Effects of Dopamine Infusion on Cerebral Blood Flow, Brain Cell Membrane Function and Energy Metabolism in Experimental<i>Escherichia coli</i>Meningitis in the Newborn Piglet

Park, Won Soon; Chang, Yun Sil; Shim, Jae Won; Kim, Mi Jung; Ko, Sun Young; Kim, Sung Shin; Hwang, Jong Hee; Choi, Chang Won; Lee, Munhyang

doi:10.3346/jkms.2003.18.6.869

Cited by 8 publications

(8 citation statements)

References 31 publications

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“…In accordance with other studies (26, 27), our data of maintenance of adequate CPP by simultaneous improvement of reduced MAP and increased ICP with HTS infusion in this study suggest the possibility that HTS could also be an attractive adjunctive therapy to prevent cerebral ischemia and the ensuing brain injury in bacterial meningitis.…”

Section: Discussionsupporting

confidence: 92%

“…The anti-inflammatory property of HTS might not be attributable to a stabilization of hemodynamics because we have observed that maintenance of adequate CPP and cerebral blood flow with dopamine infusion did not attenuate the acute inflammatory responses in our previous study of experimental bacterial meningitis ( 26 ). Which effect of HTS, either anti-inflammatory effect or improvement of CPP, might have been primary in the attenuation of brain injury observed in the present study is a subject of intricacy, because these two effects are related to each other, in which as meningeal inflammation decreases, CPP accordingly increases ( 28 ).…”

Section: Discussionmentioning

confidence: 84%

“…Besides the acute inflammatory responses, cerebral ischemia resulting from the critical reduction of CPP with intracranial hypertension and systemic hypotension may have an additional and even critical role in the pathogenesis of brain injury during bacterial meningitis ( 2 , 4 , 5 , 26 , 27 ). In accordance with other studies ( 26 , 27 ), our data of maintenance of adequate CPP by simultaneous improvement of reduced MAP and increased ICP with HTS infusion in this study suggest the possibility that HTS could also be an attractive adjunctive therapy to prevent cerebral ischemia and the ensuing brain injury in bacterial meningitis.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Hypertonic (7%) Saline on Brain Injury in Experimental Escherichia coli Meningitis

et al. 2005

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We sought to know whether hypertonic (7%) saline (HTS) attenuates brain injury by improving cerebral perfusion pressure (CPP) and down-modulating acute inflammatory responses in experimental bacterial meningitis in the newborn piglet. Twenty-five newborn piglets were assorted into three groups: 6 in the control group (C), 10 in the meningitis group (M), and 9 in the meningitis with HTS infusion group (H). Meningitis was induced by intracisternal injection of 108 colony forming units of Escherichia coli in 100 µL of saline. 10 mL/kg of HTS was given intravenously as a bolus 6 hr after induction of meningitis, thereafter the infusion rate was adjusted to maintain the serum sodium level between 150 and 160 mEq/L. HTS significantly attenuated meningitis-induced brain cell membrane disintegration and dysfunction, as indicated by increased lipid peroxidation products and decreased Na+, K+-ATPase activity in the cerebral cortex in M. HTS significantly attenuated acute inflammatory markers such as increased intracranial pressure, elevated lactate level and pleocytosis in the cerebrospinal fluid observed in M. Reduced CPP observed in M was also significantly improved with HTS infusion. These findings implicate some attenuation of the meningitis-induced alterations in cerebral cortical cell membrane structure and function with HTS, possibly by improving CPP and attenuating acute inflammatory responses.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

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Effects of Hypertonic (7%) Saline on Brain Injury in Experimental Escherichia coli Meningitis

et al. 2005

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“…Well-known neuroprotective agents, such as xenon (Chakkarapani et al, 2010 ; Faulkner et al, 2011 ) or melatonin (Robertson et al, 2013 ), have also been demonstrated to augment hypothermia neuroprotection in the brain of injured piglets. We cannot rule out the possibility that brain damage was somehow mitigated in NV animals, since the use of dopamine infusion could reduce brain damage in some experimental models of newborn pigs (Park et al, 2003 ). However, neither CBD nor the combination of the therapies were associated with acute hypotensive episodes that would require inotropic support.…”

Section: Discussionmentioning

confidence: 99%

Effects of Cannabidiol and Hypothermia on Short-Term Brain Damage in New-Born Piglets after Acute Hypoxia-Ischemia

et al. 2016

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Hypothermia is a standard treatment for neonatal encephalopathy, but nearly 50% of treated infants have adverse outcomes. Pharmacological therapies can act through complementary mechanisms with hypothermia improving neuroprotection. Cannabidiol could be a good candidate. Our aim was to test whether immediate treatment with cannabidiol and hypothermia act through complementary brain pathways in hypoxic-ischemic newborn piglets. Hypoxic-ischemic animals were randomly divided into four groups receiving 30 min after the insult: (1) normothermia and vehicle administration; (2) normothermia and cannabidiol administration; (3) hypothermia and vehicle administration; and (4) hypothermia and cannabidiol administration. Six hours after treatment, brains were processed to quantify the number of damaged neurons by Nissl staining. Proton nuclear magnetic resonance spectra were obtained and analyzed for lactate, N-acetyl-aspartate and glutamate. Metabolite ratios were calculated to assess neuronal damage (lactate/N-acetyl-aspartate) and excitotoxicity (glutamate/Nacetyl-aspartate). Western blot studies were performed to quantify protein nitrosylation (oxidative stress), content of caspase-3 (apoptosis) and TNFα (inflammation). Individually, the hypothermia and the cannabidiol treatments reduced the glutamate/Nacetyl-aspartate ratio, as well as TNFα and oxidized protein levels in newborn piglets subjected to hypoxic-ischemic insult. Also, both therapies reduced the number of necrotic neurons and prevented an increase in lactate/N-acetyl-aspartate ratio. The combined effect of hypothermia and cannabidiol on excitotoxicity, inflammation and oxidative stress, and on cell damage, was greater than either hypothermia or cannabidiol alone. The present study demonstrated that cannabidiol and hypothermia act complementarily and show additive effects on the main factors leading to hypoxic-ischemic brain damage if applied shortly after the insult.

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“…However, the maintenance of adequate cerebral perfusion pressure, by pharmacologically preventing systemic hypotension with DA infusion, has been found to prevent cerebral ischemia and attenuates energy depletion and neuronal injury in a model of newborn piglets with meningitis. In this model, the decreased cerebral cortical cell membrane NKA activity and increased lipid peroxidation products, indicative of meningitis-induced brain damage, are significantly attenuated by DA infusion (74). Similarly, the decreased DA levels in the brain may be partly responsible for the decrease in NKA activity in the striatum of newborn piglets during posthypoxic reoxygenation (75).…”

Section: Da Receptor-mediated Regulation Of Nkamentioning

confidence: 84%

Crosstalk between dopamine receptors and the Na+/K+-ATPase (Review)

Zhang

Liang³

et al. 2013

Molecular Medicine Reports

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Abstract. Dopamine (DA) receptors, which belong to the G protein-coupled receptor family, are the target of ~50% of all modern medicinal drugs and constitute a large and diverse class of proteins whose primary function is to transduce extracellular stimuli into intracellular signals. Na + /K + -ATPase (NKA) is ubiquitous and crucial for the maintenance of intracellular ion homeostasis and excitability. Furthermore, it plays a critical role in diverse effects, including clinical cardiotonic and cardioprotective effects, ischemic preconditioning in the brain, natriuresis, lung edema clearance and other processes. NKA regulation is of physiological and pharmacological importance and has species-and tissue-specific variations. The activation of DA receptors regulates NKA expression/activity and trafficking in various tissues and cells, for example in the kidney, lung, intestine, brain, non-pigmented ciliary epithelium and the vascular bed. DA receptor-mediated regulation of NKA mediates a diverse range of cellular responses and includes endocytosis/exocytosis, phosphorylation/dephosphorylation of the α subunit of NKA and multiple signaling pathways, including phosphatidylinositol (PI)-phospholipase C/protein kinase (PK) C, cAMP/PKA, PI3K, adaptor protein 2, tyrosine phosphatase and mitogen-activated protein kinase/extracellular signal-regulated protein kinase. Furthermore, in brain and HEK293T cells, D 1 and D 2 receptors exist in a complex with NKA. Among D 1 and D 2 receptors and NKA, regulations are reciprocal, which leads to crosstalk between DA receptors and NKA. In the present study, the current understanding of signaling mechanisms responsible for the crosstalk between DA receptors and NKA, as well as with specific consequent functions, is reviewed.

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Effects of Dopamine Infusion on Cerebral Blood Flow, Brain Cell Membrane Function and Energy Metabolism in ExperimentalEscherichia coliMeningitis in the Newborn Piglet

Cited by 8 publications

References 31 publications

Effects of Hypertonic (7%) Saline on Brain Injury in Experimental Escherichia coli Meningitis

Effects of Hypertonic (7%) Saline on Brain Injury in Experimental Escherichia coli Meningitis

Effects of Cannabidiol and Hypothermia on Short-Term Brain Damage in New-Born Piglets after Acute Hypoxia-Ischemia

Crosstalk between dopamine receptors and the Na+/K+-ATPase (Review)

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