L-Canavanine restores blood pressure in a rat model of endotoxic shock

Teale, David M.; Atkinson, A M

doi:10.1016/0014-2999(94)90268-2

Cited by 28 publications

(11 citation statements)

References 15 publications

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“…When activated by bacterial toxins such as LPS, macrophages inhibit the growth of a wide variety of invasive microorganisms through releasing factors such as nitric oxide (NO), result in the loss of vascular tone and hypotension primarily through the increase of NO (Teale and Atkinson, 1994).…”

Section: Introductionmentioning

confidence: 99%

San-Huang-Xie-Xin-Tang reduces lipopolysaccharides-induced hypotension and inflammatory mediators

Tsai

Huang

et al. 2005

Journal of Ethnopharmacology

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Section: Introductionmentioning

confidence: 99%

San-Huang-Xie-Xin-Tang reduces lipopolysaccharides-induced hypotension and inflammatory mediators

Tsai

Huang

et al. 2005

Journal of Ethnopharmacology

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“…In the present study, N G -nitro-L-arginine methyl ester (L-NAME ; a non-selective inhibitor of NOS [28]) and Lcanavanine (a specific inhibitor of iNOS [29,30]) were used to clarify which isoform of NOS is involved in the pathogenesis of glypressin hyposensitivity. In addition, we also investigated whether the addition of HOE 140 (a bradykinin B # receptor antagonist [31,32]) may enhance the portal-hypotensive effect of glypressin in haemor-rhage\transfused portal-hypertensive rats.…”

Section: Introductionmentioning

confidence: 99%

Splanchnic hyposensitivity to glypressin in a haemorrhage/transfused rat model of portal hypertension: role of nitric oxide and bradykinin

Chu

Lee

et al. 2000

Clinical Science

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Hyposensitivity to vasopressin is a well documented phenomenon in animals with portal hypertension and patients with cirrhosis subject to haemorrhage. Haemorrhage is associated with the endogenous release of bradykinin, which may subsequently stimulate the formation of nitric oxide (NO). The present study investigated the relative contribution of NO synthase (NOS) isoforms and the role of bradykinin in the pathogenesis of splanchnic hyposensitivity to a long-acting vasopressin analogue, glypressin, in rats with portal hypertension induced by partial portal vein ligation (PVL). At 14 days after the operation, systemic and portal haemodynamics were measured in stable or bleeding PVL rats receiving an intravenous infusion of glypressin (0.07 mg/kg). In the treatment groups, N(G)-nitro-L-arginine methyl ester (L-NAME; a non-selective NOS inhibitor), L-canavanine (a specific inhibitor of inducible NOS) or HOE 140 (a bradykinin B(2) receptor antagonist) was administered 45 min before the infusion of glypressin. In rats with a hypotensive haemorrhage, 4.5 ml of blood was withdrawn and 50% of the withdrawn blood was re-infused before the administration of glypressin or various inhibitors. Splanchnic hyposensitivity to glypressin was demonstrated in the haemorrhage/transfused PVL rats. The infusion of L-NAME elevated the mean arterial pressure in the bleeding PVL rats without the modulation of portal pressure. The addition of L-NAME or HOE 140, but not L-canavanine, significantly and similarly potentiated the portal-hypotensive effects of glypressin. It is concluded that constitutive NOS and bradykinin are responsible, at least partly, for the splanchnic hyposensitivity to glypressin observed in the early stages of the haemorrhage/transfused rat model of portal hypertension.

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“…NOS inhibition can be nonselective or selective for iNOS, which is predominantly synthesized during inflammation. In animal studies, nonselective NOS inhibition improved haemodynamics but increased mortality [97,98]. The use of nonselective NOS inhibitors in patients with septic shock was terminated early because of increased mortality [99].…”

Section: Nos Inhibitorsmentioning

confidence: 99%

Role of Mitochondrial Oxidative Stress in Sepsis

2018

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Sepsis is one of the most important causes of death in intensive care units. Despite the fact that sepsis pathogenesis remains obscure, there is increasing evidence that oxidants and antioxidants play a key role. The imbalance of the abovementioned substances in favor of oxidants is called oxidative stress, and it contributes to sepsis process. The most important consequences are vascular permeability impairment, decreased cardiac performance, and mitochondrial malfunction leading to impaired respiration. Nitric oxide is perhaps the most important and well-studied oxidant. Selenium, vitamin C, and 3N-acetylcysteine among others are potential therapies for the restoration of redox balance in sepsis. Results from recent studies are promising, but there is a need for more human studies in a clinical setting for safety and efficiency evaluation.

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L-Canavanine restores blood pressure in a rat model of endotoxic shock

Cited by 28 publications

References 15 publications

San-Huang-Xie-Xin-Tang reduces lipopolysaccharides-induced hypotension and inflammatory mediators

San-Huang-Xie-Xin-Tang reduces lipopolysaccharides-induced hypotension and inflammatory mediators

Splanchnic hyposensitivity to glypressin in a haemorrhage/transfused rat model of portal hypertension: role of nitric oxide and bradykinin

Role of Mitochondrial Oxidative Stress in Sepsis

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