal breathing movements and eye movements by 16 h of the prolonged hypoxemia. These studies indicate that the chronically catheterized sheep fetus is able to adapt behaviorally to a prolonged decrease in arterial O2 content secondary to the restriction of uterine blood flow.     

Cardiac output in exercise by impedance cardiography during breath holding and normal breathing

Estimation of cardiac output by impedance cardiography (QZ) in exercise during normal breathing (NB) has been limited by motion artifact. Our objective was to obtain readable impedance cardiograms on five subjects during upright cycle exercise at 0, 50, 100, 150, and 200 W to permit comparisons of QZ during NB, expiratory breath hold (EXP) and inspiratory breath hold (INSP). Q was also determined using an equilibration CO2 rebreathing method [Q(RB)]. QZ during NB exceeded EXP QZ at 100, 150, and 200 W, and exceeded INSP QZ at 100 W (P less than 0.05). The low EXP QZ values were due to a significantly lower stroke volume at 100, 150, and 200 W (P less than 0.05). For the INSP QZ at 100 W, heart rate was lower than during EXP (P less than 0.05). Regression of QZ (NB) against Q(RB) resulted in a linear relationship (r = 0.93) over the range of Q = 7-26 1/min. The slope of the regression differed significantly from 1.0 (P less than 0.05). We conclude that QZ values obtained during EXP or INSP should not be assumed to represent QZ during NB, at least at work rates greater than 50 W. A consequence of the linear relationship between QZ(NB) and Q(RB) over the range of 0-200 W is that estimates of CO2 rebreathing cardiac output can be obtained by impedance cardiography if QZ is adjusted using an appropriate empirical factor.     

Aldosterone response to angiotensin II during hypoxemia

Exercise in humans causes increases in plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) except when performed at high altitude or while the subjects breathe hypoxic gas. Under those conditions, PRA increases with exercise but PAC does not. We speculated that the PAC suppression during hypoxemic exercise was due to hypoxemia-induced release of a circulating inhibitor of angiotensin II-mediated aldosterone secretion. To test this hypothesis, we measured the PAC response to graded infusions of angiotensin II during hypoxemia and normoxemia. Eight normal volunteers were given increasing doses of angiotensin II (first 2 ng X kg-1 X min-1 and then 4, 8, and finally 12 ng X kg-1 X min-1, each for 20-min periods) on 2 separate days, once while breathing room air and the other day while breathing hypoxic gas adjusted to maintain the subjects' hemoglobin saturation at 90%. The PAC response to different doses of angiotensin II did not significantly differ during hypoxemia from normoxemia. We conclude that our model of hypoxemia does not cause release of an inhibitor of angiotensin II-mediated aldosterone release.