Effect of Ethanol on 15-Hydroxyprostaglandin Dehydrogenase Activity in the Brain Stem of the Near-Term Fetal Sheep

1991 ◽  
Vol 16 (1) ◽  
pp. 48-52 ◽  
Author(s):  
Deirdre Treissman ◽  
Graeme N. Smith ◽  
John Patrick ◽  
James F. Brien
Keyword(s):  
Brain Stem ◽  
Dehydrogenase Activity ◽  
Fetal Sheep ◽  
Near Term ◽  
The Brain

Thalamic Locus Mediates Hypoxic Inhibition of Breathing in Fetal Sheep

1998 ◽  
Vol 79 (5) ◽  
pp. 2383-2393 ◽  
Author(s):  
Brian J. Koos ◽  
Andrew Chau ◽  
Masahiko Matsuura ◽  
Oscar Punla ◽  
Lawrence Kruger
Keyword(s):  
Brain Stem ◽  
Ibotenic Acid ◽  
Nuclear Region ◽  
Fetal Sheep ◽  
Nuclear Complex ◽  
Fetal Breathing ◽  
The Brain

Koos, Brian J., Andrew Chau, Masahiko Matsuura, Oscar Punla, and Lawrence Kruger. Thalamic locus mediates hypoxic inhibition of breathing in fetal sheep. J. Neurophysiol. 79: 2383–2393, 1998. The effects of lesions rostral to the brain stem on breathing responses to hypoxia were determined in chronically catheterized fetal sheep (>0.8 term). These studies were designed to test the hypothesis that the diencephalon is involved in hypoxic inhibition of fetal breathing. As in normal fetuses, hypoxia inhibited breathing with transection rostral to the thalamus or transection resulting in virtual destruction of the thalamus but sparing most of the parafascicular nuclear complex. Neuronal lesions were produced in the fetal diencephalon by injecting ibotenic acid through cannulas implanted in the brain. Hypoxic inhibition of breathing was abolished when the lesions encompassed the parafascicular nuclear complex but was retained when the lesions spared the parafascicular nuclear region or when the vehicle alone was injected. A new locus has been identified immediately rostral to the midbrain, which is crucial to hypoxic inhibition of fetal breathing. This thalamic sector involves the parafascicular nuclear complex and may link central O2-sensing cells to motoneurons that inhibit breathing.

Adenosine stimulates breathing in fetal sheep with brain stem section

1992 ◽  
Vol 72 (1) ◽  
pp. 94-99 ◽  
Author(s):  
B. J. Koos ◽  
A. Chao ◽  
W. Doany
Keyword(s):  
Brain Stem ◽  
Blood Gases ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Arterial Infusion ◽  
Fetal Sheep ◽  
Stem Section ◽  
Peripheral Arterial ◽  
Arterial Po2 ◽  
The Brain ◽  
Pontomedullary Junction

Breathing responses to adenosine were determined in 12 chronically catheterized fetal sheep (greater than 0.8 term) in which hypoxic inhibition of breathing had been eliminated by brain stem section. The caudal extent of transection varied from the rostral midbrain to the pontomedullary junction. Isocapnic hypoxia [delta arterial PO2 (PaO2) of -12 Torr] doubled the incidence and depth of breathing activity and increased the incidence of eye movements. Intra-arterial infusion of adenosine (0.30 +/- 0.03 mg.min-1.kg fetal wt-1) increased the incidence and amplitude of breathing without affecting blood gases. Adenosine did not significantly alter the incidence of eye activity. Intra-arterial injection of oligomycin (120 +/- 26 micrograms/kg fetal wt), an inhibitor of mitochondrial oxidative phosphorylation, also stimulated breathing activity. In four fetuses with brain stem section, peripheral arterial chemodenervation blunted the stimulatory effects of hypoxia on breathing activity and abolished altogether the excitatory effects of adenosine. It is concluded that 1) hypoxia and adenosine likely inhibit breathing in normal fetuses by affecting similar areas of the brain stem and 2) in fetuses with brain section, hypoxic hyperpnea depends on peripheral and central mechanisms, whereas adenosine stimulates breathing via the peripheral arterial chemoreceptors.

Respiratory Effects of H+ and Dinitrophenol Injections into the Brain Stem Subarachnoid Space of Fetal Lambs

1975 ◽  
Vol 53 (5) ◽  
pp. 726-733 ◽  
Author(s):  
A. H. Jansen ◽  
B. J. Russell ◽  
V. Chernick
Keyword(s):  
Brain Stem ◽  
Subarachnoid Space ◽  
Extracellular Fluid ◽  
Ventral Surface ◽  
Metabolic Inhibitors ◽  
Blood Gas ◽  
Respiratory Response ◽  
Fetal Sheep ◽  
Arterial Ph ◽  
The Brain

Mock cerebrospinal fluid (pH 5.37–8.38) or 2,4-dinitrophenol (DNP) (0.15–1.5 mg) was injected into the subarachnoid space of the ventral brain stem of exteriorized fetal sheep. Changes in pH on the ventral surface of the medulla did not stimulate respiratory efforts or induce significant cardiovascular changes. The respiratory response to DNP injections ranged from no response to prolonged rhythmic ventilation that was independent of the peripheral chemoreceptors or the control arterial pH and blood gas tensions. This inconsistency suggests an effector site somewhat removed from the immediate surface of the medulla. The heart rate and blood pressure were not affected. It is concluded that increased H+ concentration in the extracellular fluid of the fetal ventral medulla does not initiate respiration, and any respiratory response to metabolic inhibitors applied to this area therefore is not attributable to a secondary change in surface pH.

scholarly journals Cerebral Oxygenation during Postasphyxial Seizures in Near-Term Fetal Sheep

2005 ◽  
Vol 25 (7) ◽  
pp. 911-918 ◽  
Author(s):  
Hernan Gonzalez ◽  
Christian J Hunter ◽  
Laura Bennet ◽  
Gordon G Power ◽  
Alistair J Gunn
Keyword(s):  
Blood Flow ◽  
Tissue Oxygenation ◽  
Cerebral Oxygenation ◽  
Immature Brain ◽  
Fetal Sheep ◽  
Blood Temperature ◽  
Cerebral Tissue Oxygenation ◽  
A1 Receptor ◽  
Near Term ◽  
The Brain

After exposure to asphyxia, infants may develop both prolonged, clinically evident seizures and shorter, clinically silent seizures; however, their effect on cerebral tissue oxygenation is unclear. We therefore examined the hypothesis that the increase in oxygen delivery during postasphyxial seizures might be insufficient to meet the needs of increased metabolism, thus causing a fall in tissue oxygenation, in unanesthetized near-term fetal sheep in utero (gestational age 125 ± 1 days). Fetuses were administered an infusion of the specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine, followed by 10 mins of asphyxia induced by complete umbilical cord occlusion. The fetuses then recovered for 3 days. Sixty-one episodes of electrophysiologically defined seizures were identified in five fetuses. Tissue PO2 (tPO2) did not change significantly during short seizures (<3.5 mins), 5.2 ± 0.2 versus baseline 5.6 ± 0.1 mm Hg (NS), but fell to 2.2 ± 0.2 mm Hg during seizures lasting more than 3.5 mins ( P<0.001). During prolonged seizures, cortical blood flow did not begin to increase until tPO2 had begun to fall, and then rose more slowly than the increase in metabolism, with a widening of the brain to blood temperature gradient. In conclusion, in the immature brain, during prolonged, but not short seizures, there is a transient mismatch between cerebral blood flow and metabolism leading to significant cerebral deoxygenation.

scholarly journals Hemodynamic and metabolic responses to moderate asphyxia in brain and skeletal muscle of late-gestation fetal sheep

2000 ◽  
Vol 88 (1) ◽  
pp. 82-90 ◽  
Author(s):  
J. P. Newman ◽  
D. M. Peebles ◽  
S. R. G. Harding ◽  
R. Springett ◽  
M. A. Hanson
Keyword(s):  
Redox State ◽  
Near Infrared ◽  
Metabolic Response ◽  
Hemoglobin Concentration ◽  
Late Gestation ◽  
Significant Drop ◽  
Fetal Sheep ◽  
Internal Iliac ◽  
Near Term ◽  
The Brain

The purpose of this study was to investigate metabolic and hemodynamic responses in two fetal tissues, hindlimb muscle and brain, to an episode of acute moderate asphyxia. Near-infrared spectroscopy was used to measure changes in total hemoglobin concentration ([tHb]) and the redox state of cytochrome oxidase (COX) simultaneously in the brain and hindlimb of near-term unanesthetized fetal sheep in utero. Oxygen delivery (Do 2) to, and consumption (V˙o 2) by, each tissue was derived from the arteriovenous difference in oxygen content and blood flow, measured by implanted flow probes. One hour of moderate asphyxia ( n = 11), caused by occlusion of the maternal common internal iliac artery, led to a significant fall in Do 2to both tissues and to a significant drop inV˙o 2 by the head. This was associated with an initial fall in redox state COX in the leg but an increase in the brain. [tHb], and therefore blood volume, fell in the leg and increased in the brain. These data suggest the presence of a fetal metabolic response to hypoxia, which, in the brain, occurs rapidly and could be neuroprotective.

Permeability of the microcirculation in area postrema of rat

1988 ◽  
Vol 46 ◽  
pp. 348-349
Author(s):  
Shams M. Ghoneim ◽  
Frank M. Faraci ◽  
Gary L. Baumbach
Keyword(s):  
Brain Stem ◽  
Area Postrema ◽  
Upper Body ◽  
Sprague Dawley ◽  
Sodium Cacodylate ◽  
Acute Hypertension ◽  
Sprague Dawley Rats ◽  
Ultrastructural Characteristics ◽  
The Brain ◽  
Adjacent Brain

The area postrema is a circumventricular organ in the brain stem and is one of the regions in the brain that lacks a fully functional blood-brain barrier. Recently, we found that disruption of the microcirculation during acute hypertension is greater in area postrema than in the adjacent brain stem. In contrast, hyperosmolar disruption of the microcirculation is greater in brain stem. The objective of this study was to compare ultrastructural characteristics of the microcirculation in area postrema and adjacent brain stem.We studied 5 Sprague-Dawley rats. Horseradish peroxidase was injected intravenously and allowed to circulate for 1, 5 or 15 minutes. Following perfusion of the upper body with 2.25% glutaraldehyde in 0.1 M sodium cacodylate, the brain stem was removed, embedded in agar, and chopped into 50-70 μm sections with a TC-Sorvall tissue chopper. Sections of brain stem were incubated for 1 hour in a solution of 3,3' diaminobenzidine tetrahydrochloride (0.05%) in 0.05M Tris buffer with 1% H2O2.

Surgical Approaches to the Brain Stem

1993 ◽  
Vol 4 (3) ◽  
pp. 457-468 ◽  
Author(s):  
Dennis Y. Wen ◽  
Roberto C. Heros
Keyword(s):  
Brain Stem ◽  
Surgical Approaches ◽  
The Brain

ADRENERGIC INPUTS TO THE AMYGDALA AND THE CONTROL OF GONADOTROPHIN RELEASE

1979 ◽  
Vol 90 (3) ◽  
pp. 385-393 ◽  
Author(s):  
José Borrell ◽  
Flavio Piva ◽  
Luciano Martini
Keyword(s):  
Brain Stem ◽  
Dopamine Receptor ◽  
Serum Levels ◽  
Female Rats ◽  
Receptor Blocker ◽  
Dopaminergic Drug ◽  
Gonadotrophin Secretion ◽  
Biphasic Effect ◽  
Adrenergic Blocker ◽  
The Brain

ABSTRACT Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.

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