Fetal Swallowing Research Articles

Prognostic significance of the pouch sign in fetuses with prenatally diagnosed esophageal atresia

Objective: Esophageal atresia may be diagnosed prenatally by ultrasonographic visualization of the blind-ending esophagus during fetal swallowing, which is referred to as the pouch sign. Our purpose was to determine whether this sign can be used to predict outcomes of affected fetuses. Study Design: Four cases of esophageal atresia diagnosed in our center during the past 2 years were analyzed, in conjunction with 3 cases from published series. Ultrasonographic features of the pouch sign were categorized according to localization. Results: In the neck pouch group (n = 3) 1 fetus died in utero and 1 died before a corrective operation could be undertaken. In the only fetus of this group to survive a staged repair was necessary because of a long atretic gap. Conversely, 3 of the 4 fetuses with a mediastinal pouch survived after a successful corrective operation, and primary repair was possible in all cases. Conclusions: The base of the proximal blind-ending esophagus can be clearly localized by means of ultrasonography. Our data suggest that a neck pouch may be associated with an adverse outcome. This information may be useful in counseling parents when esophageal atresia is diagnosed prenatally. (Am J Obstet Gynecol 2000;182:978-81.)

Nitric oxide modulates angiotensin II-induced drinking behavior in the near-term ovine fetus

Objective:Human and ovine fetuses demonstrate an enhanced rate of spontaneous and angiotensin II-stimulated swallowing. Angiotensin II and nitric oxide synthase have been localized to thirst centers in the brain. This study was performed to determine whether central nitric oxide contributes to the regulation of angiotensin II-induced fetal swallowing. Study Design:Six pregnant ewes with near-term singleton fetuses were chronically prepared with fetal vascular and lateral ventricle catheters and electrocorticogram and esophageal electromyogram electrodes. After a 2-hour control period, fetuses were administered serial lateral ventricle injections (1 mL) of angiotensin II (32 pg; time, 2 hours) and Nta-nitro-L-arginine methyl ester (3 mg; time, 3 hours) and a repeat angiotensin II injection (3.2 Wg; time, 5 hours). All fetuses received an additional control study of lateral ventricle injections of artificial cerebrospinal fluid on a previous day. Results:Angiotensin II injection significantly increased meant SEM fetal swallowing (0.9:t 0.1 to 2.7:t 0.4 swallows/min). Nω-nitro-l-arginine methyl ester significantly decreased fetal swallowing to below the basal rate (0.4 ± 0.1 swaliowstmin), and swallowing did not increase with the second angiotensin II dose (in the presence of nitric oxide blockade). Conclusions:These results demonstrate that inhibition of central nitric oxide suppresses fetal swallowing behavior in response to central angiotensin II. We speculate that tonic nitric oxide facilitates angiotensin II swallowing stimulation by maintenance of glutamate activation of hypothalamic AI-methyl-D-aspartate receptors.

Nitric oxide modulates spontaneous swallowing behavior in near-term ovine fetus.

Human and ovine fetuses demonstrate an enhanced rate of swallowing, an activity critical for amniotic fluid regulation. Fetal swallowing may be modulated by both systemic and central factors. Nitric oxide (NO) is a central neuromodulator that has been localized to brain regions regulating thirst and swallowing. We sought to determine if NO contributes to the regulation of spontaneous ovine fetal swallowing. Six time-dated pregnant ewes with singleton fetuses (129 +/- 1 day) were chronically prepared with fetal vascular and lateral ventricle catheters and electrocorticogram (ECoG) and esophageal electromyogram electrodes. After a 2-h control period, fetuses were given lateral ventricle injection of NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME) and monitored for 2 h. NO precursor L-arginine was then injected into the lateral ventricle, and fetuses were monitored for a final 2 h. All fetuses received an additional control study of fetal swallowing before and after lateral ventricle injection of artificial cerebrospinal fluid (aCSF). Data were analyzed with repeated-measures ANOVA and paired t-test (P < 0.05). Suppression of a central NO with central L-NAME significantly reduced mean (+/-SE) spontaneous fetal swallowing (1.2 +/- 0.1-0.6 +/- 0.1 swallows/min low-voltage ECoG; P < 0.01). Restoration of central NO by L-arginine significantly increased fetal swallowing to pre-L-NAME levels (1.2 +/- 0.1 swallows/min low voltage). There were no changes in fetal swallowing during the control study of aCSF. Fetal ECoG activity and blood pressure did not change during the study or control aCSF injection. We conclude that NO is an important neuromodulator of fetal swallowing activity. Central NO synthase activity may contribute to the heightened level of spontaneous fetal swallowing and thus amniotic fluid regulation.

Fetal distress does not affect in utero defecation but does impair the clearance of amniotic fluid

Purpose: An experimental study was performed to evaluate the effect of fetal distress on in utero defecation and clearance of amniotic fluid (AF). Methods: Sixteen pregnant New Zealand white rabbits underwent laparotomy at 25 days' gestation (full term, 31 to 32 days) as group A (n = 8) and B (n = 8). Uteroplacental ischemia was achieved by constriction of the aorta below the renal arteries to cause fetal distress in group B, whereas sham operation was done in group A. In both groups, 0.1 mL of technetium-99m ( 99mTc)-HIDA containing 1 mCi of radioactivity was injected into the gluteus muscle of each fetus, which had been exposed through the uterus. Beginning 2 hours after injection, a live fetus was killed every 2 hours for 48 hours in both groups. Tissue samples from the reference organs (lung, heart, stomach, kidney, bladder) and liver, meconium in proximal, mid and distal bowels, AF, and maternal blood were taken. The radioactivity of each sample was determined by a gamma counter and the percentage injected dose (uptake) per gram of tissue (%ID/g) was calculated. The total uptake and mean transit time (MTT) showing intestinal transport were calculated using the linear trapezoidal approximation and extrapolation. The peak concentration (C max, %ID/g) and time corresponding to the peak (t max, h) were obtained. Results: (1) Significant difference was noted between the groups with regard to uteroplacental perfusion pressure and blood pH (51.0 ± 2.6 mm Hg; pH, 6.9 ± 0.1 in group B; 80.1 ± 2.7 mm Hg, pH, 7.3 ± 0.1 in group A; P < .05). (2) 99mTc-HIDA was predominantly trapped by the liver and excreted into the gastrointestinal tract and AF in both groups. (3) In liver and bowel, shape of the profile was bimodal because of fetal swallowing and similar in both groups, t max was the same in both groups, C max was lower in group B than in group A, the total uptake was smaller in group B than in group A, and intestinal transport time was similar (44.2 hours in group A and 43.0 hours in group B). In amniotic fluid, shape of the profile was sigmoidal in group B and reached a C max value of 11.6% ID/g, whereas unimodal profiles were observed in group A with a C max value of 12.6% ID/g; radioactivity was eliminated from the AF with a rate constant of 0.48% ID/g h in group A (AUC, 273% ID/g h); whereas accumulation of radioactivity was noted in group B (AUC, 308% ID/g h). (5) In maternal blood, shape of the profile was sigmoidal in group A with a C max value of 2.9% ID/g and unimodal in group B (C max, 1.6% ID/g), accumulation of radioactivity was noted in group A (AUC, 93% ID/g h), whereas a rapid decline of radioactivity (k, 0.06% ID/g h) was noted in group B (AUC, 47% ID/g h). Conclusions: Fetal distress did not affect the intestinal transport dynamics and in utero defecation but impaired the clearance of AF and the passage into the maternal circulation, which was shown by the accumulation of radioactivity in AF only in group B and in maternal blood only in group A without any elimination rate. This finding suggests that meconium-stained AF is not related to meconium passage after fetal distress; rather, it reflects impaired clearance of AF, which already has containing meconium caused by physiological in utero defecation.

Brain and cranial disruption sequence from amniotic bands: a result of traction from fetal and embryonic swallowing of attached bands

Ultrasonographic evaluation of a 16 week fetus referred for elevated MSAFP revealed multiple amniotic bands; the right digits were tethered to a ball of umbilical cord, in turn attached by a long band to the fetal surface of the amnion. Severe hydrocephaly was present, remarkable this early in gestation. The appearance of the choroid plexes was highly unusual, as if compressed focally, with a “butterfly” appearance in the coronal plane. A disruptive cleft extended from the right orbit through the right lateral maxilla and upper lip. Because of the poor prognosis, the patient elected to terminate the pregnancy. Chromosomal analysis revealed a normal karyotype. 3 dimensional computed tomography of the fetus skull revealed irregular synostosis of the right lambdoidal and right coronal sutures, with abnormal widening of the contralateral sutures. The fetal skin over the cranium was remarkable for the presence of three skin tags. The terminal phalanges of the right hand were disrupted by the band, which attached to the cord and amnion. Fetal surgery has demonstrated how the skin can regenerate without scarring. The cranial skin showed no evidence of scarring, but what most likely happened is that the fetus swallowed the bands attached at the 3 points on the cranium marked by the skin tags, and traction caused the bands to slice down through the cranium and brain structures, disrupting the choroid, brain anatomy, and causing the asymmetric craniostenosis and facial cleft. The skin over the cranium then healed over the defect without scarring. Also presented is a neonate with focal disruption of the toes, most likely caused by a band originally attached to the lateral surface of that foot's heel, leaving only a large skin tag as evidence of the original attachment. Other fetuses are shown with an amniotic band swallowed. The caveat: whenever amniotic bands are seen, meticulous evaluation of brain structures is warranted, and asymmetry of the choroid could be an ominous sign of more severe disruption.

Maternal plasma hypo-osmolality: Effects on spontaneous and stimulated ovine fetal swallowing

Fetal swallowing is a major route of amniotic fluid resorption, and thus swallowing activity may alter amniotic fluid volume. Near-term ovine fetal swallowing increases in response to plasma and/or cerebrospinal fluid hypertonicity. As maternal hydration status alters amniotic fluid volume, we hypothesized that maternal plasma hypotonicity may alter fetal swallowing activity. Pregnant ewes (130 +/- 1 d; n = 6) were chronically prepared with maternal and fetal vascular catheters, a fetal esophageal flow probe, and fetal thyrohyoid and nuchal and thoracic esophagus electromyogram electrodes. Spontaneous fetal swallowing and hypertonic saline thresholds for stimulated swallowing were determined prior to and following maternal hypotonicity induced with water loading and intravenous DDAVP (arginine vasopressin V2 agonist). Fetal swallowing thresholds were determined with intracarotid injections (0.15 ml/kg) of increasing sodium chloride concentrations (0.15-1.2 M) at 2-min intervals. Maternal DDAVP infusion significantly decreased mean (+/-SEM) maternal and fetal plasma osmolalities (298 +/- 2-284 +/- 3; 295 +/- 2-278 +/- 3 mOsm/kg, respectively) and sodium concentrations (147.3 +/- 0.4-137.5 +/- 0.9; 142.7 +/- 0.8-133.5 +/- 1.0 mEq/l, respectively), suppressed spontaneous swallowing activity and volume (1.1 +/- 0.2-0.6 +/- 0.1 swallows/min; 0.7 +/- 0.2-0.5 +/- 0.1 ml/min, respectively) and significantly increased the osmotic threshold for swallowing stimulation (0.77 +/- 0.08-1.03 +/- 0.09 M NaCl). We conclude that: (1) maternal, and thus fetal, plasma hypotonicity results in suppression of spontaneous fetal swallowing activity and a decrease in volume swallowed, suggesting that spontaneous fetal ingestive behavior results, in part, from tonic dipsogenic stimulation, and (2) under hypotonic conditions, the intracarotid NaCl injection concentration for swallowing stimulation increases. These results suggest that the reset (lower) maternal plasma osmolality during human pregnancy may serve to minimize fetal ingestive and perhaps arginine vasopressin-mediated antidiuretic responses to acute maternal hypertonicity.

Maternal plasma hypo‐osmolality: Effects on spontaneous and stimulated ovine fetal swallowing

Maternal plasma hypo‐osmolality: Effects on spontaneous and stimulated ovine fetal swallowing

Fetal swallowing of IgE

Allergic disease is more frequently manifest by the offspring of atopic mothers than atopic fathers. Furthermore, newborn umbilical-cord blood mononuclear cells exhibit allergenspecific proliferation predicting subsequent allergic disease. Thus, intrauterine exposure to allergen and the development of immunological memory must occur in the fetus and be influenced by maternal health and environment. The key question is how does fetal-allergen exposure and sensitisation occur? Because increased IgE is a hallmark of allergy and can mediate allergen uptake via IgE receptor-mediated antigen focusing, we evaluated whether the fetus was exposed to IgE during life in utero. Matched samples of maternal blood and amniotic fluid were collected from women undergoing elective caesarean section at term ( 37 weeks of gestation), with maternal blood contamination of amniotic fluid determined by measuring IgA (in-house IgA-specific ELISA) and any sample containing above 2 g/mL IgA was excluded from the study; and also from women having amniocentesis at approximately 16 weeks of pregnancy with only samples from women who proceeded with the pregnancy included in this study. All samples were collected with the approval of the Joint Ethics Committee of Southampton University Hospitals and the consent of the mothers. Total IgE was measured in maternal plasma and in amniotic fluid with Magic Lite SQ Total IgE Extended Range and Total IgE High Sensitivity (ALK, Denmark) according to the manufacturer’s instructions. Non-parametric methods (Spearman’s correlation; SPSS 7.0) and linear regression (ANOVA; SPSS 7.0) were used for analysis. IgE was detectable in 23/23 of term amniotic fluid samples (median 0·547 IU/mL; range 0·155–2·862 IU/mL). A statistically significant correlation was found between maternal total IgE and that of amniotic fluid at both 16 weeks of pregnancy and at term (figure). Where does amniotic fluid IgE come from? Because the fetus is capable of producing IgE from 11 weeks of gestation, fetal production may account for at least some amniotic fluid IgE. However, the increasing amount of amniotic fluid IgE as maternal plasma concentrations increase, suggests that maternal IgE may pass into the amniotic fluid or that factors mediating increased maternal production of IgE similarly influence fetal production. We favour the former and, as IgE does not cross the human placenta, postulate that maternal IgE traverses the fetal membranes, a hypothesis currently under investigation. 70% of amniotic-fluid protein is turned over daily with most of this removal via fetal swallowing, since the fetus also aspirates amniotic fluid, the gastointestinal and respiratory tracts, in addition to the skin, are exposed to molecules in amniotic fluid. Whether allergen is also present and IgE receptors are expressed by cells within these tissues thereby allowing antigen focusing to occur is an ongoing study. We postulate that amnion transmission of IgE has evolved as a mechanism for sensitising and thereby protecting the fetus from parasites infesting the mother, as exposure of the newborn to these same parasites is inevitable. Filarial specific IgE was detected in the cord blood of 33/57 infants born in Madras, India, where there is a high prevalence of filariasis. Furthermore, a study in Thailand revealed that although infants at 6 months of age are infested with parasites they do not have the same parasite as their mother. This protective pathway may now be usurped for sensitisation to allergens and we hypothesise this pathway of allergen exposure as an alternative to transplacental transfer of allergen. Further elaboration of this mechanism will provide new therapeutic targets which we anticipate will reduce the current dramatically increasing prevalence of allergic diseases.

Development of ingestive behavior

Swallowing represents a primary physiological function that provides for the ingestion of food and fluid. In precocial species, swallowing activity likely develops in utero to provide for a functional system during the neonatal period. The chronically instrumented ovine fetal preparation has provided the opportunity for recent advances in understanding the regulation of in utero swallowing activity. The near-term ovine fetus swallows fluid volumes (100-300 ml/kg) that are markedly greater, per body weight, than that of the adult (40-60 ml/kg). Spontaneous in utero swallowing and ingestive behavior contribute importantly to the regulation of amniotic fluid volume and composition, the acquisition and potential recirculation of solutes from the fetal environment, and the maturation of the fetal gastrointestinal tract. Fetal swallowing activity is influenced by fetal maturation, neurobehavioral state alterations, and the volume of amniotic fluid. Furthermore, intact dipsogenic mechanisms (osmolality, angiotensin II) have been demonstrated in the near-term ovine fetus. It remains unknown to what degree, if any, fetal swallowing may be influenced by nutrient appetite, salt appetite, or taste. Nevertheless, the development of dipsogenic and additional regulatory mechanisms for ingestive behavior occurs during fetal life and may be susceptible to changes in the pregnancy environment. This review describes what is currently known regarding the in utero development of ingestive behavior and the importance of this activity for fetal and perhaps ultimately adult fluid homeostasis.

Does gut atresia cause polyhydramnios?

Fetal gut atresia is variably associated with polyhydramnios. In order to determine which pregnancies will develop polyhydramnios, the case notes of 80 babies with gut atresia and stenosis were reviewed. Maternal polyhydramnios developed in all cases of pure oesophageal atresia (n = 8), all cases of Type III duodenal atresia (DA) with a non-bifid bile duct (n = 8), 80% of cases with type I DA (n = 10), and 24% of atresias of the small intestine (n = 34). Polyhydramnios did not develop in any case where there was not total obstruction except in 1 baby with DA and a bifid bile duct (BBD). These included stenosis of the oesophagus and duodenum (n = 17) and DA type III with a BBD (n = 3). These results support the role of fetal swallowing and fluid absorption by the fetal gastro-intestinal tract in the regulation of amniotic fluid volume.

Human amniotic fluid mathematical model: Determination and effect of intramembranous sodium flux

Objective: A recently described mathematical model of human amniotic fluid dynamics used known and estimated rates of fetal fluid production (lung liquid and urine) and composition (osmolality) to enable calculation of previously unmeasured routes of amniotic fluid resorption, including fetal swallowing and intramembranous (across the amnion) water flow. This "osmolar" model assumed that only free water resorption occurred across the intramembranous route. We hypothesized that intramembranous flow also may include solutes and electrolytes because significant concentration gradients exist between amniotic fluid and fetal plasma. We used mass balance analysis to determine the direction and magnitude of intramembranous sodium flux and to assess the ability of a newly described "sodium" model to predict changes in amniotic fluid volume in response to changes in intramembranous electrolyte flow. Mathematical modeling was used to predict changes in amniotic fluid volume in response to changes in intramembranous electrolyte flow. Study Design: Model predictions were calculated using published values for human amniotic fluid and fetal urine composition and volume. Ovine studies were used to derive lung fluid volumes and composition. Fetal swallowing and intramembranous flow were independently determined using net amniotic fluid osmolar (osmolality model) and sodium (sodium model) balance. Differences between osmolality and sodium model predictions were normalized to calculate the net intramembranous sodium flux, assuming a net balance of intramembranous osmotic solute flow. Results: Both sodium and osmolality models predicted swallowed volume to be greater than intramembranous flow until 28 to 32 weeks' gestation, after which the relationship reversed. However, the sodium model predicted greater intramembranous flow and lower swallowing rates compared with the osmolality model at all gestational ages. Osmolar mass balance required daily intramembranous sodium flux into the amniotic fluid, which increased with gestational age. Furthermore, assuming stable swallowing and intramembranous water flow, the model predicts that 5% increases or decreases in amniotic fluid solute concentrations caused by intramembranous flux result in polyhydramnios or oligohydramnios, respectively. Conclusion: Sodium and osmolality models demonstrate similarities in determinations of amniotic fluid dynamics. However, mass balance equations demonstrate a net intramembranous flow of sodium into the amniotic fluid under normal conditions. Mathematical modeling suggests that small alterations in daily intramembranous sodium flux may evoke large changes in amniotic fluid volume. (Am J Obstet Gynecol 1998;178:484-90.)

Maternal Plasma Hypo-Osmolality: Effects on Spontaneous and Stimulated Ovine Fetal Swallowing

Maternal Plasma Hypo-Osmolality: Effects on Spontaneous and Stimulated Ovine Fetal Swallowing

Anticholinergic suppression of ovine fetal swallowing activity

Objective: Fetal swallowing contributes importantly to amniotic fluid volume regulation as the primary route of fluid resorption, reaching 500 to 1000 ml/day near term. Near-term ovine fetal swallowing activity occurs predominantly during low-voltage electrocortical activity. In view of the potential to pharmacologically alter electrocortical activity, we hypothesized that fetal administration of a centrally acting cholinergic antagonist may be used to modulate fetal swallowing activity. To explore cholinergic modulation of swallowing activity, we examined fetal swallowing and electrocortical activity in response to central and peripheral cholinergic suppression by atropine sulfate. Study Design: Singleton ovine fetuses ( n = 6) were chronically prepared with vascular catheters and thyrohyoid, nuchal, and thoracic esophageal electromyogram and biparietal electrocortical electrodes. Swallowing and electrocortical activity were monitored for 2 hours before and after intravenous injection (1 ml of 0.15 mol/L sodium chloride) of atropine sulfate (1 mg/kg). On a subsequent day an identical study was performed with use off atropine methyl nitrate (3 mg/kg), an atropine analog that does not cross the blood-brain barrier. Results: Atropine sulfate decreased low-voltage electrocortical activity (56% ± 5% to 14% ± 4%), increased high-voltage electrocortical activity (40% ± 5% to 81% ± 5%), and did not change intermediate electrocortical activity (4% ± 1% to 5% ± 1%). Fetal swallowing activity decreased from 46 ± 12 to 12 ± 2 swallows per hour after atropine sulfate administration. Atropine methyl nitrate had no discernible effect on either fetal electrocortical or swallowing activity. Fetal arterial pressure, plasma osmolality, pH, Pco 2, and Po 2 did not change. Conclusions: Central cholinergic antagonism suppresses low-voltage fetal electrocortical and swallowing activity in the ovine fetus. Studies exploring spontaneous or induced fetal swallowing should consider the behavioral state of the fetus when conclusions are drawn about changes in the swallowing activity.

Fetal Swallowing: Relation to Amniotic Fluid Regulation

In summary, fetal swallowing activity contributes importantly to fetal and amniotic fluid homeostasis, and fetal somatic and gastrointestinal development. Human and ovine fetal swallowing increases throughout gestational with fetal swallowed volumes markedly greater (relative to body weight) than adults. Although the regulation of swallowing activity in early gestation is unknown, intact central and systemic dipsogenic mechanisms have been shown during the last third of ovine gestation. Recent studies suggest that swallowing behavior may be modulated in accordance with neurobehavioral state changes and influenced by hypoxia, hypotension and plasma osmolality changes. Whether fetal swallowing also is regulated by the development of "hunger" sensation, salt appetite, or the development of taste is uncertain. Nevertheless, it is likely that, for species in which swallowing behavior develops in utero, there are potentially dramatic influences of the maternal-fetal pregnancy environment on the imprinting of regulatory mechanisms controlling ingestive behavior. Ultimately, the regulation of fetal swallowing may aid in the prevention and/or therapy of human amniotic fluid disorders.

Epignatic Tumtor With Intracereral Extension

Epignatic teratoma with intracerebral extension is a very rare entity, and the prognosis is always grim, with death occurring within the first month of life. Generally, the pregnancy is complicated by a rapid onset of polyhydramnions, which prompts prenatal ultrasound examination. The size of the teratoma interferes with normal fetal swallowing of amniotic fluid, which causes the onset of polyhydramnios. Prenatal ultrasound helps with the assessment of oropharangeal involvement, which can optimize care plans in the postnatal period.

Importance of milk and diet on the ontogeny and adaptation of the intestine.

Importance of milk and diet on the ontogeny and adaptation of the intestine.

Materno‐Fetal Transmission of Human Immune Deficiency Virus

Mother-to-child transmission of human immune deficiency virus (HIV) is a multifactorial event highly associated with advanced maternal HIV disease and obstetric incidents taking place during parturition. Thus, various approaches to prevention may be beneficial. Although the time and the route of materno-fetal HIV transmission are still not sufficiently clear, much speaks in favor of a late HIV transmission, most probably taking place during parturition or the phase before the delivery. The fetus is remarkably protected by the placenta and the intact fetal membranes against many viral infections during gestation. These conditions change at parturition and the chance for a transition of HIV-infected carrier cells or virus into the fetal compartment increases. Proinflammatory cytokines secreted at the materno-fetal interface accumulate in amniotic fluid and may chemoattract and stimulate potentially HIV-infected immunocytes. After rupture of membranes, maternal cells of the decidua are directly exposed to the amniotic fluid. Aside from the contamination of the fetal skin at vaginal delivery as a debatable route of infection, blood-to-blood contacts and the fetal swallowing of contaminated amniotic fluid may be the major path of fetal HIV infection. For the fetal prophylaxis of an intrauterine infection, the application of zidovudine is recommended. However, cesarian section before the onset of labor leads also to a diminution of the transmission rate. As the transmission seems to have both systemic and local causes, it makes sense to combine different intervention strategies. Whether a combination of zidovudine and elective cesarean section can lower the transmission risk further has to be evaluated.

Ovine Fetal Laryngeal Chemoreflex Thresholds and Respiratory Effects

In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome.

Ovine fetal laryngeal chemoreflex thresholds and respiratory effects

In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 ± 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38° C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 ± 0.02 vs. 0.70 ± 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 ± 0.01 mol/L. During the control period, respiratory activity averaged 14.6 ± 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 ± 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 ± 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome. (Otolaryngol Head Neck Surg 1997;116:91-6.)

Ovine fetal swallowing following systemic atropine

Ovine fetal swallowing following systemic atropine