Beagle pup model of perinatal asphyxia: nimodipine studies.

Ment, Laura R.; Stewart, William B.; Duncan, Charles C.; Pitt, Bruce R.

doi:10.1161/01.str.18.3.599

Cited by 17 publications

(10 citation statements)

References 56 publications

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“…In the present study a reduction in MABP of ap proximately 29% was observed after 15pg/ kg/min nimodipine infusion. This finding of a reduced MABP during nimodipine infusion is in agreement with several other studies [13,15,[17][18][19], and the response is not different from that reported with significantly lower dosage [13,17], This indicates that there is a plateau effect on nimodipine on MABP, prob ably at a significantly lower level than the 15 gg/kg/min used in the present investiga tion.…”

Section: Hypoxemia Followed By Nimodipine Infusion Physiological Varisupporting

confidence: 93%

“…In a study by Haws et al [13] in adult rabbits nimodipine infusion (0.1 and 1.0 pg/ kg/min) resulted in proportionately similar el evations in all brain regions (CBR, BS and CBL). On the other hand, Ment et al [18] found that nimodipine (2 pg/kg/min) reduced CBF to cortical and deep gray matter regions in a beagle pup model (24- 96 h old).…”

Section: Nimodipine Infusionmentioning

confidence: 97%

“…Experimental studies with nimodipine have resulted in variable results regarding ef fects on regional CBF and MABP [13, 15-Although most studies indicate that ni modipine increases CBF [13,16,17,19], some studies show only a slight increase [15], or even a reduction in CBF [18], In a study by Mohamed et al [ 17] in adult rats infusion of 1 and 4 gg/kg/min nimodipine resulted in sig 19].…”

Section: Nimodipine Infusionmentioning

confidence: 99%

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Effect of Nimodipine on Cerebral and Organ Blood Flow in Normal and Posthypoxemic Newborn Piglets

Odden

Roll²,

Hall³

et al. 1993

Dev Pharmacol Ther

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Using the isotope-labelled microsphere method, blood flow to the brain, the heart and the kidneys were studied in newborn piglets during nimodipine infusion. Twenty piglets were studied in two different groups. Group 1 (n = 8) was kept normoxic and given a continuous nimodipine infusion (15 µg/kg/min). Group 2 (n = 12) was made hypoxemic by breathing 10% O2 for 10 min followed by an identical nimodipine infusion as group 1. In spite of a significant systemic hypotension, nimodipine infusion alone significantly increased blood flow in the brain stem and right cardiac ventricle at 30-60 min of infusion, while blood flow to cerebellum, cerebrum and the left cardiac ventricle did not change. Blood flow to the kidneys decreased significantly. In posthypoxemic piglets nimodipine infusion gave almost similar flow patterns, however, the changes appeared at an earlier time. We conclude that in spite of a significant reduction in blood pressure, cerebral and cardiac blood flow is preserved both in normal and posthypoxemic animals even at high doses of nimodipine. However, because of the decreased blood flow to the kidneys further dose-response studies are needed before clinical use in asphyctic newborns.

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Section: Hypoxemia Followed By Nimodipine Infusion Physiological Varisupporting

confidence: 93%

Section: Nimodipine Infusionmentioning

confidence: 97%

Section: Nimodipine Infusionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Nimodipine on Cerebral and Organ Blood Flow in Normal and Posthypoxemic Newborn Piglets

Odden

Roll²,

Hall³

et al. 1993

Dev Pharmacol Ther

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“…Nimodipine did not improve CBF sagittal cortex suggested that both the duration of suppression or ECoG recovery after 5 min of total asphyxia in the beagle PUP postinsult ( r = 0.45) and the final ECoG intensity (22), and flunarizine did not reduce cerebral damage in the infant (r = -0.74, Fig. 3) were correlated with damage in the underlying rat after severe hypoxia-ischemia (23).…”

Section: Fisher's Exact Test) Of the Ecog Decreased Postinsult And Rmentioning

confidence: 97%

Flunarizine, a Calcium Channel Antagonist, Is Partially Prophylactically Neuroprotective in Hypoxic-Ischemic Encephalopathy in the Fetal Sheep

et al. 1994

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ABSTRACT. Calcium antagonist therapy has been reported to reduce neuronal death after hypoxia-ischemia; however, its potential use in prenatal hypoxic-ischemic events has received little attention. We examined the effect of pretreatment with flunarizine in chronically instrumented late gestation fetal sheep subjected to 30 min of cerebral ischemia. Eight fetuses were given 0.1 1 mmol(45 mg) of flunarizine over 2 h preischemia (high dose), 10 were given 0.07 mmol (30 mg) over 3 h preischemia (low dose), 17 were given nothing (ischemia controls), and 5 received neither the ischemic insult nor any treatment (sham controls). The fetal electrocorticogram was monitored for 3 d postinsult. Histologic outcome was quantified after 72 h. Low-dose, but not high-dose, flunarizine therapy was associated with an overall reduction in cerebral damage (p < 0.01), a greater final electrocorticogram intensity, and a reduction in the incidence of seizures ( p < 0.02) compared with ischemia controls. High-dose, but not lowdose, flunarizine was associated with a significant acute mortality and a decrease in fetal blood pressure ( p < 0.05) at the time of occlusion, although there was no effect on the initial hypertensive response to occlusion. These observations suggest that flunarizine is partially neuroprotective when given before severe global ischemia in utero, but that its hypotensive effects make it unsuitable for prophylactic administration in utero. (Pediatr Res 35: 657663, 1994)

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“…Over nearly two decades of research, these investigators stud ied a variety of issues concerning asphyxial brain disorders in the fetal and neonatal rhe sus monkey [1][2][3][4][5]. For the fetal studies, preg nant primates and the fetuses were subjected to varying types of insults at different gesta- [67] Cardiac arrest bv intravenous K.C1 administration [68] Exchange transfusion with RBC in which the Pso has been increased by the incorporation of inositol hexaphosphatc [74] (HIE studies not done using this method of insult) Hypertension to produce intracranial hemorrhage ' [64] Rodents In 7-day rat pups, ligation of left CCA. and after recov ery'.…”

Section: Nonhuman Primate Modelsmentioning

confidence: 99%

Some Animal Models for the Study of Perinatal Asphyxia

Raju¹

1992

Neonatology

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Much of our current understanding concerning the pathophysiology of perinatal brain disorders has evolved from animal studies over the past three decades. Fetal and neonatal nonhuman primate, pregnant sheep, lamb, puppy, piglet and immature rodents, all have been important animal models for perinatal brain research. Although no model can be considered Ê»perfect’ in reflecting the variety and complexity of human brain pathology, the investigator must assess the merits and limitations of each model within the framework of the research questions being asked. A variety of experimental designs have been used over the years and variations of particular interest are the animal age, the method of producing brain insult and the procedures used for evaluating outcomes. Most models relating to the study of intracranial hemorrhage, cerebral blood flow and cerebral energy metabolism have generally been acute preparations. Some important long-term survival models have also been developed in recent years for the study of hypoxicischemic encephalopathy. The latter include the nonhuman primate, piglet, sheep and immature rat models. In this article, I have reviewed some important animal models used in perinatal brain research with emphasis on those relating to perinatal asphyxia and intracranial hemorrhage.

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Beagle pup model of perinatal asphyxia: nimodipine studies.

Cited by 17 publications

References 56 publications

Effect of Nimodipine on Cerebral and Organ Blood Flow in Normal and Posthypoxemic Newborn Piglets

Effect of Nimodipine on Cerebral and Organ Blood Flow in Normal and Posthypoxemic Newborn Piglets

Flunarizine, a Calcium Channel Antagonist, Is Partially Prophylactically Neuroprotective in Hypoxic-Ischemic Encephalopathy in the Fetal Sheep

Some Animal Models for the Study of Perinatal Asphyxia

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