Intravenous dexmedetomidine prolongs bupivacaine spinal analgesia

The prolongation of spinal anesthesia by using clonidine through the oral, intravenous and spinal route has been known. The new ?2 agonist, dexmedetomidine has been proved to prolong the spinal anesthesia through the intrathecal route. We hypothesized that dexmedetomidine when administered intravenously following spinal block, also prolongs spinal analgesia. 48 patients were randomly allocated into two equal groups following receiving spinal isobaric bupivacaine 12.5 mg. Patients in group D received intravenously a loading dose of 1 microg/kg dexmedetomidine over 10 min and a maintenance dose of 0.5 microg/kg/hr. Patients in group C [the control group] received normal saline. The regression times to reach S1 sensory level and Bromage 0 motor scale, hemodynamic changes and the level of sedation were recorded. The duration of sensory block was longer in intravenous dexmedetomidine group compared with control group [261.5 +/- 34.8 min versus 165.2 +/- 31.5 min, P < 0.05]. The duration of motor block was longer in dexmedetomidine group than control group [199 +/- 42.8 min versus 138.4 +/- 31.3 min, P < 0.05]. Intravenous dexmedetomidine administration prolonged the sensory and motor blocks of bupivacaine spinal analgesia with good sedation effect and hemodynamic stability

Role of peripheral alpha2 adrenergic receptors in tonic pain during different stages of estrous cycle in rats

Estrogen and progesterone are supposed to modify pain sensitivity. However, the actual role of each of these steroid hormones in this respect is not well known. Plasma concentrations of these hormones show variation during estrous cycle. The role of alpha2 receptors in tonic pain has been pointed out. The aim of the present study was to investigate the agonist and antagonist effect of alpha2 adrenergic receptors on tonic pain sensitivity during all stages of estrous cycle in female rats. Xylasine as alpha 2 agonist and yohimbin as alpha 2 antagonist were used via intraperitoneal route [IP]. Adult rats weighing 180-200 grams were used. Animals were maintained on 12h reverse light/dark cycle for 7 days prior to the experiment. Water and food was available ad libitum. Formalin test was performed by subcutaneous injection of 50 micro l formalin [2.5%] solution into the hind paw. Formalin test was performed in all stages of estrous cycle for 60 minutes. Animals were divided into four groups; 1- control group [intact animal], 2- Sham group [animals received 0.2 ml normal saline by IP route], 3- Agonist groups [animals received 0.2 ml xylasine 1, 3 mg/kg body weight by IP route] and 4- Antagonist group [animals received 0.2 ml yohimbine 1, 3 mg/kg body weight by IP route]. Data were statistically analyzed using 2 way ANOVA test followed by Tukey's test as posthoc test. P < 0.05 was considered significant. Results showed that xylasine significantly [p < 0.05] decreases pain sensitivity in all stages of estrous cycle. Analgesic effect of xylasine was maximum in estrus stage of estrous cycle and minimum in metestrus stage of estrous cycle. Yohimbine significantly [p < 0.05] increases pain sensitivity in all stages of estrous cycle. Hyperalgesic effect of yohimbine was maximum in metestrus stage of estrous cycle and minimum in estrus stage of estrous cycle. These results indicate that alpha2 adrenergic system and endogenous steroids have an important role in pain sensitivity

Potentiation of responses to UK-14304 in rat isolated common carotid artery by angiotensin

The selective [alpha 2] -adrenoceptor agonist UK-14304 produces a small vasoconstrictor response in the rat isolated carotid artery. The purpose of the work presented here was to investigate whether stimuli that produce submaximal contraction would potentiate responses to UK-14304. Male Wistar rats were killed by overdose with pentobarbitone sodium, after which the left and right common carotid arteries were removed. The rings of arteries 3-4 mm in length were cut from each vessel and then mounted in 10 mL isolated organ bath, bathed in Krebs maintained at 37°C and gassed with 95% 02 plus 5% CO[2] The preparations were allowed to equilibrate for an hour. Cumulative concentration-response curves [CCRC] were constructed in a cumulative manner by increasing the concentration of the agonists in half-log increments. When antagonists were used, the preparations were incubated at least for 45 minutes with the drugs prior to the onset of a second CCRC. Angiotensin II [All] and other contracting factors were added approximately 10-15 min prior to the onset of CCRC to an agonist. After inducing tone with low concentrations of the thromboxane A[2] mimetic agent U-46619 [1nM], 5HT [0.5-1 [micro] M] and phenylephrine [10 [micro] M], exposure of the preparation to UK-14304 resulted in concentration dependent contractions to this agonist. The sensitivity and maximum response of the preparation to UK-14304 were not changed. Inducing tone with AII [0.01 [micro] M] produced a significant leftward shift in the CCRC to UK-14304 [p<0.05]. Thus submaximal contraction with AII [0.01 [micro] M],increased responses significantly, but inducing tone with phenylephrine, U-46619 and 5HT had no effect on responses to UK-14304. The [alpha] -adrenoceptor antagonists prazosin and rauwolscine were examined to see whether UK-14304's main action in the presence of All remained via [alpha 1]. The potentiated responses were prazosin sensitive and rauwolscine resistant, indicating an increasing effect mediated by [alpha 1] -adrenoceptotrs

Antagonism of clonidine injected intracerebroventricularly in different models of salt intake

Clonidine, and alpha2-adrenergic agonist, injected into the brain inhibits salt intake of animals treated by the diuretic model of sodium depletion. In the present study, we address the question of whether central injection of clonidine also inhibits salt intake in animals deprived of water or in the need-free state. Saline or clonidine (30 nmol) was injected into the anterior third ventricle of 24-h sodium-depleted (furosemide + removal of ambient sodium), of 24-h water-deprived and of normovolemic (need-free state) adult male rats. Clonidine injected intracerebroventricularly (icv) inhibited the 1.5 per cent NaCl intake for 120 min by 50 to 90 per cent in every model tested. Therefore, different models of salt intake are inhibited by icv injection of clonidine. Idazoxan, an alpha2-adrenergic antagonist, injected icv at a dose of 160 nmol, inhibited the effect of clonidine only in the furosemide + removal of ambient sodium model of salt intake. This indicates that the antagonism of this effect by idazoxan is dependent on the body fluid/sodium status of the animal.