Regional Cerebral Blood Flow: Studies in the Fetal Lamb during Hypoxia, Hypercapnia, Addosis, and Hypotension

Ashwal, Stephen; Dale, P.; Longo, Lawrence D.

doi:10.1203/00006450-198412000-00018

Cited by 138 publications

(76 citation statements)

References 30 publications

(60 reference statements)

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“…This supports the suggestion that impaired cerebral blood flow is critical in provoking and localizing neuronal injury (14)(15)(16). A number of studies of cerebral blood flow during short-term asphyxia have shown consistent regional variations, with reduced cortical flow and preferential brainstem and white matter blood flow despite maintenance of overall blood supply (17)(18)(19)(20). This relative reduction of cerebral blood flow to the cortex may explain the increased susceptibility of the parasagittal cortex, even in fetuses who maintained their BP.…”

Section: Discussionsupporting

confidence: 61%

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

et al. 1992

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ABSTRACT. Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebial histologic and electrophysiologic changes after as~hvxia in chronicallv instrumented late-gestation fetal sheep: We reduced uteiine blood flow to an ascending aortic blood oxygen content < 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA% region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult ( r = 0.75, p < 0.005) but not with the degree of hypoxia.No other factor was independently predictive, but, when considered separately, pH ( r = 0.54; p < 0.05) and loss of intensity of the EEG ( r = 0.61, p < 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to ~7 . 0 in six of eight fetuses with damage, whereas it remained >7.0 in five of six without damage ( p < 0.05).We conclude that severe intrauterine asphyxia for periods of 30 to 120 min can cause predominant parasagittal neuronal death and that this is associated with hypotension, severe metabolic acidosis, and suppression of EEG during the insult. These data are consistent with the suggestion that impairment of cerebral perfusion is a critical event in localizing cerebral damage during perinatal asphyxia. to the degree of cerebral damage (5, 6). Indeed, there remains considerable controversy regarding the factors that contribute to perinatal hypoxic ischemic encephalopathy. We therefore examined the histologic and electrophysiologic changes associated with asphyxia due to uterine artery occlusion of varying duration in fetal sheep. MATERIALS AND METHODSPregnant sheep from 1 19 to 128 d of gestation (term is 147 d) were instrumented under 2% halothane anesthesia with an adjustable occluder, made from Teflon-lined cardiac catheterization introducers and catheters, around the maternal common uterine artery. The ovarian arteries were ligated just proximal to the ovaries to prevent anastomotic perfusion. The fetus was then instrumented as previously described (7, 8). Polyvinyl catheters were inserted into fetal ascending aortic arteries and the amniotic cavity. Two pairs of shielded stainless steel recording electrodes were placed over the parietal dura, 10 mm lateral to bregma, and 5 mm and 15 mm anterior. In seven fetuses, a pair of stimulating electrodes was also placed 15 mm lateral and 10 mm anterior to bregma. Electrocardiographic electrodes were placed s.c. over the shoulders. In the fir...

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Section: Discussionsupporting

confidence: 61%

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

et al. 1992

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“…Furthermore, CBF and cerebral O 2 uptake values presented in this study were similar to values obtained from newborn piglets that were treated with other drugs for general anesthesia that have been shown not to alter brain oxidative metabolism and were delivered to awake newborn piglets (40,41). CBF distribution throughout the immature brain demonstrates a gradient between the brainstem (highest perfusion values) and forebrain (lowest perfusion values), thereby confirming previous findings (42). In a previous study with extensive surgical interventions, including opening the abdominal cavity, craniotomy, and ureter cannulation after retroperitoneal preparation along with 5 h of experimental performance, sham-operated newborn piglets showed no significant differences in ABP with only a slight increase in heart rate (by 20%).…”

supporting

confidence: 78%

Intrauterine Growth Restriction Ameliorates the Effects of Gradual Hemorrhagic Hypotension on Regional Cerebral Blood Flow and Brain Oxygen Uptake in Newborn Piglets

et al. 2004

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Data are scant regarding the development of cerebrovascular autoregulation in intrauterine growth-restricted (IUGR) newborns. We tested the hypothesis that IUGR improves the ability of neonates to withstand critical periods of gradual hemorrhagic hypotension by optimizing cerebrovascular autoregulation. Studies were conducted on 1-d-old anesthetized piglets divided into groups of normal weight (NW, n ϭ 14, body weight ϭ 1518 Ϯ 122 g) and IUGR (n ϭ 14, body weight ϭ 829 Ϯ 50 g) animals. Physiologic parameters, including regional cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO 2 ), were similar in NW and IUGR piglets under baseline conditions. Controlled arterial blood loss [hemorrhagic hypotension (HH)] induced a stepwise reduction of the mean arterial blood pressure of 49 Ϯ 3 mm Hg (mild HH), 39 Ϯ 3 mm Hg (moderate HH), and 30 Ϯ 3 mm Hg (severe HH) in seven NW and seven IUGR piglets (p Ͻ 0.05). In NW piglets, cortical CBF and CMRO 2 was reduced already at moderate HH (p Ͻ 0.05). A similar CMRO 2 reduction occurred during severe HH in NW and IUGR piglets (p Ͻ 0.05). In addition, during mild and moderate HH, primarily in IUGR piglets, an increase in regional CBF of brainstem, cerebellum, and thalamus was shown compared with baseline values (p Ͻ 0.05). Furthermore, under these conditions, cerebral cortex blood flow was maintained in newborn IUGR animals. In contrast, NW piglets exhibited a significant reduction in CBF (p Ͻ 0.05) during moderate HH. Thus, IUGR resulted in an improved ability to withstand critical periods of gradual oxygen deficit as shown by improved cerebrovascular autoregulation during hemorrhagic hypotension. Asymmetric IUGR (type II) is still an unresolved problem in perinatal medicine. Perinatal mortality is markedly increased (1-3), as well as the incidence of perinatal asphyxia, because placental insufficiency is the main cause of IUGR (4).The perinatal morbidity and mortality of neonates after IUGR is mainly caused by postasphyxial encephalopathy (4). The most dangerous complication is brain injury secondary to hypoxic-ischemic disease, which is the predominant form of all brain injuries encountered in the perinatal period (5). Periods of arterial hypotension are frequently involved in the initial period of acute perinatal asphyxia (6). Cerebrovascular autoregulation protects against brain hypoperfusion, provided arterial pressure does not fall below the lower limit of the autoregulatory range. The efficiency of autoregulation to prevent hypoperfusion generally improves with increasing fetal age and maturity of the brain (7-9). This implies that the immature brain is susceptible to ischemia during hypotension (10). Therefore, poor autoregulation may place the immature brain at risk for injury (11,12).The slow down of fetal growth late in gestation after intrauterine malnutrition, although resulting in IUGR, can be regarded as a compensatory process, which enables the fetus to survive (13,14). Growth reduction is primarily achieved by altering the endocrine milieu, possi...

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“…Although increase in cerebral blood flow due to hypoxia, hypercapnia and acidosis [2] is considered to be an etiological factor in PIVH, we were unable to analyse this in our study, since monitoring of Ρθ2, Pco2 and pH was not standardized in the various units. Statistical analyses were based on logistic regression techniques.…”

Section: Curriculum Vitaementioning

confidence: 62%

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

Bor¹,

Verloove-Vanhorick²,

Brand³

et al. 1987

Journal of Perinatal Medicine

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Regional Cerebral Blood Flow: Studies in the Fetal Lamb during Hypoxia, Hypercapnia, Addosis, and Hypotension

Cited by 138 publications

References 30 publications

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

Cerebral Histologic and Electrocorticographic Changes after Asphyxia in Fetal Sheep

Intrauterine Growth Restriction Ameliorates the Effects of Gradual Hemorrhagic Hypotension on Regional Cerebral Blood Flow and Brain Oxygen Uptake in Newborn Piglets

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

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