Regional blood flow and metabolism in ovine fetuses during severe cord occlusion

Ball, Robert H.; Parer, Julian T.; Caldwell, Larry E.; Johnson, Judy

doi:10.1016/0002-9378(94)90400-6

Cited by 45 publications

(14 citation statements)

References 14 publications

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“…The baseline values of BF to supra-and infratentorial brain regions as well as those to the heart in the present study are 1.5-to 2-fold higher than corresponding baseline values for unanesthetized, chronically instrumented sheep fetuses (11)(12)(13). The increased values of BF to the heart and brain before cord occlusion represent a fetal response to metabolic acidosis and hypoxemia and might in turn have affected the subsequent hemodynamic response to total cord occlusion.…”

Section: Discussioncontrasting

confidence: 65%

“…The early decrease in CBF associated with an increase in cerebrovascular resistance is characteristic of insults of rapid onset and has not been observed in studies with slower or graded decreases of umbilical or uterine BF (12,23). Sheep fetuses were acidemic and hypoxic before the acute asphyxial insult and therefore the differentiated vascular response to cord occlusion represents that of the partially asphyxiated fetus and not necessarily that of the healthy fetus.…”

Section: Discussionmentioning

confidence: 99%

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Different Responses of Myocardial and Cerebral Blood Flow to Cord Occlusion in Exteriorized Fetal Sheep

et al. 2004

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Type and duration of fetal asphyxial insult affect the distribution of blood flow to the heart and brain. The purpose of this study was to describe dynamic and quantitative changes in regional myocardial and cerebral blood flow (CBF) during fetal asphyxia induced by total occlusion of the umbilical cord. Eleven exteriorized fetal sheep were subjected to total umbilical cord occlusion and five fetal sheep served as sham controls. Regional blood flow (BF) to the brain and heart was quantified using radioactive microspheres before and after 5 min of occlusion and finally when fetal mean arterial blood pressure had decreased below 25 mm Hg, 9.8 (0.8) [mean (SD)] min after occlusion. Right coronary arterial (RCA) blood flow velocity and carotid BF were registered continuously. Mean values of arterial pH and oxygen content (mL O 2 /100 mL) were 7.08 (0.11) and 4.4 (2.9) before cord occlusion and decreased to 6.83 (0.05) and 1.4 (0.9) at 5 min after occlusion (p Ͻ 0.01, respectively). Carotid BF was significantly below preocclusion values by 2.5 min (p Ͻ 0.05), whereas RCA velocity time integral per minute remained above preocclusion values for 9 min. CBF decreased from 316 (24) before cord occlusion to 156 (30) mL/min/100 g at 5 min (p Ͻ 0.01), whereas right myocardial BF was maintained at 792 (125) and 751 (183) mL/min/100 g, respectively. CBF decreased rapidly after total cord occlusion whereas myocardial BF increased and was maintained until shortly before cardiac arrest, suggesting the myocardium to be better preserved during this type of insult in already partially asphyxiated fetuses. The vascular response of the heart and brain to acute asphyxia in the late gestation fetus varies according to type and rapidity of insult. As opposed to the centralization of flow in fetal hypoxemia with a well-established compensatory increase to the brain and heart, acute asphyxia may result in a variety of vascular responses. Total cord occlusion has resulted in an early decrease in carotid blood flow, suggesting a vulnerability of the fetal brain during an early stage of the insult (1). The decrease in carotid blood flow and cerebral blood volume was accompanied by an increase in carotid vascular resistance.Localization of regional brain damage has been attributed to differences in timing of the asphyxial insult (2, 3). The regional vascular response within the brain during the asphyxial insult has been sparsely investigated. Thus, differences in vascular reactivity within the brain due to variations in type and timing of the insult may predispose to selective regional vulnerability of brain structures.A previous study reporting an early decrease in carotid blood flow during acute asphyxia with maintained blood pressure suggested that this decrease was not due to cardiac compromise (1). We postulated that myocardial and cerebral perfusion are differentially regulated during acute asphyxia. Studies of early concomitant changes in CBF and myocardial BF in response to sustained periods of total cord occlusion have not been per-

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Section: Discussioncontrasting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Different Responses of Myocardial and Cerebral Blood Flow to Cord Occlusion in Exteriorized Fetal Sheep

et al. 2004

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“…Earlier results support this possibility to some extent, although previous findings vary considerably depending on experimental circumstances. After partial cord occlusion, increases in cerebral blood flow range from 43 to 100% [3,10], and could account for significant reductions in brain temperature. However during complete occlusion of the cord for 5 min, as carried out here, cerebral blood flow does not increase at all when measured directly with ultra-670 Fig.…”

Section: Increases In Cerebral Blood Flowmentioning

confidence: 99%

Brain temperature and metabolic responses during umbilical cord occlusion in fetal sheep

Kubonoya

Yoneyama

Sawa

et al. 1998

Pfl�gers Archiv European Journal of Physiology

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The purpose of this study was to compare core body and brain temperatures after complete but intermittent occlusions of the umbilical cord. Thermocouple probes were placed in the parasagittal parietal cortex, ascending aorta, and jugular vein of eight near-term fetal sheep and in the maternal descending aorta. Three days later, after an initial control period, the umbilical cord was occluded for 5 min, followed by a 30-min recovery period, and this cycle was repeated 4 times. Temperature changes, blood gases, and plasma glucose, lactate and adenosine were measured. In the first occlusion period, body core temperature increased 0.12 degreesC over control, and then declined to baseline after cord release, and this pattern was repeated with subsequent occlusions. Brain temperature, however, did not increase in response to any of the cord occlusions. Plasma adenosine increased 2.4-fold during the first occlusion, but not during subsequent occlusions, despite a continuing pattern of constant brain temperature, a result which minimizes adenosine's importance as a continuing regulator of cerebral metabolism. We conclude that brain temperature fails to increase because of diminished heat production by the brain and increases in cerebral blood flow, responses which delay complete depletion of adenosine 5'-triphosphate stores in brain tissue.

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“…This mechanism is the same with fetal hypoxia also. During fetal hypoxia, blood flow is shunted away from nonvital organs, such as intestine, the skin, and kidney [9,37,38]. Whereas the pathogenesis of NEC is not obvious, it is very difficult to explain how maternal nicotine exposure increases the severity of hypoxic intestinal injury in the newborn rats.…”

Section: Discussionmentioning

confidence: 99%

Does maternal nicotine exposure during gestation increase the injury severity of small intestine in the newborn rats subjected to experimental necrotizing enterocolitis

Özkan

Özokutan

İnanç

et al. 2005

Journal of Pediatric Surgery

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Regional blood flow and metabolism in ovine fetuses during severe cord occlusion

Cited by 45 publications

References 14 publications

Different Responses of Myocardial and Cerebral Blood Flow to Cord Occlusion in Exteriorized Fetal Sheep

Different Responses of Myocardial and Cerebral Blood Flow to Cord Occlusion in Exteriorized Fetal Sheep

Brain temperature and metabolic responses during umbilical cord occlusion in fetal sheep

Does maternal nicotine exposure during gestation increase the injury severity of small intestine in the newborn rats subjected to experimental necrotizing enterocolitis

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