Mesenteric vascular bed responsiveness in bile duct-ligated rats: roles of opioid and nitric oxide systems

Namiranian, Khodadad; Samini, Morteza; Mehr, Shahram Ejtemaei; Gaskari, Seyed Ali; Rastegar, Hossein; Homayoun, Houman; Dehpour, Ahmad Reza

doi:10.1016/s0014-2999(01)01091-3

Cited by 46 publications

(48 citation statements)

References 29 publications

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“…Sham-naltrexone (n = 8) or cirrhotic-naltrexone (n = 8) rats were injected with sub-cutaneous naltrexone hydrochloride (20 mg/kg/ day, s.c.) for 28 days post sham procedure or bile duct ligation [4,5]. In chronic naltrexone treatment, the last doses of the drugs were injected 16 h before the experimental protocol.…”

Section: Study Groupsmentioning

confidence: 99%

“…Opioid peptides contribute partly to the manifestations of liver disease such as fatigue, pruritis, ascitis and hepatic encephalopathy. There are also emerging reports on the role of opioid system in the pathophysiology of cardiovascular hyporesponsiveness in short-term cholestasis [4,5]. However there is not any data regarding the contribution of endogenous opioid system to hyperdynamic circulation of cirrhosis which is a more common clinical situation with worldwide importance.…”

Section: Introductionmentioning

confidence: 99%

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Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis

et al. 2008

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Arterial vasodilation with concomitant hyperdynamic circulation is a common finding in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritus, ascitis, and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20 mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGregor method and then phenylephrine vasoconstrictor response of mesenteric vessels (10(-10) to 10(-6 )mol) was examined. In order to evaluate the effects of acute opioid receptor blockade, additional groups of animals were treated by acute single intraperitoneal naltrexone injection (20 mg/kg). Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P < 0.01). Chronic opioid receptor blockade significantly increased this parameter (P < 0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while chronic naltrexone treatment completely improved it (P < 0.01). Acute single injection of naltrexone could not influence the understudied homodynamic parameters. Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidence on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis which is not directly correlated to high plasma NO levels.

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Section: Study Groupsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis

et al. 2008

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“…The administration of L-NAME at 1 mg/kg dose decreased apoptosis [3]. Other studies indicated that administration of guanidine as a nitric oxide inhibitor reduces the rate of apoptosis [4,13]. In this study, Namiranian et al showed that L-NAME at 1 mg/kg dosage did not have meaningful effects on the testis of cholestatic rats.…”

Section: Discussionmentioning

confidence: 48%

“…It will protect the stomach from indometacin side effects [1]. Namiranian et al displayed that nitric oxide synthase inhibitor (L-NAME) at a dose of 1 mg/kg did not have any effect on complications of cholestasis [4].…”

Section: Introductionmentioning

confidence: 99%

Effects of nitric oxide synthase inhibitor (L-NAME) on cytopathologic changes due to cholestasis in hepatic cells of adult male rats

Monsef

2012

pjp

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Obstructive cholestasis is associated with overproduction of endogenous opioids, nitric oxide (NO) and cytokines in the blood stream. Nitro-L-arginine methyl ester (L-NAME) administration decreases the NO serum level and it is able to reduce related complications. The aim of this research is to survey the effects of the NO inhibitor on complications relating to cholestasis in liver cells and intrahepatic biliary ducts. We used five groups of animals: control, sham-operated (surgical control), bile duct ligated (BDL) group, BDL and normal saline infused group, and BDL with L-NAME administrated group. After 3 weeks all animals were killed, histopathology of liver cells and intrahepatic biliary ducts were evaluated by hematoxylin-eosin (HE), PAS (periodic acid-Schiff) and trichrome staining. The status of inflammation and fibrosis was evaluated by the modified Knodell score system. Microscopic study of different groups showed that the necro-inflammatory score in the control group was 0.36, it was 1 in the sham-operated group and it raised to 15.2 in the cholestatic group. After administration of L-NAME it had a meaningful decrease to 7, but in the saline-treated group, the score was 16. L-NAME with the mentioned dose was capable of decreasing the serum nitric oxide level, although it is able to decrease the unfavorable complications of cholestatic jaundice.

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“…Namiranian et al [89] reported that acetylcholine (ACh)-induced vasodilatation, but not SNP-induced vasodilatation, in isolated perfused mesenteric artery was impaired in bile duct-ligated rats, and chronic treatment with L-NAME or naltrexone partially restored the response to ACh, suggesting that the impaired AChinduced vasodilatation in cholestatic rats was due to a defect in endothelial function. These authors speculated that an increased level of endogenous opioids in bile duct-ligated rats chronically increased [Ca 2+ ]i [90]; thus, ACh could no longer increase the [Ca 2+ ]i level to stimulate cNOS to release NO.…”

Section: Vascular Endothelium and Smooth Musclementioning

confidence: 99%

Interactions between morphine and nitric oxide in various organs

Toda¹,

Kishioka

Hatano

et al. 2009

J Anesth

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Nitric oxide (NO) plays obligatory roles as an important intercellular messenger in the control of physiological functions and it also participates in pathophysiological interventions. This labile, gaseous molecule is also involved in mechanisms underlying the beneficial and untoward actions of therapeutic agents. Endogenous NO is formed by endothelial and neurogenic NO synthases that are constitutively present mainly in the endothelium and nervous system, respectively, and is induced by lipopolysaccharides or cytokines mainly in mitochondria, glial cells, and vascular smooth muscle cells. NO modulates the effects of morphine on processes involving the central nervous system, such as learning, memory, convulsion, thermoregulation, and penile erection. This molecule is also involved in the modification of morphine actions on the cardiovascular, digestive, and respiratory systems. Morphine regulates NO bioavailability in various organs. NO formed by inducible NO synthase participates in some morphine actions in the immune system. Information concerning interactions between NO and morphine and other opioids in a variety of organs and tissues is quite useful in establishing new strategies for minimizing the noxious and unintended reactions that are frequently encountered during analgesic therapy.

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Mesenteric vascular bed responsiveness in bile duct-ligated rats: roles of opioid and nitric oxide systems

Cited by 46 publications

References 29 publications

Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis

Opioid Receptor Blockade Improves Mesenteric Responsiveness in Biliary Cirrhosis

Effects of nitric oxide synthase inhibitor (L-NAME) on cytopathologic changes due to cholestasis in hepatic cells of adult male rats

Interactions between morphine and nitric oxide in various organs

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