morphine and Necrosis

Topics: Birth Weight; Contrast Media; Enterocolitis, Pseudomembranous; Female; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature, Diseases; Intestinal Mucosa; Intestinal Perforation; Intestines; Male; Meconium; Necrosis; Pneumatosis Cystoides Intestinalis; Pneumoperitoneum; Radiography

Zinc coproporphyrin I (ZnCP-I) is a photosensitive molecule and a major component of meconium. Here, we examined the effects of ZnCP-I as a potential photosensitizer in photodynamic therapy for tumors.. (1) Aqueous ZnCP-I was irradiated with a pulsed YAG-SHG laser (wavelength: 532 nm)/YAG-SHG dye laser (wavelength: 566 nm). (2) HeLa cells were incubated in 200 mM ZnCP-I, and accumulation of ZnCP-I in HeLa cells was evaluated with ZnCP-I-specific fluorescence over 500 nm. (3) Aqueous ZnCP-I was administered intravenously to HeLa tumor-bearing mice at a dose of 10.2 mg/kg body weight. The tumors were irradiated with a filtered halogen lamp (wavelength: 580 nm) at 100 J/cm(2) 20 min after administration.. (1) An intense near-infrared emission spectrum was observed at around 1,270 nm after irradiation. The emission intensity was proportional to the laser power between 10 and 80 mW and was completely inhibited by addition of NaN3, a singlet oxygen scavenger. (2) ZnCP-I-specific fluorescence was detected in the HeLa cell cytoplasm. (3) Irradiated tumors treated with ZnCP-I were mostly necrotized.. ZnCP-I accumulated in tumor cells, produced singlet oxygen upon irradiation, and necrotized the tumor cells. These results suggest that ZnCP-I may be an effective photosensitizer.

Topics: Animals; Antineoplastic Agents; Biological Transport; Coproporphyrins; Female; Free Radical Scavengers; HeLa Cells; Humans; Lasers, Dye; Lasers, Solid-State; Meconium; Mice; Mice, Inbred BALB C; Mice, Nude; Necrosis; Neoplasms; Oxidants; Photochemotherapy; Photosensitizing Agents; Singlet Oxygen; Xenograft Model Antitumor Assays; Zinc

Meconium-associated vascular necrosis (MAVN) is a histological abnormality of human placental chorionic vessels that is associated with poor neonatal outcome. We tested the hypothesis that MAVN shows apoptosis in the walls of chorionic vessels. Archival placental specimens with MAVN (n = 5) were compared with specimens from uncomplicated pregnancies at term (n = 5) and from placentas with intense chorionic vasculitis associated with acute chorioamnionitis with (n = 5) or without (n = 5) a clinical history of meconium in the amniotic fluid. Sections from all placentas were processed by the TUNEL method, and 2 observers who were blinded to specimen diagnosis quantified the immunofluorescent TUNEL staining in both the amnion-facing and villous-facing walls of the larger chorionic vessels in each specimen. Compared with the other 3 groups, only the amnion-facing wall of chorionic vessels in MAVN showed a significantly greater number of apoptotic cells. This was verified by morphological criteria and caspase 3 staining. There were limited or no detectable TUNEL-stained cells in either the villous-facing walls of vessels in the MAVN specimens or in any of the vessels of the placentas from uncomplicated pregnancies. There was a negligible level of apoptosis in chorionic vessels of placentas with intense chorionic vasculitis, with or without meconium, despite the inflammatory response or presence of meconium. We conclude that apoptosis contributes to the pathophysiology of MAVN.

Topics: Apoptosis; Blood Vessels; Caspase 3; Caspases; Chorion; Female; Humans; Immunohistochemistry; In Situ Nick-End Labeling; Meconium; Muscle Cells; Necrosis; Placenta; Placenta Diseases; Pregnancy; Vasculitis

The rationale for in utero repair of myelomeningocele has been supported experimentally by the observation of preserved neural function after prenatal closure of surgically created defects compared with nonrepaired controls. The mechanism of injury to the exposed neural elements is unknown. Postulated mechanisms include trauma to the herniated neural elements or progressive injury from amniotic fluid exposure as gestation proceeds. A component of amniotic fluid that may contribute to neural injury is meconium. In the current study the effect of human meconium on the exposed spinal cord in a fetal rat model of myelomeningocele was examined.. Twenty time-dated pregnant rats underwent laparotomy at 181/2 days of gestation. The exposed uterus was bathed in ritrodrine for tocolysis. The amniotic cavity was opened over the dorsal midline of the fetal rat, and, under a dissecting microscope (x25), a 2- to 3-level laminectomy was performed. Under magnification (x40), the translucent dura was opened using a 25-gauge needle as a knife. Two fetuses per dam were operated on. In the control group, the amniotic fluid was restored with saline solution, whereas in the experimental group a solution of Human meconium diluted (10%) in saline was used to restore the amniotic fluid. Fetuses were harvested by cesarean section at 211/2 days' gestational age. The liveborn pups were then killed and fixed in 10% formaline. Sections 10 micrometer thick were stained with H&E and studied by light microscopy for evidence of spinal cord injury.. Seven of 20 (35%) experimental rat pups and 6 of 20 (30%) control rat pups were liveborn. All liveborn pups had severe paralysis of the hindlimbs and tail, so that functional differences between the 2 groups could not be detected. Histologic examination of 13 spinal cords at the site of surgical exposure showed that necrosis of neural tissue in 5 of 7 meconium-exposed rat pups was increased when compared with that observed in the 6 fetuses exposed to amniotic fluid without meconium. In general, inflammation was greater and repair processes appeared delayed in meconium-exposed rat pups.. Exposure of the spinal cord of fetal rats to amniotic fluid by surgically created myelomeningocele leads to severe functional impairment. Histologically recognizable necrosis of neural elements was increased in those animals that were exposed to diluted human meconium in the amniotic fluid. The results support the hypothesis that meconium may contribute to the pathophysiology of spinal cord injury observed in myelomeningocele.

Topics: Amniotic Fluid; Animals; Disease Models, Animal; Female; Humans; Infant, Newborn; Male; Meconium; Meningomyelocele; Necrosis; Pregnancy; Rats; Spinal Cord; Uterus

To show that meconium causes fetal morbidity and death at earlier gestations than reported previously.. We searched for specimens from 1997 and 1998 with pathologic diagnosis of meconium-induced umbilical vascular necrosis in placentas of nonmalformed fetuses and newborns. Because intra-amniotic infection is known to activate cytokines, and blood pigment is often microscopically indistinguishable from meconium, we removed those confounding considerations by excluding placentas with chorioamnionitis and signs of intra-amniotic bleeding. Light microscopic identification of vacuolar amniotic epithelial degeneration was used to select specimens with meconium because blood does not cause that histopathologic abnormality. We used histochemical procedures to show absence of hemosiderin and presence of bilirubin, and immunocytochemical labeling with interleukin-1beta to show cytokine.. Four cases had meconium-induced umbilical vascular necrosis. The gestational ages were 16, 19, 29, and 38 weeks. Two cases were abortuses, the third was stillborn, and the fourth was a small-for-gestational-age liveborn, delivered by cesarean because of repetitive variable decelerations. Luna-Ishak staining showed bilirubin in macrophages between umbilical vascular myocytes and in the Wharton's jelly. Immunocytochemical methods showed interleukin-1beta in those same macrophages.. Cytokines and other meconium-associated factors may contribute to the pathogenesis of fetal death. Survivors may suffer intraventricular hemorrhage, periventricular leukomalacia, and other morbidity.

Topics: Adult; Bilirubin; Female; Fetal Diseases; Humans; Infant, Newborn; Interleukin-1; Macrophages; Meconium; Necrosis; Pregnancy; Umbilical Arteries; Umbilical Veins

Topics: Adult; Fatal Outcome; Female; Fetal Distress; Humans; Meconium; Necrosis; Pregnancy; Rupture, Spontaneous; Umbilical Cord; Umbilical Veins

The literature lacks epidemiologic study of pregnancy outcome with light-microscopic meconium-related lesions. We recently described previously unreported meconium-induced necrosis of placental and umbilical cord vessels and hypothesized that the lesions represent preceding vasocontraction and fetal hypoperfusion. Preliminary experiments then confirmed that meconium produces vasocontraction in isolated umbilical venous tissue. In the present study, we examined whether clinically meaningful abnormalities occur with these vascular signs of remote fetal meconium discharge. In a light-microscopic review of 1100 meconium-stained placentas, we found ten with meconium-induced vascular necrosis. In six of these ten cases, fetal distress necessitated cesarean delivery. Seven newborns had Apgar scores of 3 or less at 1 minute, and each of the seven cases tested had umbilical arterial pH less than 7.19. Because seven of the ten infants were born after December 1, 1989, clinical follow-up was limited. One died, another has neurodevelopmental deficiency, and a third has experienced enlargement of head circumference from the 50th percentile at birth to the 95th percentile at 10 months of age. Two placentas had umbilical cord ulceration, a lesion that has rarely been reported in the literature. We conclude that meconium-induced vascular necrosis seems to be a meaningful, detrimental lesion.

Topics: Amniotic Fluid; Apgar Score; Blood Vessels; Female; Humans; Infant, Newborn; Meconium; Necrosis; Placenta; Pregnancy; Pregnancy Outcome; Ulcer; Umbilical Arteries; Umbilical Cord; Umbilical Veins

Gastroschisis is a rare congenital birth defect of the abdominal wall that invariably is fatal if not managed appropriately. Early in utero diagnosis is now possible using maternal serum alpha-fetoprotein and ultrasound. As with other serious congenital disorders, antenatal diagnosis allows therapeutic options and time for preparation. Even if the diagnosis is made late, however, efforts to achieve prenatal maternal transport are still reasonable. The neonatal outcome of an unplanned delivery of an anomalous child requiring immediate attention is likely to be better if the delivery occurs in a tertiary center. These facilities generally have specialized services and teams available for critical care around the clock. The authors describe the maternal transport and delivery of a neonate with a serious disorder that required specialized attention at an hour when most hospitals are staffed with a skeleton crew. The necessary resources were available immediately, and the neonatal outcome was favorable. Although this report describes gastroschisis specifically, the concept of tertiary site delivery for potentially seriously ill neonates applies to any condition. With a late diagnosis, possible other anomalies, and a logistically unfavorable hour, the advantages of maternal transport are evident. This report also briefly reviews the area of antenatal ultrasound diagnosis and the newer mechanisms used to develop a perinatal care plan.

Topics: Abdominal Muscles; Adult; Female; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Intestine, Small; Meconium; Necrosis; Obstetric Labor, Premature; Patient Care Team; Pregnancy; Prenatal Diagnosis; Ultrasonography

Gastrografin (methylglucamine diatrizoate) enemas were carried out in 2 newborn infants with meconium ileus. Evacuation was slow and incomplete. Both patients died within 72 hours following enemas from bowel necrosis, perforation and peritonitis. Although it is not possible to implicate Gastrografin directly as the cause, it is suggested that it may have contributed substantially to bowel necrosis. Recent experimental evidence of colonic inflammation and occasionally necrosis caused by Gastrografin lends support to this hypothesis. Caution should be exercised to prevent not only the systemic osmotic effects of Gastrografin, but also potential local injury to the bowel, especially when underlying disease interferes with intestinal viability.

Topics: Diatrizoate; Diatrizoate Meglumine; Enema; Female; Humans; Infant, Newborn; Intestinal Diseases; Intestinal Obstruction; Meconium; Necrosis; Radiography

Topics: Amnion; Extraembryonic Membranes; Female; Humans; Inflammation; Meconium; Microscopy, Electron; Necrosis; Neutrophils; Placenta; Pregnancy; Pregnancy Complications; Rupture