Association of clonidine and ropivacaine in brachial plexus block for shoulder arthroscopy / Associação de clonidina e ropivacaína no bloqueio de plexo braquial para artroscopia de ombro

Abstract Background and objectives: Arthroscopy for shoulder disorders is associated with severe and difficult to control pain, postoperatively. The addition of clonidine to local anesthetics for peripheral nerve block has become increasingly common, thanks to the potential ability of this drug to reduce the mass of local anesthetic required and to prolonging analgesia postoperatively. The present study aimed to evaluate the success of brachial plexus block for arthroscopic rotator cuff surgery using local anesthetic with or without clonidine. Method: 53 patients of both genders, between 18 and 70 years old, American Society of Anesthesiologists I or II, who were scheduled to undergo arthroscopic shoulder surgery were selected. Patients were then randomized into two groups. The verbal numerical pain scale and the presence of motor block were obtained in the post-anesthetic recovery room and 6, 12, 18 and 24 h postoperatively. Results: The association of clonidine (0.15 mg) to a solution of 0.33% ropivacaine (30 mL) in brachial plexus block for shoulder arthroscopy has not diminished the visual numeric pain scale values, nor the need for opioid rescue postoperatively. There was a lower incidence of nausea/vomiting postoperatively and a significant motor block time prolongation in the group of patients who received clonidine as adjuvant. Conclusions: The use of brachial plexus block with local anesthetic for analgesic postoperative control is well established in the literature. The addition of clonidine in the dose proposed for prolongation of the analgesic effect and reduction of opioid rescue proved unhelpful.

Resumo Justificativa e objetivos: A artroscopia para afecções do ombro associa-se a dor de forte intensidade no pós-operatório, de difícil manejo. A adição de clonidina ao anestésico local em bloqueios periféricos tornou-se progressivamente maior graças à potencial habilidade dessa droga em reduzir a massa de anestésicos locais necessários e prolongar a analgesia no pós-operatório. O presente estudo teve como objetivo avaliar o sucesso do bloqueio de plexo braquial para a cirurgia artroscópica de manguito rotador com o uso de anestésico local associado ou não à clonidina. Método: Foram selecionados 53 pacientes de ambos os sexos, entre 18 e 70 anos, ASA I ou II, que seriam submetidos à cirurgia de ombro por artroscopia. Os pacientes foram então randomizados em dois grupos. A escala numérica verbal de dor e a presença de bloqueio motor eram obtidas na sala de recuperação pós-anestésica (SRPA) e com seis, 12, 18 e 24 horas de pós-operatório. Resultados: A associação de clonidina (0,15 mg) à solução de ropivacaína 0,33% (30 mL) no bloqueio de plexo braquial para artroscopia de ombro não diminuiu os valores da escala visual numérica de dor, nem a necessidade de resgate com opioides no pós-operatório. Houve uma menor incidência de náuseas e vômitos no pós-operatório (NVPO) e aumento considerável do tempo de bloqueio motor no grupo de pacientes que recebeu clonidina como adjuvante. Conclusões: O uso do bloqueio de plexo braquial com anestésico local para controle analgésico pós-operatório está consolidado na literatura. A adição de clonidina na dose proposta para prolongamento do efeito analgésico e redução de resgate com opioides mostrou-se pouco útil.

Association of clonidine and ropivacaine in brachial plexus block for shoulder arthroscopy.

BACKGROUND AND OBJECTIVES: Arthroscopy for shoulder disorders is associated with severe and difficult to control pain, postoperatively. The addition of clonidine to local anesthetics for peripheral nerve block has become increasingly common, thanks to the potential ability of this drug to reduce the mass of local anesthetic required and to prolonging analgesia postoperatively. The present study aimed to evaluate the success of brachial plexus block for arthroscopic rotator cuff surgery using local anesthetic with or without clonidine. METHOD: 53 patients of both genders, between 18 and 70 years old, American Society of Anesthesiologists I or II, who were scheduled to undergo arthroscopic shoulder surgery were selected. Patients were then randomized into two groups. The verbal numerical pain scale and the presence of motor block were obtained in the post-anesthetic recovery room and 6, 12, 18 and 24h postoperatively. RESULTS: The association of clonidine (0.15mg) to a solution of 0.33% ropivacaine (30mL) in brachial plexus block for shoulder arthroscopy has not diminished the visual numeric pain scale values, nor the need for opioid rescue postoperatively. There was a lower incidence of nausea/vomiting postoperatively and a significant motor block time prolongation in the group of patients who received clonidine as adjuvant. CONCLUSIONS: The use of brachial plexus block with local anesthetic for analgesic postoperative control is well established in the literature. The addition of clonidine in the dose proposed for prolongation of the analgesic effect and reduction of opioid rescue proved unhelpful.

Condicionamento anestésico e cardioproteção / Anesthetic conditioning and cardioprotection

O envelhecimento populacional e suas consequências aumentaram progressivamente a necessidade de o médico anestesiologista realizar técnicas capazes de reduzir o risco cardiovascular durante o per e o pós-operatório. É cada vez mais forte a evidência dos benefícios anestésicos sobre o aparelho cardiovascular, por ativação de vias protetoras intracelulares. Esse benefício mimetiza a resposta do organismo frente a um evento isquêmico. Este artigo objetiva a descrição dos fenômenos de pré e pós-condicionamento isquêmico e anestésico. Aborda as possíveis vias de ativação do fenótipo protetor das células, descrevendo e comentando as principais evidências experimentais e clínicas das quais dispomos no momento, tanto para o aparelho cardiovascular, quantopossíveis benefícios em outros órgãos e sistemas.

Ageing and its consequences progressively increased the physician?s needs to perform anesthesia techniques able to reduce the cardiovascular risk during per and postoperative period. The evidence from the anesthetic benefits on the cardiovascular system increases with time, through activation of protective intracellular pathways. These benefits mimic the body?s answer for an ischemic event. The aim of this paper is to describe the ischemic and anesthetic pre and post conditioning phenomena, the possible activation pathways of the protective cell phenotype and the main experimental and clinical evidence available nowadays, for the cardiovascular system and other organs.

Evidence for Mas-mediated bradykinin potentiation by the angiotensin-(1-7) nonpeptide mimic AVE 0991 in normotensive rats.

We evaluated the effect of the nonpeptide mimic of angiotensin (Ang)-(1-7), AVE 0991, on the hypotensive effect of bradykinin (BK). Increasing doses of intra-arterial or intravenous BK were administered before and 30 minutes after the beginning of AVE 0991 infusion. The effect of AVE 0991 on plasma Ang-converting enzyme activity was tested using Hip-His-Leu as the substrate. The interaction of AVE 0991 with Ang-converting enzyme in vivo was tested by determining its effect on the pressor action of Ang I or Ang II. AVE 0991 produced a significant and similar potentiation of intra-arterial or intravenous bradykinin. AVE 0991 did not inhibit plasma Ang-converting enzyme activity in vitro or the pressor effect of Ang I in vivo. N(W)-nitro-l-arginine methyl ester or D-Ala(7)-Ang-(1-7) administration abolished the BK potentiating effect of AVE 0991. We further examined the BK-potentiating effect of AVE 0991, evaluating its effect on NO production in rabbit endothelial cells. The NO release was measured using the 4-amino-5-methylamino-2'-7'-difluorofluorescein diacetate. A synergistic effect of AVE 0991 and BK on NO release was observed. These results suggest that AVE 0991 potentiates bradykinin through an Ang-converting enzyme-independent, NO-dependent receptor Mas-mediated mechanism. This effect may contribute to the improvement of endothelial function by AVE 0991 in vivo.

Angiotensin-(1-7) through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways.

Angiotensin-(1-7) [Ang-(1-7)] causes endothelial-dependent vasodilation mediated, in part, by NO release. However, the molecular mechanisms involved in endothelial NO synthase (eNOS) activation by Ang-(1-7) remain unknown. Using Chinese hamster ovary cells stably transfected with Mas cDNA (Chinese hamster ovary-Mas), we evaluated the underlying mechanisms related to receptor Mas-mediated posttranslational eNOS activation and NO release. We further examined the Ang-(1-7) profile of eNOS activation in human aortic endothelial cells, which constitutively express the Mas receptor. Chinese hamster ovary-Mas cells and human aortic endothelial cell were stimulated with Ang-(1-7; 10(-7) mol/L; 1 to 30 minutes) in the absence or presence of A-779 (10(-6) mol/L). Additional experiments were performed in the presence of the phosphatidylinositol 3-kinase inhibitor wortmannin (10(-6) mol/L). Changes in eNOS (at Ser1177/Thr495 residues) and Akt phosphorylation were evaluated by Western blotting. NO release was measured using both the fluorochrome 2,3-diaminonaphthalene and an NO analyzer. Ang-(1-7) significantly stimulated eNOS activation (reciprocal phosphorylation/dephosphorylation at Ser1177/Thr495) and induced a sustained Akt phosphorylation (P<0.05). Concomitantly, a significant increase in NO release was observed (2-fold increase in relation to control). These effects were blocked by A-779. Wortmannin suppressed eNOS activation in both Chinese hamster ovary-Mas and human aortic endothelial cells. Our findings demonstrate that Ang-(1-7), through Mas, stimulates eNOS activation and NO production via Akt-dependent pathways. These novel data highlight the importance of the Ang-(1-7)/Mas axis as a putative regulator of endothelial function.

Short-term angiotensin(1-7) receptor MAS stimulation improves endothelial function in normotensive rats.

In this study we evaluated the effect of angiotensin(1-7) and its nonpeptide analog, AVE 0991, on the endothelial function in vivo. The experiments were performed in conscious adult male Wistar rats, with polyethylene catheters implanted into the descending aorta (through left carotid artery), for injection of acetylcholine or sodium nitroprusside, femoral artery for mean arterial pressure and heart rate measurement; and femoral vein for drug administration. Increasing doses of acetylcholine (3.1 ng to 25.0 ng) or nitroprusside (1.0 microg to 10.0 microg) were administered before and 30 minutes after the start of the infusion of: angiotensin(1-7) (0.7 and 7.0 pmol/min); A-779 (180 pmol/min); angiotensin(1-7) (7.0 pmol/min) combined with A-779 (180 pmol/min); AVE 0991 (11, 45, and 230 pmol/min); AVE 0991 (45 pmol/min) combined with A-779 (180 pmol/min), or vehicle (6 microL/min). Baseline mean arterial pressure and heart rate were not altered during angiotensin(1-7) or AVE 0991 infusion. Angiotensin(1-7) (0.7 pmol/min) infusion produced a significant potentiation of the hypotensive effect of acetylcholine (3.1 ng: -9+/-1 mm Hg before; -18+/-2 mm Hg after; P<0.05). A similar potentiation was observed with the higher dose of angiotensin(1-7). As observed for angiotensin(1-7), infusion of AVE 0991 at 230 pmol/min potentiated the acetylcholine effect (3.1 ng: -8+/-2 mm Hg before; -16+/-2 mm Hg after; P<0.05). The potentiating effect was not observed for nitroprusside. A-779 or l-NAME treatment blocked the potentiation produced by angiotensin(1-7) or AVE 0991. Our data indicate that short-term stimulation of angiotensin(1-7) receptors improve endothelial function through facilitation of nitric oxide release.