Cardiovascular responses and nitric oxide production in cerebral ischemic rats

Shin, Chang Yell; Lee, Nam In; Je, Hyun Dong; Kim, Jeong Soo; Sung, Ji Hyun; Kim, Do Kyung; Lee, Doo Won; Bae, Ki Lyong; Sohn, Uy Dong

doi:10.1007/bf02976947

Cited by 4 publications

(3 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another investigation has reported that nimodipine (0.3 mg/Kg, i.p.) did not inhibit the increases of NO concentration during ischemia, suggesting that increased NO was due to induction of Ca 2+ -independent NOS (56). Analysis of the effects of nimodipine (i.v.…”

mentioning

confidence: 98%

“…Of 14 studies investigating the effect of pharmacological treatment in ischemia-induced brain damage, 10 (44-53) reported a positive effect of nimodipine and four did not (54)(55)(56)(57). Another investigation has assessed only the displacement of 1,4-dihydropiridine Ca 2+ channel binding sites, labeled by (+)-[ 3 H]PN 200-110, after oral administration of nimodipine.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

120

View full text Add to dashboard Cite

Nimodipine is a 1,4-dihydropyridine-derivative Ca(2+)-channel blocker developed approximately 30 years ago. It is highly lipophilic, crosses the blood-brain barrier, and reaches brain and cerebrospinal fluid. Early treatment with nimodipine reduces the severity of neurological deficits resulting from vasospasm in subarachnoid haemorrhage (SAH) patients. In SAH, nimodipine reduced spasm-related deficits of all severities, but no spasm-unrelated deficits. This paper has reviewed preclinical studies on the influence of nimodipine in various animal models of cerebral ischemia, with particular attention toward investigations published in the last 10 years. These studies further support the main indication of nimodipine, by clarifying some mechanisms of the anti-ischemic activity of the compound. Papers reporting a possible role of nimodipine in epileptogenesis were also examined. Clinical studies on nimodipine were grouped into subarachnoid hemorrhage, acute ischemic stroke, cerebral ischemia without stroke, dementia disorders, and migraine. Clinical investigations have shown that the drug improves neurological outcome by reducing the incidence and severity of ischemic deficits in patients with SAH from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition. No relevant effects of treatment with nimodipine were reported for acute ischemic stroke, cerebral ischemia without stroke, and migraine, except than for cluster headache. The less pronounced cardiovascular effects of nimodipine compared to other dihydropyridine-type Ca(2+)-channel blockers probably accounts for its use out of label for treating patients affected by chronic cerebral ischemia and vascular cognitive impairment. However, the blood pressure-lowering effects of nimodipine should not be minimized, as clinical studies have documented lowering blood pressure in small groups of patients, including cases of withdrawn due to pronounced hypotension induced by nimodipine administration. In the area of vascular cognitive impairment, short-term benefits of nimodipine do not justify its use as a long-term anti-dementia drug, and benefits obtained in elderly patients affected by subcortical vascular dementia require to be confirmed by other groups and in larger scale trials. In conclusion, nimodipine is a safe drug with an important place in pharmacotherapy and with the main documentation for reduction in the severity of neurological deficits resulting from vasospasm in SAH patients.

show abstract

mentioning

confidence: 98%

mentioning

confidence: 99%

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Tomassoni

Lanari

Silvestrelli

et al. 2008

Clinical and Experimental Hypertension

120

View full text Add to dashboard Cite

show abstract

“…These results were consistent with the reported anxiolytic effects of NOS inhibitors [ 18 , 19 ] and compatible with the reports of Bonassoli et al [ 22 ] and Gonzaga et al [ 23 ] revealing that infusion of a nonselective NOS inhibitor, a selective nNOS inhibitor, or a selective inducible NOS (iNOS) inhibitor (N-([3-(aminomethyl)phenyl]methyl) ethanimidamide dihydrochloride) into the dorsolateral periaqueductal gray matter or into the dorsal raphe nucleus, respectively, attenuated EtOHW anxiety in rats 24 or 48 hours after discontinuation of EtOH. The expression of iNOS is induced in response to inflammatory and immune stimuli [ 29 ], and chronic EtOH may cause dysregulation of the immune system in the brain that can persist over a certain withdrawal time, while increased production of proinflammatory factors has shown to sensitize EtOHW anxiety [ 30 – 32 ]. However, in the present study, we did not examine the involvement of solitary iNOS, since it was not detected in the NTS of the protracted EtOHW rats in a preliminary experiment.…”

Section: Discussionmentioning

confidence: 99%

Solitary Nitric Oxide Signaling Mediates Mild Stress-Induced Anxiety and Norepinephrine Release in the Bed Nucleus of the Stria Terminalis during Protracted Ethanol Withdrawal

Zhao

Kim

Jiao

et al. 2021

Behavioural Neurology

View full text Add to dashboard Cite

Ethanol withdrawal (EtOHW) alters the pattern of neurohormonal and behavioral response toward internal and external stimuli, which mediates relapse to alcohol use even after a long period of abstinence. Increased noradrenergic signaling from the nucleus tractus solitarius (NTS) to the bed nucleus of the stria terminalis (BNST) during EtOHW underlies withdrawal-induced anxiety, while nitric oxide synthase (NOS) inhibitors injected into the periaqueductal area attenuate EtOHW-induced anxiety. Therefore, this study investigated the involvement of NOS within the NTS in anxiety and increased norepinephrine (NE) release in the BNST during protracted EtOHW in rats exposed to a mild stress. Rats were intraperitoneally administered 3 g/kg/day EtOH for 21 days followed by 28 days of withdrawal, and on the 28th day of withdrawal, the rats were subjected to restraint stress for 7 minutes. The elevated plus maze test was employed to evaluate anxiety-like behavior in rats, and in vivo microdialysis was used to measure the extracellular NE level in the BNST. In elevated plus maze tests, EtOHW rats but not EtOH-naive rats exhibited anxiety-like behavior when challenged with 7-minute mild restraint stress, which was, respectively, mitigated by prior intra-NTS infusion of the nitric oxide scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), nonselective NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME), or selective neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI). Each of these agents also decreased the plasma corticosterone levels in EtOHW rats. In in vivo microdialysis, prior intra-NTS infusion of carboxy-PTIO, L-NAME, or 7-NI attenuated the mild stress-induced NE release in the BNST of EtOHW rats. Additionally, EtOHW rats showed increased solitary nNOS gene and protein expression. Moreover, the anxiolytic effect of intra-NTS administration of 7-NI was abolished by subsequent intra-NTS administration of sodium nitroprusside. These results suggest that elevation of solitary nitric oxide signaling derived from nNOS mediates stress-precipitated anxiety and norepinephrine release in the BNST during protracted EtOHW.

show abstract

Goat cerebrovascular reactivity to ADP after ischemia–reperfusion. Role of nitric oxide, prostanoids and reactive oxygen species

et al. 2006

View full text Add to dashboard Cite

Cardiovascular responses and nitric oxide production in cerebral ischemic rats

Cited by 4 publications

References 31 publications

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Nimodipine and Its Use in Cerebrovascular Disease: Evidence from Recent Preclinical and Controlled Clinical Studies

Solitary Nitric Oxide Signaling Mediates Mild Stress-Induced Anxiety and Norepinephrine Release in the Bed Nucleus of the Stria Terminalis during Protracted Ethanol Withdrawal

Goat cerebrovascular reactivity to ADP after ischemia–reperfusion. Role of nitric oxide, prostanoids and reactive oxygen species

Contact Info

Product

Resources

About