Effect of hyperglycemia on brain nitric oxide production in a rat model of forebrain ischemia and reperfusion: an in vivo microdialysis study

Background This study examined the influences of isoflurane versus halothane anesthesia on basal and agonist-stimulated nitric oxide in the cerebellum of intact rats. Nitric oxide was measured using the hemoglobin-trapping method in an in vivo microdialysis technique. This method uses the stoichiometric reaction of nitric oxide with oxyhemoglobin to produce methemoglobin and nitrate; the change in methemoglobin concentration is measured spectrophotometrically to estimate nitric oxide concentration. Methods Male Wistar rats were anesthetized with isoflurane (1.4%) or halothane (1.2%), mechanically ventilated and paralyzed (intravenous pancuronium, 1 mg/kg). Microdialysis probes were implanted into the cerebellum. Bovine oxyhemoglobin dissolved in artificial cerebrospinal fluid was pumped through the probe (2 microl/min) and assayed at 15-min intervals. The glutamatergic agonist, kainic acid (KA, 5 mg/kg, intraarterially), was used to stimulate nitric oxide production. NG-nitro L-arginine methyl ester (L-NAME, 40 mg/kg, intravenously) was used to inhibit nitric oxide synthase. Results Unstimulated cerebellar nitric oxide concentrations were stable and greater during anesthesia with isoflurane (532+/-31 nM; mean +/- SEM) than with halothane (303+/-23 nM). L-NAME pretreatment reduced nitric oxide concentrations during isoflurane, but not halothane, anesthesia. Infusion of KA increased nitric oxide in both groups; however, the increase in nitric oxide was significantly greater during isoflurane anesthesia. Pretreatment with L-NAME inhibited the response to KA in both groups. Conclusions Nitric oxide production in the cerebellum, monitored by microdialysis, was greater during isoflurane anesthesia than during halothane anesthesia. Increased nitric oxide production during isoflurane anesthesia would be expected to impact central neuronal function and cerebral blood flow and vascular resistance.

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Effects of Periodic Body Acceleration on the In Vivo Vasoactive Response to N-w-nitro–L-arginine and the In Vitro Nitric Oxide Production

Annals of Biomedical Engineering ◽

10.1114/1.1623486 ◽

2003 ◽

Vol 31 (11) ◽

pp. 1337-1346 ◽

Cited By ~ 28

Author(s):

Jose A. Adams ◽

James E. Moore, Jr. ◽

Michael R. Moreno ◽

Jaqueline Coelho ◽

Jorge Bassuk ◽

...

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Production ◽

Body Acceleration ◽

Oxide Production

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Modulation of in vivo alloreactivity by inhibition of inducible nitric oxide synthase.

Journal of Experimental Medicine ◽

10.1084/jem.181.1.63 ◽

1995 ◽

Vol 181 (1) ◽

pp. 63-70 ◽

Cited By ~ 158

Author(s):

N K Worrall ◽

W D Lazenby ◽

T P Misko ◽

T S Lin ◽

C P Rodi ◽

...

Keyword(s):

Nitric Oxide ◽

Immune Response ◽

Nitric Oxide Synthase ◽

Inducible Nitric Oxide Synthase ◽

Biologically Active ◽

Nitric Oxide Production ◽

Oxide Production ◽

Oxide Synthase ◽

Inducible Nitric Oxide

The role of nitric oxide in the immune response to allogeneic tissue was explored in an in vivo cardiac transplant model in the rat. Nitric oxide production during organ rejection was demonstrated by elevations in systemic serum nitrite/nitrate levels and by electron paramagnetic resonance spectroscopy. Messenger RNA for the inducible nitric oxide synthase enzyme was detected in the rejecting allografted heart, but not in the nonrejecting isografted heart. The enzyme was demonstrated to be biologically active by the in vitro conversion of L-arginine to L-citrulline and was immunohistochemically localized to the infiltrating inflammatory cells. Treatment with aminoguanidine, a preferential inhibitor of the inducible nitric oxide synthase isoform, prevented the increased nitric oxide production in the transplanted organ and significantly attenuated the pathogenesis of acute rejection. Aminoguanidine treatment prolonged graft survival, improved graft contractile function, and significantly reduced the histologic grade of rejection. These results suggest an important role for nitric oxide in mediating the immune response to allogeneic tissue. Inhibition of inducible nitric oxide synthase may provide a novel therapeutic modality in the management of acute transplant rejection and of other immune-mediated processes.

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Dithiocarbamate spin traps for in vivo detection of nitric oxide production in mice

Bioradicals Detected by ESR Spectroscopy ◽

10.1007/978-3-0348-9059-5_12 ◽

1995 ◽

pp. 163-171 ◽

Cited By ~ 4

Author(s):

C.-S. Lai ◽

A. M. Komarov

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Production ◽

Spin Traps ◽

Oxide Production ◽

In Vivo Detection

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Bioflavonoid-Induced Apoptosis and DNA Damage in Amastigotes and Promastigotes of Leishmania donovani: Deciphering the Mode of Action

Molecules ◽

10.3390/molecules26195843 ◽

2021 ◽

Vol 26 (19) ◽

pp. 5843

Author(s):

Shaila Mehwish ◽

Sanjay Varikuti ◽

Mubarak Ali Khan ◽

Tariq Khan ◽

Imdad Ullah Khan ◽

...

Keyword(s):

Nitric Oxide ◽

Dna Damage ◽

Leishmania Donovani ◽

Genetic Material ◽

Mechanisms Of Action ◽

Pcr Analysis ◽

Nitric Oxide Production ◽

Oxide Production ◽

Ic50 Values

Natural products from plants contain many interesting biomolecules. Among them, quercetin (Q), gallic acid (GA), and rutin (R) all have well-reported antileishmanial activity; however, their exact mechanisms of action are still not known. The current study is a step forward towards unveil the possible modes of action of these compounds against Leishmania donovani (the causative agent of visceral leishmaniasis). The selected compounds were checked for their mechanisms of action against L. donovani using different biological assays including apoptosis and necrosis evaluation, effects on genetic material (DNA), quantitative testing of nitric oxide production, ultrastructural modification via transmission electron microscopy, and real-time PCR analysis. The results confirmed that these compounds are active against L. donovani, with IC50 values of 84.65 µg/mL, 86 µg/mL, and 98 µg/mL for Q, GA, and R, respectively. These compounds increased nitric oxide production and caused apoptosis and DNA damage, which led to changes in the treated cells’ ultrastructural behavior and finally to the death of L. donovani. These compounds also suppressed essential enzymes like trypanothione reductase and trypanothione synthetase, which are critical for leishmanial survival. The selected compounds have high antileishmanial potentials, and thus in-vivo testing and further screening are highly recommended.

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