Effect of hypoxia on the auditory system of goat fetuses during extrauterine incubation

J Obstet Gynaecol Res 2002; 2: 109–114
Aim:  To investigate the effect of hypoxia on the auditory system in fetuses, we attempted to analyze the auditory brainstem response, the middle latency response, and changes of several physiological parameters of goat fetuses during extrauterine incubation.
Methods:  We conducted extrauterine incubation of five goat fetuses at around 127 days of gestation (term = 148 days). Their physiological parameters, such as fetal heart rate, mean blood pressure, flow rate of carotid artery, as well as the auditory brainstem response and middle latency response, were recorded prior to and during hypoxia, and the two sets of data were compared with each other.
Results:  In all five cases, the fetal heart rate decreased from 178 ± 12.2 b.p.m. to 144 ± 15.2 b.p.m. during hypoxia, while mean blood pressure and flow rate of carotid artery increased from 37.3 ± 3.7 mmHg to 43.2 ± 5.1 mmHg, and from 38.5 ± 5.5 mL/min to 47.0 ± 5.1 mL/min, respectively. The latency of the auditory brainstem response's wave V and of the middle latency response's Pa wave elongated from 5.24 ± 0.24 ms to 5.69 ± 0.20 ms, and from 19.2 ± 1.6 ms to 20.9 ± 1.4 ms, respectively.
Conclusion:  Although fetal compensatory reactions, such as increases in mean blood pressure and flow rate of carotid artery during hypoxia were recognized, elongation of latency, and decrement of amplitude were observed in the auditory brainstem response and middle latency response. These results suggest that hypoxia itself influences the auditory system of the fetus.     

Doppler assessment of fetal blood flow velocity waveforms during acute maternal oxygen administration as predictor of fetal outcome in post-term pregnancy

The changes in fetal blood flow velocity waveforms during maternal administration of 60% humidified oxygen were assessed by Doppler ultrasonography in 45 post-term fetuses. During oxygen treatment, nine fetuses exhibited temporary increases (24.3 +/- 2.0% [1 standard deviation] above pretreatment values) in the pulsatility index at the level of internal carotid artery. Although no significant changes (2.9 +/- 5.1%) were found in the remaining 36 fetuses. In this former group a higher incidence of emergency cesarean delivery due to fetal distress and more neonatal complications were observed. Also, meconium staining of the amniotic fluid and low 1- and 5-minute Apgar scores occurred more frequently in the group of fetuses who responded to maternal oxygen administration. An increase of at least 20% in the pulsatility index of internal carotid artery during maternal hyperoxygenation may be a useful marker of adverse outcome in post-term fetuses.     

Endocrinological and Biophysical Responses to Further Reduction in Oxygenation Following Sustained Hypoxemia in Fetal Goats

Objective: The purpose of this study was to determine fetal endocrinological and biophysical responses to the further reduction in oxygenation following prolonged nonacidemic hypoxemia in fetal goats.

Methods: Seven further hypoxic experiments were performed after prolonged (24-h) nonacidemic hypoxemia, caused by an infusion of nitrogen into the maternal trachea and by reducing uterine arterial blood flow in four chronically instrumented goat fetuses at 123–131 days' gestation. We measured arginine vasopressin, adrenocorticotropic hormone, cortisol, and cathecolamines as endocrinological parameters. Fetal heart rate, fetal blood pressure, and fetal breathing movement were observed as biophysical parameters.

Results: Fetal arterial pO₂ was significantly decreased from 27.0± 1.2 mmHg (control) to 18.0 ± 0.7 mmHg and 11.3 ± 1.3 mmHg at the end of the prolonged hypoxemia and the further hypoxia, respectively. The further hypoxia induced reductions in fetal heart rate, increases in fetal blood pressure, and a series of gasping. Arginine vasopressin and cathecolamines were elevated significantly by the further hypoxia. Although adrenocorticotropic hormone and cortisol were increasingly elevated, they did not reach a significant level.

Conclusions: Some specific fetal responses—excessive elevations of fetal cathecolamines, arginine vasopressin, accompanied with fetal gasping—were observed during further severe hypoxia.     

Middle cerebral artery Doppler flow velocity waveforms

Doppler flow velocity-time waveforms of the middle cerebral arteries at their origin from the internal carotid arteries were obtained serially on 14 patients to determine the alterations of these waveforms with gestational age. Satisfactory recordings were obtained from all patients. The middle cerebral artery waveforms demonstrated a typically biphasic pattern with continuing forward flow in diastole. The peak systolic to end-diastolic ratio (A/B ratio) showed a progressive and significant decline from 6.89 +/- 1.48 at around 25 weeks to 4.23 +/- 0.67 at term. Elevation of diastolic velocities and diminished A/B ratio in the middle cerebral arteries were noted in four fetuses, in whom severe antepartum compromise was diagnosed. The ratio also appeared to decrease with worsening of fetal condition. Because the fetus compensates for hypoxia by increasing blood flow to the brain, Doppler middle cerebral artery waveforms may permit evaluation of fetal compromise and hypoxia.     

The effects of veno-venous extracorporeal membrane oxygenation on hypoxic fetal lambs.

OBJECTIVE: The purpose of this study was to determine the applicability of veno-venous extracorporeal membrane oxygenation (V-V ECMO) to support fetal oxygenation in utero. METHODS: An ECMO system with a centrifugal pump was applied to ten chronically instrumented fetal lambs, at 126 or 127 days of gestation. Blood was obtained through a double-lumen catheter inserted into the right atrium. After oxygenation, the blood was returned through a single-lumen catheter into either the carotid artery (veno-arterial; V-A ECMO) or the right atrium (V-V ECMO). After fetal hypoxia had been experimentally produced, V-A ECMO or V-V ECMO was instituted to maintain fetal oxygenation. We compared fetal blood gases with both routes of ECMO. RESULTS: Oxygen partial pressure (pO(2)) in the fetal cranial carotid artery decreased to 12.9 +/- 0.6 mmHg after reducing the fraction inspiratory oxygen of the mother. After instituting V-A ECMO, pO(2) was found to be 23.5 +/- 2.6 mmHg; after instituting V-V ECMO, pO(2) was found to be 20.3 +/- 1.9 mmHg. Thus, fetal acidosis increased under both procedures. Fetal heart rate and blood pressure were not altered significantly during the experiments. CONCLUSIONS: This study indicates that V-V ECMO could more effectively and less traumatically maintain oxygenation in hypoxic fetal lambs.     

The pattern of breathing of fetal sheep in graded hypoxia

We examined the effects on fetal breathing movements (FBM) and electrocortical activity (ECoG) of maintaining fetal arterial PO2 (PaO2) at 16.9 +/- 1.9 mmHg for 20 min in unanaesthetized, chronically instrumented fetal sheep in utero at 122-132 days gestation. In 82% of trials, a pattern of regular FBM occurred characterised by its large (35 +/- 7 mmHg) excursions in tracheal pressure and its low frequency (ca. 3 per min) compared to the irregular FBM occurring during normoxia (ca. 5 mmHg and ca. 90 per min, respectively) (PaO2 ca. 23 mmHg). The occurrence of FBM in mild hypoxia was independent of the ECoG state of the fetus and it also occurred in fetuses in which the carotid sinus nerves and cervical vagosympathetic trunks had been sectioned bilaterally. Reducing PaO2 to between 16 and 11 mmHg produced a cessation of FBM, as reported by other workers. The FBM in mild hypoxia were distinct from 'gasping', which occurs only when PaO2 was reduced to much lower levels. The FBM in mild hypoxia are discussed in terms of central respiratory mechanisms excited by hypoxia, as opposed to the well-documented mechanisms which inhibit FBM in more intense hypoxia.     

Unloading of baroreceptors by carotid occlusion does not increase heart rate in fetal sheep

Unloading of baroreceptors by carotid occlusion does not increase heart rate in fetal sheep; Objectives: To test the hypothesis that in fetal sheep reduction of carotid sinus pressure by carotid occlusion increases heart rate. Study design: Fetal sheep (gestational age 121-132 days) were chronically instrumented with bilateral carotid occluders, catheters and electrodes (ECG) to measure systemic arterial and carotid sinus (CSP) blood pressures, and fetal heart rate. Results: Bilateral carotid occlusion (BCO) increased mean arterial blood pressure from 46+/-7 mmHg to 53+/-8 mmHg (mean+/-S.D.) while CSP decreased from 44+/-7 mmHg to 17+/-7 mmHg. Fetal heart rate fell during occlusion significantly from 186+/-34 bpm to 159+/-26 bpm (n=20 animals). Infusion of phenylephrine (8.5-20 microg min(-1)kg(-1)) or methoxamine (60-200 microg min(-1)kg(-1)) increased mean blood pressure from 44+/-6 to 61+/-9 mmHg, and fetal heart rate decreased from 186+/-30 to 132+/-31 bpm (n=12). BCO increased systemic arterial pressure further to 70+/-11 mmHg whereas carotid sinus pressure was reduced to 31+/-13 mmHg. However, average heart rate did not increase significantly (136+/-28 bpm). Conclusion: We conclude that in contrast to adult animals, in fetal sheep carotid occlusion with subsequent unloading of baroreceptors does not increase heart rate even when the baroreflex had been activated by arterial hypertension. It seems likely that stimulation of carotid chemoreceptors prevents the expected baroreceptor mediated heart-rate response.     

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic blocking agents in fetal lambs.

Fetal heart rate decelerations resembling the late deceleration FHR pattern were produced in fetal sheep by periodic occlusion of the maternal common hypogastric artery for 30-60 sec. Transient fetal hypertension also occurred during the occlusions. Alpha-adrenergic blockade with phentolamine eliminated or markedly reduced the hypertensive response. FHR decelerations still occurred intermittently with some occlusions; however, their character was greatly altered. After parasympathetic blockade with atropine, the decelerations were replaced by periodic FHR accelerations during the occlusions. These accelerations were, in turn, eliminated by the beta-adrenergic blocking agent, propranolol. In the presence of combined parasympathetic, alpha- and beta-adrenergic blockade, the FHR remained essentially constant during the hypogastric artery occlusions in non-acidemic fetuses. FHR decelerations persisted after parasympathetic or total autonomic blockade when the fetuses were significantly hypoxic, as judged by depressed arterial blood pH and base excess values. Beat-to-beat variability of the baseline FHR persisted in the face of severe hypoxia and acidosis. These observations demonstrate that reflex mechanisms are involved importantly in the genesis of late deceleration FHR patterns in the acutely hypoxemic fetus, but that direct depression of myocardial rhythmicity becomes a factor as hypoxic acidosis develops.     

Doppler investigation of the fetal circulation

Doppler ultrasound provides a non-invasive method for the study of fetal haemodynamics. Animal studies on effects of hypoxia have provided evidence of a redistribution of cardiac output to favour perfusion of the fetal heart, adrenals and brain, at the expense of the carcass, gut and kidneys. This paper summarises the changes in fetal Doppler parameters with advancing gestation. Furthermore, it examines the alterations in fetal haemodynamics in relation to fetal blood oxygen tension in samples obtained by cordocentesis from small for gestational age (SGA) fetuses. In SGA fetuses increased downstream impedence to flow in the umbilical artery, as demonstrated by the absence of end-diastolic frequencies in the flow velocity waveforms (FVW), is associated with fetal hypoxia. This presumably reflects the underlying derangement of placental structure and function. The impedence to flow and mean blood velocity were also measured in FVWs from the descending thoracic aorta and common carotid artery, obtained by pulsed Doppler ultrasound, and from the middle cerebral and renal arteries obtained by colour flow imaging. There were significant correlations between the degree of fetal hypoxia and alterations in Doppler parameters, which were compatible with the brain sparing effect. Thus, in fetal hypoxia impedence to flow in the common carotid and middle cerebral arteries was decreased, whereas impedence in the aorta and renal artery was increased. There were simultaneous alterations in the mean blood velocity in the opposite direction to those in impedence.     

Development of artificial placenta: oxygen metabolism of isolated goat fetuses with umbilical arteriovenous extracorporeal membrane oxygenation

To assess the oxygen utilization of extrauterine goat fetuses with arteriovenous extracorporeal membrane oxygenation via umbilical vessels, oxygen delivery (OD) and oxygen consumption (OC) were investigated in 19 long-term incubations (incubation periods 58-236 h). The OCs did not change (6.4 +/- 1.3 ml/min/kg, mean +/- SD, n = 227) when the ODs were more than 10 ml/min/kg, but were significantly suppressed when the ODs were less than 10 ml/min/kg. It was suggested that the oxygen metabolism of extrauterine goat fetuses is equivalent to that of fetuses in utero.     

Effect of maternal oxygenation on fetal blood gas status in shiba goat fetuses

The purpose of this study is to investigate the effect of maternal oxygen administration on the fetal blood gas status. Five Shiba goat fetuses were used whose gestational days were 134 +/- 4 days. Maternal and fetal pH, pO2, pCO2, B.E., and hematocrit were measured every 30 minutes during 4 l/min oxygen administration for 60 minutes. Maternal arterial blood pO2 increased from 95.5 +/- 19.6 mmHg to 262.6 +/- 75.8 mmHg at 30 minutes and to 207.8 +/- 110.1 mmHg at 60 minutes. Fetal arterial blood pO2 increased significantly from 18.4 +/- 3.0 mmHg to 24.4 +/- 5.8 mmHg and 23.6 +/- 6.9 mmHg, respectively. There was a significant positive correlation between maternal pO2 and fetal pO2. The increase in fetal pO2 was small when the control pO2 was less than 17 mmHg. Although maternal pH did not change significantly, fetal pH decreased significantly from 7.29 +/- 0.07 to 7.25 +/- 0.07 at 60 minutes. Also fetal hematocrit decreased significantly from 33.9 +/- 5.2% to 32.8 +/- 5.4% at 60 minutes. Neither maternal nor fetal pCO2 and B.E. changed significantly. Therefore, we concluded that the effect of maternal oxygen administration on fetal pO2 was small when the fetus was already hypoxic. Also 60 minutes' oxygen administration may cause the decrease in fetal pH and hemodilution.     

Tocolysis and delayed delivery versus emergency delivery in cases of non-reassuring fetal status during labor

AIM: To determine whether fetal intrauterine resuscitation using tocolysis and delayed delivery is better for the fetus than emergency delivery when fetal hypoxia is suspected because of a non-reassuring fetal heart-rate (FHR) pattern using conventional heart rate monitoring. METHODS: This was a prospective and randomized study, conducted between 2001 and 2004 at Pereira Rossell Hospital, Montevideo, Uruguay. The population consisted of 390 fetuses, in which intrauterine distress was diagnosed using electronic FHR monitoring. Of these, 197 were randomly assigned to the emergency delivery group and 193 to the fetal intrauterine resuscitation group. The inclusion criteria were: term singleton pregnancy, in labor, cephalic presentation, and no placental accidents. RESULTS: The time between randomization and birth was 16.9 +/- 7.6 min (mean +/- SD) for the emergency delivery group, and 34.5 +/- 11.7 min (mean +/- SD) for the resuscitation group. The relative risk (RR) of acidosis in the umbilical artery (pH < 7.1) in the emergency delivery group was 1.47 (0.95-2.27). The RR of base deficit < or =12 mEq/L in the emergency delivery group was higher than in the resuscitation group (RR = 1.48 [1.0-2.2], P = 0.04). When considering the need for admission to the neonatal care unit, the relative risk was higher in the emergency delivery group than in the resuscitation group (RR = 2.14 [1.23.3.74], P = 0.005). No maternal adverse effects were reported. CONCLUSION: Tocolysis and delayed delivery renders better immediate neonatal results than emergency delivery when fetal distress is suspected because of a non-reassuring fetal heart pattern. In addition, it may decrease the need for emergency delivery without increasing maternal and fetal adverse side-effects.     

Efficacy of carotid collateral perfusion in anaesthetized sheep fetuses

The purpose of this study was to learn to what extent carotid collateral circulation is efficient in maintaining cephalic blood flow in the sheep fetus. Under halothane anaesthesia six fetal sheep at 124-135 days of gestation were instrumented with inflatable occluders around both common carotid arteries, an inductive flow probe around one external carotid artery, and arterial catheters to measure carotid sinus and aortic pressure. In acute experiments, the occluders were inflated on one side, or the other, or both sides simultaneously, while carotid blood flow, driving pressures and fetal heart rate were determined. Ipsi- and bilateral occlusion reduced carotid blood flow from about 42 ml/min to 10-0 ml/min and decreased sinus pressure from 39 mmHg to 29.1+/-2.9 (mean+/-s.d.) and 16.7+/-3.7 mmHg, respectively. Occlusion of the contralateral carotid artery increased ipsilateral carotid blood flow from 45+/-10 ml/min to 64+/-14 ml/min within 0.2 sec. Heart rate and aortic and sinus pressures did not change appreciably. Analysis of an analogue resistance network demonstrated that the observed carotid flow increases (less than twice normal) do not require changes of vascular resistances.It is concluded that the fetal sheep, as in the adult of many species, possesses an efficient carotid collateral system.     

Left ventricular isovolumic relaxation and renin-angiotensin system in the growth restricted fetus

OBJECTIVE: To determine left ventricular isovolumic relaxation time (LV IRT) in normally developing and growth restricted fetuses (FGR) as an indicator of fetal cardiac afterload and neonatal systolic blood pressure. STUDY DESIGN: A prospective longitudinal study in 124 normally developing and 47 growth restricted fetuses (FGR). LV IRT, fetal heart rate (FHR) and umbilical artery pulsatility index (PI) were determined at 2-3 week intervals starting at 22-26 weeks of gestation until delivery. Renin and angiotensin I levels were measured by radioimmunoassay in umbilical venous blood after delivery. Systolic blood pressure was measured at day 1 and day 5 of postnatal life. To evaluate the association between LV IRT, gestational age and FHR, bivariate regression analyses were performed. RESULTS: Mean LV IRT (62+/-8ms) was 29 percent longer in FGR as compared to the normal subset (47+/-6ms) at all gestational ages (p<0.001). Mean postnatal active plasma renin level (7.78+/-S.D. 1.03ng/ml) and postnatal angiotensin I level (4.21+/-0.70ng/ml) in the FGR subset were significantly higher (p<0.001) than in the normal subset (4.81+/-1.04ng/ml, renin and 2.69+/-0.44ng/ml, angiotensin I). There was a significant difference (p<0.01) in systolic blood pressure between the two subsets on postnatal day 1 (FGR 52+/-6mmHg vs. normal 46+/-4mmHg) and day 5 (FGR 76+/-5mmHg vs. normal 60+/-6mmHg). CONCLUSION: Left ventricular isovolumic relaxation time may act as a sensitive index of increased arterial afterload in the growth retarded fetus and may herald raised systolic blood pressure in the early neonatal period.     

Influence of gestational age and fetal heart rate on the fetal mechanical PR interval.

OBJECTIVE: The fetal mechanical PR interval obtained via pulsed Doppler has previously been demonstrated to correlate with electrocardiographic PR interval measured in the neonate. We sought to further analyze the influence of fetal heart rate and gestational age upon the fetal mechanical PR interval. METHODS: We searched our database for mechanical PR intervals, which were obtained during fetal echocardiography performed in our antenatal diagnostic unit. We included fetuses with a normal cardiac structural survey. The mechanical PR interval is measured from the A wave of the mitral valve to the beginning of ventricular systole corresponding to the opening of the aortic valve. Linear regression curves were generated to examine the correlation of mechanical PR interval with gestational age and fetal heart rate. Analysis of variance was used to compare the mean variation across three gestational age groups: 17-21.9 weeks (n = 24), 22-25.9 weeks (n = 52) and 26-38 weeks (n = 20). RESULTS: Mechanical PR intervals were measured in 96 fetuses with normal fetal echocardiography. The mechanical PR interval was 123.9 +/- 10.3 ms (mean +/- SD), with a range of 90-150 ms. Linear regression curves correlating mechanical PR interval with fetal heart rate and gestational age demonstrated a flat slope with R2 = 0.016, p = 0.22 and R2 = 0.0004, p = 0.85, respectively. The mechanical PR interval measured over the three gestational ages was as follows (mean +/- SD): 122.3 +/- 10.5 ms for 17-21.9 weeks; 125.0 +/- 9.6 ms for 22-25.9 weeks; and 123.1 +/- 11.9 ms for 26-38 weeks. Analysis of variance revealed no difference among the mechanical PR interval means measured over the three gestational age groups (p = 0.53). CONCLUSIONS: Fetal mechanical PR interval ranges from 90 to 150 ms in fetuses with sonographically normal fetal cardiac structure and rate. The mechanical PR interval appears to be independent of gestational age and fetal heart rate.     

Doppler ultrasound assessment of cerebral blood flow in the human fetus

A mechanical sector and linear array real-time scanner combined with a pulsed Doppler system was used for recording the flow velocity waveform in the internal carotid artery, the lower thoracic part of the descending aorta and umbilical artery in the human fetus. A total of 42 fetuses in normal pregnancy and nine growth-retarded fetuses between 26 and 41 weeks gestation was studied. In normal pregnancy the mean pulsatility index (PI) in the internal carotid artery varied between 1.5 and 1.6, in the descending aorta between 1.7 and 1.8 and in the umbilical artery between 0.7 and 1.3. In the growth-retarded fetuses the PI was reduced in the internal carotid artery and raised in the descending aorta and umbilical artery, suggesting an increased peripheral vascular resistance in the fetal body and placenta and a compensatory reduction in peripheral vascular resistance in the fetal cerebrum, i.e. a brain-sparing effect in the presence of fetal hypoxia.     

Role of adenosine in regulation of brain temperature in fetal sheep.

OBJECTIVE: The purpose of this study was to test adenosine's possible suppression of heat production by the ovine fetal brain during acute hypoxia. STUDY DESIGN: Hypoxia was induced by occluding the umbilical cord for 5 minutes in 8 fetal sheep with and without an adenosine receptor blocker, theophylline, and fetal brain and core temperatures were recorded. RESULTS: In 8 untreated fetuses, cord occlusion induced severe but reversible hypoxemia (decrease in carotid arterial PO (2) from 23 +/- 1 to 5 +/- 1 mm Hg (P <.01), a 2.3-fold increase in plasma adenosine, and an increase in body core temperature of 0.19 degrees C +/- 0.03 degrees C (P <.01), yet brain temperature remained constant. However, after cord occlusion with prior and continuing administration of theophylline, brain temperature did not increase as hypothesized but rather decreased, suggesting marked reductions in cerebral metabolic rate. This response occurred despite similar degrees of hypoxemia and similar increases in plasma adenosine and body core temperature. CONCLUSION: We conclude that the temperature of the fetal ovine brain remains constant or decreases during severe reversible hypoxemia by mechanisms other than those dependent on adenosine.     

Plasma endothelin-1 and atrial natriuretic peptide levels during prolonged (24-h) non-acidemic hypoxemia in fetal goats.

OBJECTIVE: The purpose of this study was to investigate the effects of prolonged (24-h) non-acidemic hypoxemia on plasma endothelin-1 and atrial natriuretic peptide (ANP) in fetal goats. METHODS: During continuous infusion of nitrogen into the maternal trachea, fetal plasma endothelin-1 and ANP levels were measured in nine chronically instrumented goat fetuses at 117-129 days' gestation. Endothelin-1 and ANP were measured by radioimmunoassay. RESULTS: Fetal arterial pO(2) decreased significantly from 23.1 +/- 1.0 mmHg (control) to 15.2 +/- 0.9 mmHg during the first 2 h of hypoxemia and to 15.7 +/- 1.1 mmHg at the end of the experimental period of hypoxemia. The plasma endothelin-1 concentration increased from 10.6 +/- 1.9 pg/ml to 20.4 +/- 4.3 pg/ml (p < 0.05) during the first 2 h and was 19.7 +/- 2.4 pg/ml (p < 0.01) at the end of the experimental period. The plasma ANP concentration also increased, from 20.3 +/- 5.5 pg/ml to 23.0 +/- 4.7 pg/ml in the first 2 h and then to 58.0 +/- 8.8 pg/ml (p < 0.05) at the end of the experimental period. There was a significant negative correlation between fetal plasma endothelin-1 and pO(2), but no significant correlation was found between fetal plasma ANP and pO(2). CONCLUSIONS: Prolonged non-acidemic hypoxemia induces a continuous increase in fetal plasma endothelin-1 and ANP levels. Fetal plasma ANP increases time-dependently but endothelin-1 remains constant during hypoxemia.     

窒息早产儿最大长度序列脑干听觉诱发电位的变化及意义

目的 研究围产期窒息缺氧对早产儿脑干听觉功能的影响,分析能够早期反映脑干听觉功能变化的敏感指标以及最大长度序列脑干听觉诱发电位(maximum length sequence brainstem auditory evoked potential,MLS BAEP)是否较常规法对脑干听觉功能异常的检出具有优越性. 方法窒息早产儿组:胎龄29～33<'+6>"周有围产期窒息缺氧病史的早产儿51例.对照组:正常早产儿47例,正常足月儿38例.MLS BAEP检测时间分别为生后3～7 d、纠正胎龄37～42周、3个月.常规法声刺激速率为21次/s,MLS声刺激速率为91、227和455次/s,采用t检验比较组间Ⅰ、Ⅲ、Ⅴ波潜伏期和振幅,Ⅰ-Ⅲ、Ⅲ-Ⅴ、Ⅰ-Ⅴ峰间期的差异. 结果生后3～7 d,窒息早产儿较正常早产儿Ⅲ波、Ⅴ波潜伏期,Ⅰ-Ⅲ、Ⅲ-Ⅴ和Ⅰ-Ⅴ峰问期延长,Ⅴ波振幅降低(P<0.05).声刺激速率为455次/s时,窒息早产儿组Ⅲ波潜伏期为(6.64±0.58)ms,V波潜伏期为(10.57±0.93)ms Ⅰ-Ⅲ峰间期为(3.69±0.55)ms,Ⅲ-Ⅴ峰间期为(3.93±0.53)ms,Ⅰ-Ⅴ峰间期为(7.60±0.73)ms,明显低于正常早产儿.纠正胎龄足月时窒息早产儿组Ⅰ-Ⅲ峰间期已恢复正常,但Ⅴ波潜伏期、Ⅲ-Ⅴ和Ⅰ-Ⅴ峰间期仍相对延长且Ⅴ波振幅减低(P<0.01).在纠正年龄3个月时窒息早产儿组常规BAEP与足月儿组的差异已不明显,仅在较高声刺激速率时仍有部分参数异常. 结论围产期窒息缺氧可以对早产儿BAEP造成影响,但随早产儿生长发育有一定程度恢复.脑干听觉通路的近中枢部位对缺氧损伤易感,波形变化出现早,恢复慢.Ⅴ波潜伏期和振幅、Ⅲ-Ⅴ和Ⅰ-Ⅴ峰间期可作为判断早产儿缺氧损伤的早期敏感指标.MLS BAEP通过提高声刺激速率,可以提高诊断价值.     

Swallowing, urine flow, and amniotic fluid volume responses to prolonged hypoxia in the ovine fetus

OBJECTIVE: Four days of hypoxia produce an extensive fetal polyuria with little change in amniotic fluid volume in the ovine fetus. We hypothesized that fetal swallowing and intramembranous absorption would increase with prolonged hypoxia to offset the polyuria. STUDY DESIGN: After a 24-hour normoxic period, nine ovine fetuses were subjected to 4 days of hypoxia induced by lowering maternal inspired oxygen content. Seven fetuses were monitored for 5 days as normoxic time controls. Measurements included fetal swallowed volume by a computerized system with Transonic flow probes, urine production by gravity drainage, and amniotic fluid volume by an indicator dilution technique. Data were averaged over 12-hour intervals, and a three-factor repeated-measures analysis of variance was used for statistical testing. RESULTS: During days 2 to 5, arterial oxygen tension was 20.7+/-1.1 (SE) mm Hg in the normoxic and 13.9+/-0.8 mm Hg in the hypoxic fetuses (P<.0001). Urine flow was unchanged over time in the normoxic fetuses and increased gradually from 693+/-88 to 2189+/-679 mL per day during hypoxia (P<.0001). The prehypoxia swallowed volume was similar in the two groups, averaging 447+/-95 mL per day. Although transiently decreased in eight of nine hypoxic fetuses, the 12-hour average swallowed volumes were not significantly different at any time in the hypoxic versus normoxic fetuses (P=.62). Amniotic fluid volume increased in the hypoxic fetuses relative to that in the normoxic fetuses (520+/-338 mL vs -226+/-136 mL, P<.01), although the increase was small (P<.01) relative to the excess volume of urine (4269+/-1306 mL). Estimated intramembranous absorption increased from 209+/-95 mL per day during normoxia to average 1032+/-396 mL per day during hypoxia. CONCLUSIONS: The current study supports the concept that prolonged hypoxia produces a progressive fetal polyuria with relatively small changes in amniotic fluid volume. Concomitantly, hypoxia does not induce prolonged changes in fetal swallowing; rather, intramembranous absorption greatly increases, thereby preventing severe polyhydramnios.