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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2005.03.069 Byline: Jesmin I. Noor (a), Tomoaki Ikeda (a), Yuto Ueda (b), Tsuyomu Ikenoue (a) Abstract: The purpose of this study was to elucidate a role for edaravone, a free radical scavenger 3-methyl-1-phenyl-2-pyrazolin-5-one, in neonatal hypoxic-ischemic brain damage. We determined the level of thiobarbituric acid reactive substances as an index of lipid peroxidation and nitric oxide metabolites as nitric oxide production. Author Affiliation: (a) Departments of Obstetrics and Gynecology (b) Psychiatry, Faculty of Medicine, University of Miyazaki, Japan Article History: Received 15 November 2004; Revised 28 February 2005; Accepted 30 March 2005

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2005.01.029 Byline: Tomoaki Ikeda (a), Masanori Iwai (b), Takeshi Hayashi (b), Isao Nagano (b), Mikio Shogi (b), Tsuyomu Ikenoue (a), Koji Abe (b) Abstract: We examined whether progenitor neural stem cells can differentiate successfully into mature neurons and astrocytes in a rat model of neonatal hypoxic-ischemic encephalopathy. Author Affiliation: (a) Department of Obstetrics and Gynecology, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan (b) Department of Neurology, Graduate School of Medicine and Dentistry, Okayama University, Okayama, Japan Article History: Received 19 October 2004; Revised 3 December 2004; Accepted 11 January 2005 Article Note: (footnote) Supported in part by Grants-in-Aid for Scientific Research (B) 15390273 and (Hoga) 15659338 and the National Project on Protein Structural and Functional Analyses from the Ministry of Education, Science, Culture and Sports of Japan and by grants from the Ministry of Health and Welfare of Japan.

A study is conducted to examine whether progenitor neutral cells can differentiate successfully into mature neutrons and atrocities in a rat model of neonatal hypoxic-ischemic encephalopathy. The intrinsic ability for neurologic self-repair is limited at the maturation step after hypoxic-ischemic stress in the neonatal rat brain.

A study was conducted to examine neuroprotective effect of glial cell line-derived neurotrophic factor with the use of a delivery system. It was concluded that grafting of encapsulated glial cell line-derived neurotrophic factor-secreting cells was a promising way to protect the neonatal brain from hypoxic/ischemic insult.

The effect of glial cell line-derived neurotrophic factors on long-term learning and memory impairment and morphological changes up to 18 weeks after hypoxic-ischemic stress in neonatal rats was examined. It was concluded that glial cell line-derived neurotrophic factor treatment is effective in reducing brain damage as well as inhibiting learning and memory impairment, following hypoxic-ischemic insult in neonatal rats.

The effect of dexamathasone on both histologic and behavioral changes in rats that were exposed to a combination of endotoxin and hypoxia-ischemia (HI) on postnatal day 7 is examined. Dexamethasone is useful for preventing infection and inflammation-induced perinatal brain damage.

The effect of dexamathasone on both histologic and behavioral changes in rats that were exposed to a combination of endotoxin and hypoxia-ischemia (HI) on postnatal day 7 is examined. Dexamethasone is useful for preventing infection and inflammation-induced perinatal brain damage.

The long-term of perinatal hypoxia-ischemia and endotoxin on attention and short- and long-term memory in neonatal rats with the use of behavioral tasks and brain histologic results is assessed. The results reveal that the lipopolysaccharide, hypoxia-ischemia, and lipopolysaccharide + hypoxia-ischemia groups showed significantly poorer performance than controls in the choice reaction time task.

Intrapartum fetal heart rate patterns of cytomegalovirus-infected fetuses are studied. As the heart rate patterns of fetuses affected with this virus is abnormal, it is necessary that perinated detection of cytomegalovirus is made.

A study was conducted to evaluate the clinical validity of electronic fetal heart rate monitoring to detect fetal acidemia and to evaluate the prevalence of cerebral palsy in unselected low-risk pregnancies. Cerebral palsy caused by intrapartum asphyxia was restricted to unavoidable accidents under continuous fetal heart rate monitoring.

Byline: Tomoaki Ikeda, Yuji Murata, Edward J. Quilligan, Julian T. Parer, Toshihiko Murayama, Masashi Koono Keywords: Fetal sheep; brain; heart; kidney; liver; oxidative stress Abstract: Objective: We sought to determine the relationship between the degree of histologic changes in the brain, heart, kidney, and liver in fetal lambs after severe asphyxia and to analyze the role of oxidative stress in the pathogenesis of fetal multiple organ failure. Study Design: Eight chronically instrumented near-term fetal lambs were asphyxiated by partial umbilical cord occlusion for approximately 60 minutes until the fetal arterial pH reached Author Affiliation: Irvine and San Francisco, California, and Miyazaki, Japan From the Departments of Obstetrics and Gynecology, University of California, Irvine,.sup.a the Cardiovascular Research Institute, University of California, San Francisco,.sup.b and the Department of Pathology, Miyazaki Medical College..sup.c Article History: Received 10 September 1998; Revised 21 December 1998; Accepted 4 October 1999 Article Note: (footnote) [star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan.

Byline: Tomoaki Ikeda, Tsuyomu Ikenoue, Xiao Y. Xia, Yi X. Xia Keywords: Heat shock protein 72; hyperthermia; hypoxic-ischemic insult; immature rat; tolerance Abstract: Objectives: Hypoxic-ischemic tolerance can be induced in neonatal rats through hyperthermic preconditioning. The purposes of this study were to determine the interval between hyperthermic preconditioning and a subsequent hypoxic-ischemic insult that would provide optimal neuroprotection against the insult and to examine the relationship between tolerance induction and heat shock protein expression. Study Design: On postnatal day 7 Wistar rat pups were separated into the following 2 groups: a heated group (those exposed to 15 minutes of hyperthermic pretreatment at a brain temperature of 41.5[degrees]C-42.0[degrees]C) and an unheated control group. At 6, 12, 24, 48, and 72 hours after the hyperthermic stress, rats from both groups were exposed to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen and 92% nitrogen) at 33[degrees]C. Twenty animals from each group were used at each time point. All rats were killed at 1 week after hypoxia-ischemia, at which time the brains were processed and neuronal damage in the cortex and hippocampus was assessed histologically. Another set of 7-day-old rats (n = 30) was studied immunohistochemically at 6, 12, 24, 48, and 72 hours after the same hyperthermic treatment. Expression of 72-kd heat shock protein was measured in neuronal, glial, and vascular endothelial cells. Results: Hyperthermia-induced hypoxic-ischemic tolerance was observed at 6, 12, and 24 hours but not at 48 and 72 hours after hyperthermic preconditioning. Heat shock protein 72 expression in the vascular endothelial cells, rather than in the glial or neuronal cells, was most strongly associated with hypoxic-ischemic tolerance. Conclusion: These findings suggest that heat shock protein 72 in endothelial cells plays an important role in the acquisition of hypoxic-ischemic tolerance at postnatal day 7, a time when maximal angiogenesis occurs and the blood-brain barrier is still immature. (Am J Obstet Gynecol 2000;182:380-6.) Author Affiliation: Department of Obstetrics and Gynecology, Miayzaki Medical College. Miyazaki, Japan Article History: Received 26 March 1999; Revised 2 August 1999; Accepted 19 August 1999 Article Note: (footnote) [star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan.

Asphyxia appears to damage the heart, kidneys and liver in addition to the brain. This was the conclusion of a study on lambs. In the liver, the damage appears to be caused by oxidative stress.

Heat shock protein 72 appears to protect the brain from low blood levels of oxygen, according to a study in rats. This protein is produced when the body is exposed to high temperatures.

Very young rats appear to produce heat shock protein (HSP) 72 sooner after a stressful event than older rats and this may protect their brains from injury. HSP72 is a protein that is released after some shock to the body, such as excessive heat, low oxygen levels or an interruption in the blood supply. It is believed to protect the body from being damaged by these stressful conditions. In a study of rats, 5-day-old rats produced HSP72 sooner than 14-day-old rats after the rats were exposed to low oxygen levels. Their brains also showed less damage from the stress.

Byline: Xiao Y. Xia, Tomoaki Ikeda, Arturo Ota, Yi X. Xia, Hiroshi Sameshima, Tsuyomu Ikenoue, Kiyotaka Toshimori Keywords: Brain damage; developmental change; heat shock protein; hypoxia-ischemia; microtubule-associated protein 2; rat Abstract: Objective: This study was intended to investigate the temporal changes in heat shock protein 72 expression and microtubule-associated protein 2 disappearance in rat brain at 2 different ages after hypoxic-ischemic insult. Study Design: Both 5-day-old and 14-day-old Wistar rats were subjected to unilateral common carotid artery ligation and hypoxia in 8% oxygen for 2 hours at 33[degrees]C. Brain sections were examined sequentially for heat shock protein 72 expression at 0.5, 3, 6, 12, 24, 48, and 72 hours of recovery after hypoxia-ischemia and for microtubule-associated protein 2 disappearance at 0, 24, 48, and 72 hours of recovery and at 7 days of recovery after hypoxia-ischemia. Results of immunohistochemical staining for heat shock protein 72 and microtubule-associated protein 2 were used as markers for detection of early hypoxic-ischemic brain damage. Permanent neuronal damage was assessed with hematoxylin and eosin staining at 7 days after hypoxia. Results: In 5-day-old rats microtubule-associated protein 2 expression was lost as early as 0 hours after hypoxia-ischemia in the cerebral cortex and hippocampus, with a peak at 48 hours after which expression recovered. Expression of heat shock protein 72 was detected in the ligated hemisphere at 0.5 hours after hypoxia-ischemia and peaked at 6 to 24 hours of recovery. In 14-day-old rats microtubule-associated protein 2 was stained in the cortex at 0 hours after hypoxia-ischemia but gradually disappeared in the cerebral cortex and hippocampus after 24 hours of recovery. The expression of heat shock protein 72 was not detected by 6 hours of recovery in the cerebral cortex and by 3 to 12 hours of recovery in the hippocampus, but heat shock protein 72 was persistently expressed in the cortex and hippocampus after 48 hours of recovery. Neuronal damage was significantly less in 5-day-old rats than in 14-day-old rats. Conclusion: In 5-day-old rats hypoxia-ischemia causes earlier changes in heat shock protein 72 and microtubule-associated protein 2 immunostaining results and causes less severe brain damage than in 14-day-old rats. (Am J Obstet Gynecol 1999;180:1254-62.) Author Affiliation: Miyazaki, Japan From the Department of Obstetrics and Gynecology.sup.a and the First Department of Anatomy,.sup.b Miyazaki Medical College Article History: Received 3 June 1998; Revised 28 December 1998; Accepted 14 January 1999 Article Note: (footnote) [star] Reprint requests: Tsuyomu Ikenoue, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan., [star][star] 0002-9378/99 $8.00 + 0 6/1/97170

A synchronized sinusoidal heart rate pattern may reveal a serious health problem in fetuses who are on extracorporeal membrane oxygenation. Extracorporeal membrane oxygenation is used to support the lungs and heart when the fetus has severe heart or lung disease. Researchers compared the health of 32 fetal lambs who developed a sinusoidal heart rate pattern while on extracorporeal membrane oxygenation. Two types of sinusoidal heart rate occurred: synchronized and reciprocal, depending on whether heart rate was synchronized with blood pressure or out-of-phase. The synchronized pattern was associated with more severe acid-base abnormalities and alterations in cerebral blood flow.

The fetus may produce a protein called heat shock cognate protein 70 under stressful conditions to protect the heart and brain from damage. Researchers measured the amount of this protein in the heart, brain, and liver of seven-day-old rats who had been subjected to low levels of oxygen. This caused blood oxygen levels and brain temperature to drop. It also caused the level of heat shock cognate protein 70 to increase in brain and heart but not in liver.

Byline: Tomoaki Ikeda, Yuji Murata, Edward J. Quilligan, Paula Cifuentes, Shigeharu Doi, Soung-Day Park Keywords: Extracorporeal membrane oxygenation; fetal lamb; phase-angle analysis; sinusoidal heart rate pattern Abstract: Objectives: The study analyzed the phase relationship between fetal heart rate and arterial blood pressure fluctuation during sinusoidal heart rate patterns in fetal lambs. Study Design: Thirty-two fetal lambs were placed on extracorporeal membrane oxygenation after cesarean delivery at ages ranging between 113 and 133 days' gestation. Sinusoidal heart rate patterns persisting for >10 minutes were analyzed. The relationships between the sinusoidal heart rate cycles and the arterial blood pressure cycles were quantitatively expressed in degrees by timing the zenith and the nadir of each and assigning a phase-angle index (with 0 [360] and 180 degrees being synchronized and reciprocal, respectively). Simultaneous blood samples were taken from the 4 different sites of the fetal circulation for blood gas and acid-base analysis when the sinusoidal heart rate pattern appeared. Regional cerebral blood flow was determined by means of the colored microsphere technique in 8 fetuses with sinusoidal patterns and 7 control fetuses. Results: Sinusoidal heart rate patterns were observed in 13 (40.6%) of the 32 fetal lambs. Two types of fetal heart rate and arterial blood pressure relationship could be recognized during sinusoidal pattern, the reciprocal type (n = 7) and the synchronized type (n = 9). A reciprocal type of sinusoidal pattern preceded a synchronized type pattern in 3 lambs that showed sinusoidal patterns at different stages of the experiment. The reciprocal type was associated with a higher baseline heart rate and amplitude of the sinusoidal heart rate pattern than was the synchronized type. The synchronized type was associated with a lower pH and base excess than was the reciprocal type. The cerebral blood flow in the medulla oblongata was significantly lower during the synchronized type pattern than during the reciprocal type pattern. Conclusion: There are 2 types of sinusoidal heart rate pattern. A synchronized type sinusoidal heart rate pattern may indicate more advanced fetal compromise than is associated with a reciprocal type pattern. (Am J Obstet Gynecol 1999;180:462-8.) Author Affiliation: Department of Obstetrics and Gynecology, University of California, Irvine. Orange, California Article History: Received 15 April 1998; Revised 7 July 1998; Accepted 22 September 1998 Article Note: (footnote) [star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan., [star][star] 6/1/94600

Byline: Tomoaki Ikeda (a), Koji Abe (b), Arturo Ota (a), Tsuyomu Ikenoue (a) Keywords: Brain; heart; heat shock cognate protein 70; heat shock protein 70; liver; neonatal rat Abstract: Objective: The aim of this study was to examine the production of 2 types of heat shock protein 70 in the organs of neonatal rats during an episode of mild hypoxic stress that was insufficient to produce histologic changes. Study Design: Seven-day-old rats were subjected to hypoxia (inspired gas of 8% oxygen and 92% nitrogen) at 33[degrees]C for 2 hours (n = 5), 3 hours (n = 5), and 4 hours (n = 5). Control rats (n = 5) inspired room air for 4 hours. The brains, hearts, and livers were removed after 4 hours of recovery. The levels of heat shock protein 70 and heat shock cognate protein 70 messenger ribonucleic acid were measured by Northern blot analysis. Arterial pH, Pao.sub.2 , PACO.sub.2 , and brain temperature were measured before, during, and at 4 hours of hypoxia in another 16 animals. Histologic examinations were carried out in these 16 animals 7 days after hypoxic stress. Results: PaO.sub.2 , PACO.sub.2 , and brain temperature decreased during the hypoxic stress and returned to prehypoxic values at recovery time. Arterial pH did not change. No histologic changes were observed in any areas of the brain. Heat shock cognate protein 70 messenger ribonucleic acid was normally expressed in the brain, heart, and liver and was further induced after hypoxia in the brain and the heart. There was, however, no additional increase of heat shock cognate protein 70 messenger ribonucleic acid in the liver. there were no increments of the stress-induced form of heat shock protein 70 messenger ribonucleic acid in these organs. Conclusion: Mild hypoxia selectively induced messenger ribonucleic acid of heat shock cognate protein 70, which may play an important role in protecting the brain and the heart against stress. (Am J Obstet Gynecol 1999;180:457-61.) Author Affiliation: (a) Department of Obstetrics and Gynecology, Miyazaki Medical College, Miyazaki, Japan (b) Department of Neurology, Okayama University Medical School. Miyazaki, Japan Miyazaki, Japan Article History: Received 6 January 1998; Revised 29 July 1998; Accepted 14 September 1998 Article Note: (footnote) [star] Supported in part by grant-in-aid for scientific research (B) number 09470151., [star][star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan., a 6/1/94470

Decreased fetal heart rate variability and characteristic heart rate patterns are associated with brain damage from fetal asphyxia. Researchers induced asphyxia in fetal lambs while monitoring the heart beat and other physiological parameters, then examined the brains for asphyxia-induced damage. A loss of heart rate variability, a check-shaped heart rate pattern, and changes in the normal sinus rhythm following asphyxia, were characteristic of progressively greater damage to the brain.

Preconditioning with four hours of hypoxic exposure significantly reduced hypoxic-ischemic brain damage in neonatal rats. An elevation in heat shock cognate protein messenger ribonucleic acid may account for the increased hypoxic-ischemic tolerance in the brain. Brain damage involved either generalized infarction or neuronal loss in the hippocampus.

Byline: Arturo Ota, Tomoaki Ikeda, Koji Abe, Hiroshi Sameshima, Xiao Y. Xia, Yi X. Xia, Tsuyomu Ikenoue Keywords: Brain damage; hypoxic-ischemic tolerance; neonatal rat Abstract: Objective: Our purpose was to determine whether hypoxic-ischemic brain damage would be protected against by advance conditioning of the animal with 4 hours of hypoxic exposure. Study Design: Neonatal rats were exposed on postnatal day 7 to (1) 4 hours of hypoxia with 8% oxygen (preconditioning hypoxic group) or (2) 4 hours of normoxia (sham-preconditioning group). At 24 hours after the conditioning, rats from both groups were exposed to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen). All the rats were killed 1 week after hypoxia-ischemia, and their brains were extracted for histologic study. Results: Two types of brain damage were histologically observed at 1 week after hypoxia-ischemia in both groups: (1) generalized infarction in the ligated hemisphere and (2) predominant neuronal loss in the hippocampal region. The total incidence of brain damage was significantly decreased in the preconditioning hypoxic group (10/24 rats, 41.7%) compared with the sham-preconditioning hypoxic group (17/22 rats, 77.3%; P < .05). Conclusion: Our results show that the hypoxic-ischemic tolerance phenomenon may be induced in the hypoxic-ischemic brain damage model by conditioning the animal before the insult with 4 hours of hypoxic exposure. (Am J Obstet Gynecol 1998;179:1075-8.) Author Affiliation: Miyazaki, Japan Article History: Received 13 October 1997; Revised 16 February 1998; Accepted 25 March 1998 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, Miyazaki Medical College,a and the Department of Neurology, Tohoku University School of Medicine.b , [star][star] Reprint requests: Arturo Ota, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-16, Japan., a 0002-9378/98 $5.00 + 0 6/1/90522

Oxidative stress may cause brain damage in fetuses deprived of oxygen. Researchers measured physiologic indicators of free radical activity in the brains of six fetal lambs subjected to umbilical cord compression and six in which normal umbilical blood flow was maintained. Thiobarbituric acid reactive substance levels were elevated in the frontal and parietal white matter, basal ganglia, and thalamus brain regions. Concentrations of superoxide dismutase, an protective antioxidant, were also elevated in these brain regions. Asphyxiation may induce free radical damage to nerve cells.

Byline: Tomoaki Ikeda, Yuji Murata, Edward J. Quilligan, Julian T. Parer, Shigeharu Doi, Soung-Day Park Keywords: Fetal lamb; asphyxia; brain damage; oxygen free radical Abstract: OBJECTIVES: The purpose of this study was to explain the role of oxidative stress in the pathogenesis of brain damage caused by intrauterine fetal asphyxia. STUDY DESIGN: Six chronically instrumented near-term fetal lambs were subjected to asphyxia by partial umbilical cord occlusion for approximately 60 minutes until fetal arterial pH diminished to less than 6.9 and base excess to less than -20 mEq. Another six fetuses surgically prepared but not occluded were used as control. Fetuses were killed after 72 hours and eight different brain regions (frontal and parietal gray matter, frontal and parietal white matter, basal ganglia, thalamus, hippocampus, and cerebellum) were dissected and assayed for thiobarbituric acid reactive substances, glutathione, and superoxide dismutase. RESULTS: Thiobarbituric acid reactive substance levels in asphyxiated animals were elevated in frontal and parietal white matter, basal ganglia, and thalamus compared with those in controls. The concentrations of superoxide dismutase in the asphyxiated group were also higher in frontal and parietal white matter, basal ganglia, and cerebellum compared with those in the control group. Between the two groups, however, glutathione concentrations did not differ significantly. CONCLUSION: These results suggest that oxidative stress may be a major contributing factor to the development of brain damage in intrauterine fetal asphyxia. (Am J Obstet Gynecol 1998;178:474-8.) Author Affiliation: Irvine and San Francisco, California Article History: Received 27 January 1997; Revised 4 April 1997; Accepted 5 September 1997 Article Note: (footnote) [star] From the Departments of Obstetrics and Gynecology, University of California., [star][star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan., a 6/1/85861

Asphyxia appears to produce different kinds of damage in the fetal brain. Asphyxia occurs when the fetus does not receive enough oxygen. Researchers caused asphyxia in fetal lambs by blocking the umbilical cord for about one hour. Three days later the lambs were killed and their brains were examined. Asphyxia produced a wide variety of changes, ranging from severe damage to mild damage. Even lambs that recovered from the asphyxia had brain damage.

Byline: Tomoaki Ikeda, Yuji Murata, Edward J. Quilligan, Ben H. Choi, Julian T. Parer, Shigeharu Doi, Soung-Day Park Keywords: fetal lamb; asphyxia; brain damage; partial umbilical; cord occlusion Abstract: OBJECTIVE: Our purpose was to characterize the histologic changes in the asphyxiated fetal lamb brain and to correlate the severity of these changes with fetal physiologic parameters during and after asphyxia. STUDY DESIGN: Seventeen near-term fetuses were used for analysis: control group without manipulation (n = 4, 132 [+ or -] 1.1 days of gestation at autopsy, mean [+ or -] SEM), sham-asphyxia control group (n = 3, 132 [+ or -] 1.3 days), and asphyxiated group, which successfully survived 72 hours after asphyxia (n = 10, 130 [+ or -] 1.0 days). Asphyxia was produced by umbilical cord occlusion lasting for approximately 60 minutes until fetal arterial pH diminished to Author Affiliation: Irvine and San Francisco, California Article History: Received 21 November 1996; Revised 11 February 1997; Accepted 13 August 1997 Article Note: (footnote) [star] From the Departments of Obstetrics and Gynecologya and Pathology,b University of California, Irvine, and University of California, San Francisco.c , [star][star] Reprint requests: Tomoaki Ikeda, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake-Cho, Miyazaki 889-16, Japan., a 6/1/85388

Heat shock protein-72 (HSP-72) and microtubule-associated protein-2 (MAP-2) levels appear to reflect cell damage seen after oxygen deprivation in an area of the brain called the hippocampus. HSP-72 and MAP-2 levels were measured in the brains of seven-day-old rats killed at designated time points between one and 72 hours after the main blood vessel supplying oxygen to one half of the brain was tied off. Brain damage was examined microscopically after death. HSP-72 levels peaked and MAP-2 levels reached their lowest point 24 hours after injury. Most of the brain damage occurred in the CA3 region of the hippocampus.

Byline: Arturo Ota, Tomoaki Ikeda, Tsuyomu Ikenoue, Kiyotaka Toshimori Keywords: Hypoxia-ischemia; newborn rat brain; heat shock protein-72; microtubule-associated protein-2 Abstract: Objective: Our purpose was to study the neuronal responses of heat shock protein-72 (a stress-inducible protein) and microtubule-associated protein-2 (a constitutive protein of the neuronal cytoskeleton) after hypoxia-ischemia and their relationship with permanent damage in the newborn rat brain. Study design: Seven-day-old rats were exposed to unilateral carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen) and then killed at time points ranging from 1 to 72 hours after injury. Brains were removed for immunohistochemical and routine staining. Results: Heat shock protein-72 appearance and microtubule-associated protein-2 disappearance occurred from 1 hour after injury, mainly in the dentate gyrus of the hippocampal formation and the cerebral cortex. Such alterations reached maximal levels at 24 hours for both proteins. Microtubule-associated protein-2 staining recovered in almost all parts of the brain. However, the hippocampal CA3 showed a delay in the responses for both proteins, and microtubule-associated protein-2 did not recover the response to immunostaining. Histologic evaluation at 72 hours after hypoxia by routine methods showed predominant damage in the hippocampal CA3. Conclusion: Our results show that delayed responses of heat shock protein-72 and microtubule-associated protein-2 are related to a high incidence of neuronal cell loss in the hippocampal CA3 region. Author Affiliation: Miyazaki, Japan Article History: Received 6 August 1996; Revised 6 March 1997; Accepted 16 April 1997 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecologya and the First Department of Anatomy,b Miyazaki Medical College., [star][star] Reprint requests: Arturo Ota, MD, Department of Obstetrics and Gynecology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-16, Japan., a 0002-9378/97 $5.00 + 0, aa 6/1/82776

Women may experience a significant increase in cerebral blood flow during the early stages of pregnancy except in the occipital lobe of the brain. Cerebral blood flow was studied in 10 women who were between seven and 19 weeks pregnant the day before undergoing an abortion and again an average of 43 days after. Cerebral blood flow decreased by an average of 8% after the abortion. The average drop in cerebral blood flow was 8% in the frontal lobe of the brain, 9% in the temporal lobe, 13% in the parietal lobe, 10% in the basal ganglia and 17% in the cerebellum. The average blood flow to the occipital lobe of the brain was approximately the same both before and after the abortion.

Pregnancy is associated with significant changes in the cardiovascular system, which includes the heart and blood vessels. The cardiac output, or amount of blood pumped by the heart per unit time, and the blood flow of certain organs such as the uterus and kidneys are altered in pregnant women. There is limited knowledge about the effects of pregnancy on the cerebrovascular system and blood flow within the brain, although pregnancy is thought to increase the risk of cerebrovascular disorders. Doppler ultrasound is a method of using sound waves to evaluate blood flow in an organ, and can be used to detect cerebrovascular complications such as narrowing or blockage of the major blood vessels within the brain. Doppler ultrasound, or velocimetry, was used to assess the circulation within the brain in 77 women with uncomplicated pregnancies. Blood flow measurements were made within the internal carotid artery, a major blood vessel supplying the head and neck. Blood flow in the first and second trimesters of pregnancy was similar to that of nonpregnant women, but was slower in the third trimester of pregnancy. Pulsatility index, a measure of the pulse or rhythm of blood flow, was higher in pregnant women from four to 31 weeks gestation as compared with nonpregnant women, but decreased to nonpregnant values at 32 weeks gestation. These results show that Doppler velocimetry is a useful method of assessing blood flow within the brain during pregnancy. (Consumer Summary produced by Reliance Medical Information, Inc.)

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2009.03.015 Byline: Keiko Ueda (a), Tomoaki Ikeda (a), Naoko Iwanaga (a), Shinj Katsuragi (a), Kaoru Yamanaka (a), Reiko Neki (a), Jun Yoshimatsu (a), Isao Shiraishi (b) Keywords: congenital heart disease; fetal heart rate monitoring; variant FHR pattern Abstract: We evaluated the intrapartum fetal heart rate (FHR) patterns in fetuses with congenital heart disease (CHD). Author Affiliation: (a) Department of Perinatology, National Cardiovascular Center, Osaka, Japan (b) Department of Pediatric Cardiology, National Cardiovascular Center, Osaka, Japan Article History: Received 25 September 2008; Revised 4 January 2009; Accepted 6 March 2009 Article Note: (footnote) Authorship and contribution to the manuscript is limited to the 8 authors indicated. There was no outside funding or technical assistance with the production of this article., Cite this article as: Ueda K, Ikeda T, Iwanaga N, et al. Intrapartum fetal heart rate monitoring in cases of congenital heart disease. Am J Obstet Gynecol 2009;201:64.e1-6.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2007.03.037 Byline: Julian T. Parer (1), Tomoaki Ikeda (2) Keywords: fetal acidemia; fetal heart rate management; intrapartum Abstract: The purpose of this study was to classify fetal heart rate (FHR) monitor patterns according to risk of fetal acidemia and risk of evolution to a more serious pattern and to use this information to construct a standardized process for FHR pattern management, with the ultimate aim of minimizing newborn infant acidemia without excessive obstetric intervention. Author Affiliation: (1) Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, School of Medicine (2) Department of Perinatology, National Cardiovascular Center, Osaka, Japan. Article History: Received 6 November 2006; Accepted 12 March 2007 Article Note: (footnote) Cite this article as: Parer JT, Ikeda T. A framework for standardized management of intrapartum fetal heart rate patterns. Am J Obstet Gynecol 2007;197:26.e1-26.e6.