[A 23-gauge pars plana vitrectomy after induction of general anesthesia: effect of additional retrobulbar anesthesia on postoperative pain]. / 23-Gauge-Pars-plana-Vitrektomien in Allgemeinanästhesie : Effekt einer additiven Retrobulbäranästhesie auf das postoperative Schmerzempfinden.

PURPOSE: Some studies have shown a significant reduction of postoperative pain by additional regional anesthesia in 20-gauge pars plana vitrectomy (20-G-ppV) with the patient under general anesthesia (AN). This observational study examined whether the advantages of additional retrobulbar anesthesia can also be observed with 23-gauge vitrectomy in AN. MATERIAL AND METHODS: Surgery was performed in 130 patients under AN of which 88 received an additional retrobulbar block (group AN+) and 42 patients were treated without additional injection of retrobulbar anesthesia (group AN) using bupivacaine 0.5 % and mepivacaine 1%. The AN was performed with fentanyl and propofol. Postoperatively, the subjective patient pain was recorded using a numeric scale and the use and amount of analgesic drugs in the postoperative course were monitored. RESULTS: The mean age of the patients was 53.6 ± 16.8 years, 52.6% of the patients were male, 31.5% were staged as American Society of Anesthesiologists (ASA) level I, 52.3% as ASA II and 15.4% as ASA III. At no time did the study show a statistically significant difference in pain frequency, intensity and analgesic consumption. However, the results suggest that patients in the AN+ group tended to experienced delayed and more intense postoperative pain, which is also reflected in the postoperative use of pain relief medications. CONCLUSIONS: This study did not show any advantage by additional retrobulbar anesthesia regarding postoperative analgesia compared to an adequate treatment with peripheral acting analgesics during surgery and the early postoperative period.

Isoflurane inhalation after induction of endotoxemia in rats attenuates the systemic cytokine response.

BACKGROUND/AIMS: Volatile anesthetics are frequently utilized in clinical routine. Isoflurane has been shown to attenuate the response to inflammatory stimuli such as lipopolysaccharide (LPS) when administered before induction of endotoxemia. We aimed therefore to evaluate the effect of isoflurane after administration of LPS on the cytokine release as a therapeutic option. MATERIALS AND METHODS: 21 male Sprague-Dawley rats were randomly assigned to the following groups: animals that received LPS (5 mg/kg, i.v.) without further intervention (LPS group), animals that received continuous inhalation of 1 minimum alveolar concentration (MAC) isoflurane 15 min after administration of LPS (Iso group) and no specific intervention (sham group). Four hours following LPS injection, plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6 and IL-10 were determined. Furthermore, nitrite release from cultured alveolar macrophages was analyzed. RESULTS: Inhalation of isoflurane after induction of endotoxemia attenuated the release of TNF-alpha (-52%, p < 0.05) and IL-1 beta (-39%, p < 0.05) as compared to the LPS group, while IL-6 and IL-10 levels were not significantly altered. Nitrite release was significantly increased in the Iso group as compared to the LPS group (+115%, p < 0.05). CONCLUSION: Inhalation of 1 MAC isoflurane after induction of endotoxemia in rats attenuates the systemic release of proinflammatory cytokines and concurrently enhances the production of nitrite in cultured alveolar macrophages.

Anti-inflammatory effects of sevoflurane and mild hypothermia in endotoxemic rats.

BACKGROUND: Volatile anesthetics and hypothermia attenuate the inflammatory response. We aimed to compare the anti-inflammatory effects of sevoflurane and mild hypothermia during experimental endotoxemia in the rat. METHODS: Anesthetized, ventilated Sprague-Dawley (SD) rats were randomly treated as follows (n = 6 per group): lipopolysaccharide (LPS) only, animals received LPS [LPS 5 mg/kg, intravenously (i.v.)] with no further treatment. In the LPS-hypothermia group, rats were cooled down to a temperature of 33 degrees C 15 min after LPS-injection (LPS 5 mg/kg i.v.). In animals of the LPS-sevoflurane group, sevoflurane inhalation (1 MAC) was initiated 15 min after induction of endotoxemia. The LPS-sevoflurane-hypothermia group received combined sevoflurane and hypothermia 15 min after induction of endotoxemia. A Sham group served as control without endotoxemia or treatment. After 4 h of endotoxemia, plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-10 were measured. Alveolar macrophages (AM) were ex vivo cultured for nitrite assay. RESULTS: Inhalation of sevoflurane significantly attenuated plasma levels of TNF-alpha (-60%, P < 0.05) and IL-1beta (-68%, P < 0.05) as compared with the LPS-only group. Hypothermia and its combination with sevoflurane significantly reduced TNF-alpha levels (-46% and -58%, each P < 0.05), but not IL-1beta. Application of mild hypothermia and also its combination with sevoflurane resulted in a significant increase in plasma IL-10 as compared with endotoxemic controls. Nitrite release from AM was found to be significantly suppressed by sevoflurane (-83%), hypothermia (-73%) and by the combination of both (-67%) (P < 0.05, each). CONCLUSION: Our data suggest that sevoflurane and mild hypothermia attenuate the inflammatory response during endotoxemia in vivo thus contributing to their beneficial role in clinical organ protection.

The beta-adrenoceptor antagonist propranolol counteracts anti-inflammatory effects of isoflurane in rat endotoxemia.

BACKGROUND: Recent studies suggest that volatile anaesthetics have anti-inflammatory and preconditioning properties and that beta-adrenoceptors are involved in the signalling pathways for these effects. Concurrently, the blockade of beta-adrenoceptors has been shown to augment the release of inflammatory mediators in response to pro-inflammatory stimuli. We therefore aimed to investigate whether the beta-adrenoceptor antagonist propranolol might modulate the anti-inflammatory effects of isoflurane on the systemic and pulmonary release of pro-inflammatory cytokines in endotoxemic rats. METHODS: Forty anaesthetized and ventilated Sprague-Dawley rats were randomly treated as follows. Lipopolysaccharide (LPS) only (n = 8), endotoxemia with LPS [5 mg/kg, intravenously (i.v.)]. LPS-isoflurane (n = 8): endotoxemia and continuous inhalation of 1 minimum alveolar concentration (MAC) of isoflurane. LPS-isoflurane-propranolol (n = 8): administration of propranolol (3 mg/kg) before continuous inhalation of isoflurane and induction of endotoxemia. LPS-propranolol (n = 8): administration of propranolol (3 mg/kg) before endotoxemia without inhalation of isoflurane. Sham (n = 8): control-group only with surgical preparation. After 4 h of endotoxemia, levels of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-10 (IL-10) in plasma and bronchoalveolar fluid (BALF) were analysed. Release of nitric oxide (NO) and amount of inducible nitric oxide synthase (iNOS) protein in alveolar macrophages was measured by Griess assay or determined by Western Blotting, respectively. RESULTS: Inhalation of isoflurane reduced the release of TNF-alpha (P < 0.05) and IL-1beta (P < 0.05) in plasma and IL-1beta (P < 0.05) in BALF. Co-administration of propranolol significantly inhibited these effects. During inhalation of isoflurane, the increased release of NO and iNOS protein from alveolar macrophages was also completely inhibited by propranolol. CONCLUSION: Our results indicate for the first time, that blockade of beta-adrenoceptors counteracts the anti-inflammatory effects of isoflurane in endotoxemic rats.