Effects Of Clonidine Pretreatment Research Articles

The effect of clonidine pretreatment on epidural resiniferatoxin in a neuropathic pain rat model.

Resiniferatoxin (RTX) is an ultrapotent synthetic TRPV1 (transient receptor potential vanilloid subtype 1) agonist with significant initial transient hyperalgesia followed by a prolonged analgesic effect in response to thermal stimulus. Using a rat model of neuropathic pain, we evaluated the effect of pretreatment with clonidine-which has been shown to relieve intradermal capsaicin-induced hyperalgesia-on the initial hyperalgesic response and the thermal analgesic property of RTX. Thirty-six male rats were divided into 6 treatment groups (n=6 each):RTX 500 ng, RTX 1 μg, clonidine 20 μg (Cl), Cl＋RTX 500 ng, Cl＋RTX 1 μg, or normal saline 20 μL (control). We evaluated the short-term (180 min) and long-term (20 days) analgesic effects of RTX after thermal stimulation and mechanical stimulation. RTX had significant initial transient hyperalgesia followed by a prolonged analgesic effect in response to the thermal stimulus, but the RTX 500 ng and RTX 1 μg groups showed no initial short-term thermal hyperalgesic responses when pretreated with clonidine. The Cl＋RTX 1 μg rats' behavior scores indicated that they were more calm and comfortable compared to the RTX 1 μg rats. Even though we cannot precisely confirm that pretreatment with clonidine potentiates or adds to the analgesic effect of RTX, clonidine pretreatment with epidural RTX eliminated the initial RTX-associated hyperalgesic response and systemic toxicity in this neuropathic pain rat model.

Clonidine pre-treatment prevents hemorrhagic shock-induced endotoxemia and oxidative stress in the gut, liver, and lungs of the rat

ObjectivesTo study the effect of clonidine pre-treatment on hemorrhagic shock (H/S)-induced endotoxemia and oxidative stress (OS) in three vital organs of the rat.MethodsThe study protocol consisted of two arms: one for the measurement of organic hydroperoxide (LOOH) and superoxide radical (O2−·) production in the gut, liver, and lungs (n = 32 rats) and one for the measurement of endotoxin in portal and systemic circulation (n = 32 rats). Four animal groups (sham, clonidine, H/S, and clonidine-H/S group) were used in each arm. Three hours after H/S and concominant blood resuscitation, tissues were collected for LOOHs and O2−· measurement and blood samples were obtained for endotoxin determination.ResultsClonidine pre-treatment prior to H/S resulted in a significant reduction of LOOHs and O2−· production in all vital organs (P < 0.05–0.001), while additionally, clonidine reduced H/S-induced endotoxemia in portal (P < 0.05) and systemic circulation as well (P < 0.01).DiscussionClonidine pre-treatment prevents endotoxemia and OS in the gut, liver, and lungs of rats subjected to severe H/S. The improved intestinal barrier function probably stems from the antioxidant effect of clonidine on the intestinal epithelium, whereas the reduced endotoxemia may contribute to a decreased OS observed in the liver and lungs.

The Effect of Clonidine Pretreatment on Cardiovascular Response and Seizure Duration according to Electroconvulsive Therapy

The Effect of Clonidine Pretreatment on Cardiovascular Response and Seizure Duration according to Electroconvulsive Therapy

Effects of Clonidine Pretreatment on Bupivacaine-Induced Cardiac Toxicity Resuscitation in Dogs

Effects of Clonidine Pretreatment on Bupivacaine-Induced Cardiac Toxicity Resuscitation in Dogs

Regional extracellular norepinephrine responses to amphetamine and cocaine and effects of clonidine pretreatment

Microdialysis in behaving animals was used to characterize the hippocampus (HP) and prefrontal cortex (PFC) norepinephrine (NE) responses to amphetamine (AMPH) and cocaine (COC). NE exhibited regionally similar dose- and time-dependent increases to each drug. However, peak NE concentrations were ∼ 2-fold greater at behaviorally similar doses of AMPH compared with COC. To examine the role of noradrenergic impulse flow in the mechanism(s) by which these stimulants enhance extracellular NE, groups of animals were pretreated with the α 2 autoreceptor agonist, clonidine (CLON), prior to stimulant administration. CLON (50 μg/kg) administration completely blocked the NE response to both 20 and 30 mg/kg COC. By contrast, CLON decreased the NE response to 0.5 mg/kg AMPH by 75%, but became progressively less effective on the response as the dose was increased to 1.75 and 5.0 mg/kg. CLON also had no effect on the caudate dopamine responses to either AMPH or COC, consistent with the presumed specificity of this drug for α 2 receptors and suggesting the absence of any significant pharmacokinetic interactions. These results indicate that COC acts as an uptake blocker at NE-containing neurons and suggest that AMPH increases extracellular NE through two consequences of its interaction with the neuronal transport carrier: (1) reuptake blockade which predominates at lower doses; (2) release which becomes more prevalent at higher doses. Behavioral analyses revealed effects of CLON which varied as a function of stimulant and dose.

Effect of Clonidine Pretreatment on the Cardiovascular Toxicity Induced by Inrravenous Bupivacaine in Rabbits

This study was performed to evaluate the influence of clonidine pretreatment on the car- diovascular toxic effects of bupivacaine overdose induced by constant intravenous infusion. Thirty male rabbits were used for this study and they were divided into saline pretreatment group(15) and clonidine-pretreatment group(15). The changes of mean arterial pressure, heart rate and electrocardiogram by the bupivacaine-induced toxic effect during intravenous infusion of bupivacaine were observed. The results were as follows; 1. Mean arterial pressure was significantly decreased in clonidine-premedicated group compared with control group (P<0.01) before infusion of bupivacaine, but the times occuring 25% and 50% decrease of mean arterial pressure were significantly prolonged in clonidine group compared with control group (P <0.001 ). 2. Heart rate was significantly decreased in clonidine group compared with control group (P<0.01) before infusion of bupivacaine, but the times occuring 25% and 50% decrease of heart rate were significantly prolonged in clonidine group compared with control group (P< 0.001). 3. The times occuring the first QRS modification and first dysrhythmia and the final systole were significantly prolonged in clonidine group compared with control group (P < 0.001). In conclusion, clonidine given prophylactically delays the cardiotoxicity caused by bupivacaine overdose snd does not accentuate the subsequent hypotension.