Need for placental and experimental pathologicexamination to determine pathogenetic influences of chronicallypresent intraamniotic meconium
1996; Elsevier BV; Volume: 174; Issue: 5 Linguagem: Inglês
10.1016/s0002-9378(96)70639-7
ISSN1097-6868
AutoresScott Hyde, Geoffrey Altshuler,
Tópico(s)Fetal and Pediatric Neurological Disorders
ResumoTo the Editors:We have hypothesized that after soluble meconium components diffuse to placental and umbilical vessels they produce fetal vasoactivity and hypoperfusion.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar Montgomery et al. retorted (Montgomery LD, Belfort MA, Saade GR, Moise KJ Jr, Vedernikov YP. Meconium inhibits the contraction of umbilical vessels induced by the thromboxane A2 analog U46619. AM J OBSTET GYNECOL 1995;173:1075-8). They performed experiments to investigate our findings but used radically different methods. Their discussion did not mention a highly relevant article of 1991.2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google Scholar With experimental findings similar to ours, Sepulveda et al. explained the risk of stillbirth complicating maternal cholestatic disease of pregnancy. They wrote, “This is the first report that provides experimental evidence of the possible role of bile acids in those mechanisms that trigger fetal asphyxia in pregnancies complicated by intrahepatic cholestasis of pregnancy.”2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google ScholarOur methods included placement of umbilical cord venous segments in 37° C Krebs solution transport media controlled for temperature, pH, and 95% oxygen and 5% carbon dioxide.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar To avoid influences induced by labor and delivery, we used tissue from umbilical cords of mothers delivered by scheduled repeat cesarean section. These considerations enabled accurate investigation of intrinsic vasocontractility and of effects induced by fresh 1% meconium solution.Montgomery et al. used umbilical cords obtained after vaginal delivery or cesarean section done because of prolonged labor. That would have altered intrinsic properties of the vessels, as would have their subsequent immersion of vascular segments in cold Krebs solution. They later used the thromboxane A2 analog U46619 as a terminal vasoconstrictor. This agent exerts its effect on smooth muscle through a cell surface receptor. Because meconium contains bile, a powerful detergent, exposure of biologic membranes to meconium disrupts the biologic activity of membrane-bound hormone receptors. We therefore understand why Montgomery et al. observed inhibition of vasoactivity by 1% meconium, even after the meconium had been washed out of the organ bath.Because only a minority of fetuses are exposed to intraamniotic meconium for many hours or days, fetal meconium discharge usually is not complicated by a detrimental outcome. Placental findings can identify chronic exposure, the most severe manifestation of which is meconium-induced vascular necrosis. Those cases have the highest risk of cerebral palsy and other disorders. Naeye has recently endorsed this consideration.3Naeye RL Can meconium in the amniotic fluid injure the fetal brain?.Obstet Gynecol. 1995; 86: 720-724Crossref PubMed Scopus (39) Google ScholarFurther investigations should resolve whether fetal vasoactivity and hypoperfusion are important pathophysiologic mechanisms and whether diffusible meconium components enter the fetal circulation and directly inflict cellular damage in vital organs.6/8/72214 To the Editors:We have hypothesized that after soluble meconium components diffuse to placental and umbilical vessels they produce fetal vasoactivity and hypoperfusion.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar Montgomery et al. retorted (Montgomery LD, Belfort MA, Saade GR, Moise KJ Jr, Vedernikov YP. Meconium inhibits the contraction of umbilical vessels induced by the thromboxane A2 analog U46619. AM J OBSTET GYNECOL 1995;173:1075-8). They performed experiments to investigate our findings but used radically different methods. Their discussion did not mention a highly relevant article of 1991.2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google Scholar With experimental findings similar to ours, Sepulveda et al. explained the risk of stillbirth complicating maternal cholestatic disease of pregnancy. They wrote, “This is the first report that provides experimental evidence of the possible role of bile acids in those mechanisms that trigger fetal asphyxia in pregnancies complicated by intrahepatic cholestasis of pregnancy.”2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google ScholarOur methods included placement of umbilical cord venous segments in 37° C Krebs solution transport media controlled for temperature, pH, and 95% oxygen and 5% carbon dioxide.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar To avoid influences induced by labor and delivery, we used tissue from umbilical cords of mothers delivered by scheduled repeat cesarean section. These considerations enabled accurate investigation of intrinsic vasocontractility and of effects induced by fresh 1% meconium solution.Montgomery et al. used umbilical cords obtained after vaginal delivery or cesarean section done because of prolonged labor. That would have altered intrinsic properties of the vessels, as would have their subsequent immersion of vascular segments in cold Krebs solution. They later used the thromboxane A2 analog U46619 as a terminal vasoconstrictor. This agent exerts its effect on smooth muscle through a cell surface receptor. Because meconium contains bile, a powerful detergent, exposure of biologic membranes to meconium disrupts the biologic activity of membrane-bound hormone receptors. We therefore understand why Montgomery et al. observed inhibition of vasoactivity by 1% meconium, even after the meconium had been washed out of the organ bath.Because only a minority of fetuses are exposed to intraamniotic meconium for many hours or days, fetal meconium discharge usually is not complicated by a detrimental outcome. Placental findings can identify chronic exposure, the most severe manifestation of which is meconium-induced vascular necrosis. Those cases have the highest risk of cerebral palsy and other disorders. Naeye has recently endorsed this consideration.3Naeye RL Can meconium in the amniotic fluid injure the fetal brain?.Obstet Gynecol. 1995; 86: 720-724Crossref PubMed Scopus (39) Google ScholarFurther investigations should resolve whether fetal vasoactivity and hypoperfusion are important pathophysiologic mechanisms and whether diffusible meconium components enter the fetal circulation and directly inflict cellular damage in vital organs. We have hypothesized that after soluble meconium components diffuse to placental and umbilical vessels they produce fetal vasoactivity and hypoperfusion.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar Montgomery et al. retorted (Montgomery LD, Belfort MA, Saade GR, Moise KJ Jr, Vedernikov YP. Meconium inhibits the contraction of umbilical vessels induced by the thromboxane A2 analog U46619. AM J OBSTET GYNECOL 1995;173:1075-8). They performed experiments to investigate our findings but used radically different methods. Their discussion did not mention a highly relevant article of 1991.2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google Scholar With experimental findings similar to ours, Sepulveda et al. explained the risk of stillbirth complicating maternal cholestatic disease of pregnancy. They wrote, “This is the first report that provides experimental evidence of the possible role of bile acids in those mechanisms that trigger fetal asphyxia in pregnancies complicated by intrahepatic cholestasis of pregnancy.”2Sepulveda WH Gonzalez C Cruz MA Rudolph MI Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.Eur J Obstet Gynecol Reprod Biol. 1991; 42: 211-215Abstract Full Text PDF PubMed Scopus (159) Google Scholar Our methods included placement of umbilical cord venous segments in 37° C Krebs solution transport media controlled for temperature, pH, and 95% oxygen and 5% carbon dioxide.1Altshuler G Hyde S Meconium-induced vasocontraction: a potential cause of cerebral and other fetal hypoperfusion and of poor pregnancy outcome.J Child Neurol. 1989; 4: 137-142Crossref PubMed Scopus (126) Google Scholar To avoid influences induced by labor and delivery, we used tissue from umbilical cords of mothers delivered by scheduled repeat cesarean section. These considerations enabled accurate investigation of intrinsic vasocontractility and of effects induced by fresh 1% meconium solution. Montgomery et al. used umbilical cords obtained after vaginal delivery or cesarean section done because of prolonged labor. That would have altered intrinsic properties of the vessels, as would have their subsequent immersion of vascular segments in cold Krebs solution. They later used the thromboxane A2 analog U46619 as a terminal vasoconstrictor. This agent exerts its effect on smooth muscle through a cell surface receptor. Because meconium contains bile, a powerful detergent, exposure of biologic membranes to meconium disrupts the biologic activity of membrane-bound hormone receptors. We therefore understand why Montgomery et al. observed inhibition of vasoactivity by 1% meconium, even after the meconium had been washed out of the organ bath. Because only a minority of fetuses are exposed to intraamniotic meconium for many hours or days, fetal meconium discharge usually is not complicated by a detrimental outcome. Placental findings can identify chronic exposure, the most severe manifestation of which is meconium-induced vascular necrosis. Those cases have the highest risk of cerebral palsy and other disorders. Naeye has recently endorsed this consideration.3Naeye RL Can meconium in the amniotic fluid injure the fetal brain?.Obstet Gynecol. 1995; 86: 720-724Crossref PubMed Scopus (39) Google Scholar Further investigations should resolve whether fetal vasoactivity and hypoperfusion are important pathophysiologic mechanisms and whether diffusible meconium components enter the fetal circulation and directly inflict cellular damage in vital organs. 6/8/72214
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