Mitochondria and Pharmacologic Cardiac Conditioning-At the Heart of Ischemic Injury.

Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.

Balancing patient needs with environmental impacts for best practices in general anesthesia: Narrative review and clinical perspective.

Discussions of the environmental impacts of general anesthetics have focused on greenhouse gas (GHG) emissions from inhaled agents, with those of total intravenous anesthesia (TIVA) recently coming to the forefront. Clinical experts are calling for the expansion of research toward life cycle assessment (LCA) to comprehensively study the impact of general anesthetics. We provide an overview of proposed environmental risks, including direct GHG emissions from inhaled anesthetics and non-GHG impacts and indirect GHG emissions from propofol. A practical description of LCA methodology is also provided, as well as how it applies to the study of general anesthesia. We describe available LCA studies comparing the environmental impacts of a lower carbon footprint inhaled anesthetic, sevoflurane, to TIVA/propofol and discuss their life cycle steps: manufacturing, transport, clinical use, and disposal. Significant hotspots of GHG emission were identified as the manufacturing and disposal of sevoflurane and use (attributed to the manufacture of the required syringes and syringe pumps) for propofol. However, the focus of these studies was solely on GHG emissions, excluding other environmental impacts of wasted propofol, such as water/soil toxicity. Other LCA gaps included a lack of comprehensive GHG emission estimates related to the manufacturing of TIVA plastic components, high-temperature incineration of propofol, and gas capture technologies for inhaled anesthetics. Considering that scarce LCA evidence does not allow for a definite conclusion to be drawn regarding the overall environmental impacts of sevoflurane and TIVA, we conclude that current anesthetic practice involving these agents should focus on patient needs and established best practices as more LCA research is accumulated.

[Recommendations of the new S1 guidelines on airway management]. / Empfehlungen zur neuen S1-Leitlinie Atemwegsmanagement.

The German guidelines for airway management aim to optimize the care of patients undergoing anesthesia or intensive care. The preanesthesia evaluation is an important component for detection of anatomical and physiological indications for difficult mask ventilation and intubation. If predictors for a difficult or impossible mask ventilation and/or endotracheal intubation are present the airway should be secured while maintaining spontaneous breathing. In an unexpectedly difficult intubation, attempts to secure the airway should be limited to two with each method used. A video laryngoscope is recommended after an unsuccessful direct laryngoscopy. Therefore, a video laryngoscope should be available at every anesthesiology workspace throughout the hospital. Securing the airway should primarily be performed with a video laryngoscope in critically ill patients and patients at risk of pulmonary aspiration. Experienced personnel should perform or supervise airway management in the intensive care unit.

Endothelial nitric oxide synthase mediates the first and inducible nitric oxide synthase mediates the second window of desflurane-induced preconditioning.

OBJECTIVES: Nitric oxide synthases (NOSs) mediate the first window of anesthetic-induced preconditioning (APC). The authors tested the hypothesis that endothelial NOS (eNOS) mediates the first window and inducible NOS (iNOS) mediates the second window of APC. DESIGN: Randomized, prospective, blinded laboratory investigation. SETTING: Experimental laboratory. PARTICIPANTS: Mice. INTERVENTIONS: Mice were subjected to a 45-minute coronary artery occlusion (CAO) and a 180-minute reperfusion. C57BL/6 mice received desflurane, 1.0 minimum alveolar concentration, for 30 minutes or 12, 24, 48, or 96 hours before CAO. In eNOS(-/-) and iNOS(-/-) mice, desflurane was given 30 minutes and 48 hours before CAO. In the control groups, no desflurane was administered. Myocardial infarct size (IS) was determined after staining with Evans blue and triphenyltetrazolium chloride. MEASUREMENTS AND MAIN RESULTS: The second window of APC was detectable at 48 hours but not at 12, 24, and 96 hours after preconditioning. In the control groups, IS was not different among the wild-type (50 ± 10%), eNOS(-/-) (52 ± 14%), and iNOS(-/-) (46 ± 10%) mice. The IS decreased significantly (p < 0.05) when desflurane was administered 30 minutes (10 ± 6%) or 48 hours (16 ± 7%) before CAO in wild-type mice, 48 hours (21 ± 13%) before CAO in eNOS(-/-) mice, and 30 minutes (13 ± 6%) before CAO in iNOS(-/-) mice. Desflurane given 30 minutes before CAO in eNOS(-/-) mice (60 ± 10%) and 48 hours before CAO in iNOS(-/-) mice (48 ± 21%) did not decrease the IS significantly compared with controls. CONCLUSIONS: Endothelial NOS and iNOS work independently to mediate the first and second windows of APC, respectively. Endothelial NOS is not necessary to trigger the second window of APC.

History-based preoperative evaluation of antibiotic-related allergies and design of an easy to use questionnaire.

BACKGROUND: An unconfirmed history of antibiotic allergies may negatively influence prescribing patterns for preoperative antibiotic prophylaxis and increase rates of postoperative wound infections through unnecessary use of alternative antibiotics. METHODS: After a literature search, we developed a questionnaire for the structured collection of antibiotic allergy history in the anesthesia consultation center and tested it over 2 years at a tertiary care hospital under everyday conditions as part of a quality assurance project. All data were evaluated completely anonymously in the context of standard care. RESULTS: After refining the questionnaire, we analyzed 4866 recorded optimized questionnaires, of which 51 were incomplete. An antibiotic allergy was denied 4312 times and affirmed 503 times, which corresponds to 10% in our sample. The most frequent single substances or groups in the 503 respondents with a positive history of antibiotic allergy were penicillin in 271 (54%), amoxicillin in 65 (13%), an unknown single agent in 50 (10%) and multiple substances in 25 (5%). The reported event occurred more than 10 years ago in 192 (38%) of the respondents, less than 10 years ago in 116 (23%), and 195 (39%) could not provide information. The time from exposure to symptom onset was less than 1h in 96 (19%), between 1 and 24 h in 75 (15%), more than 24 h in 106 (21%), and the remainder could not provide information. Allergy-specific treatment was recalled by 75 (15%) respondents, 287 (57%) reported not having received specific treatment, and the remainder could not recall. A specific allergy test was reported by 55 (11%) respondents, 337 (67%) said no allergy test had been made, and the rest could not recall. A substance-specific allergy passport was issued in 80 (16%) respondents. According to expert assessment, symptoms compatible with an IgE-mediated reaction were present in 96 (19%) of the respondents. An IgE-mediated reaction was considered possible in 70 (14%) and could be excluded by history in 337 (67%) of respondents. Out of 503 respondents with a positive history 51 (10%) could not remember the allergic substance but 7 (14%) of the 51 reported symptoms compatible with severe anaphylaxis or anaphylactic shock and 6 of the 51(12%) reported symptoms possibly related to an IgE-mediated reaction. DISCUSSION: Our survey revealed approximately 10% of respondents reporting an antibiotic allergy, which is in the upper range of data published in international literature and corresponds most closely to American data. Thus, the topic is also relevant to German anesthesia consultation centers, given the high rate of respondents who could have been "delabeled" based on the comprehensive assessment of their history. More expert allergy testing is needed in patients who report symptoms related or probably related to an IgE-mediated reaction. In our opinion, a special issue exists in those patients who did not remember the exact antibiotic but reported symptoms compatible with severe anaphylaxis putting them at high risk of unintended re-exposure.

[Anesthesia in obesity surgery : Recommendations from the practice for the practice]. / Anästhesie in der Adipositaschirurgie : Empfehlungen aus der Praxis für die Praxis.

BACKGROUND: Due to unsuccessful conservative treatment concepts and the steady increase in the prevalence of obesity, obesity surgery has gained importance worldwide. In Germany alone, around 20,000 surgical operations for obesity are performed each year. In addition to patient history and physical examination a close interdisciplinary cooperation taking into account the currently applicable standards and guidelines of the professional societies are prerequisites for best patient care and to evaluate and mitigate patient risks. AIM: The aim of this work was to compile and consent experiences of experts in the implementation of applicable standards and guidelines for anesthesia in obesity surgery for daily clinical practice. METHOD: Anesthesiologists from five bariatric centers, comprising about 10% of the obesity surgery caseload of Germany per year, have collated their clinical experiences to agree on a consensus for procedures. The procedures for preoperative patient evaluation, drug premedication and PONV prophylaxis, induction of anesthesia and drug dosage recommendations for anesthetics were consented based on the authors' practice. RESULTS AND CONCLUSION: The procedures described herein were developed as part of a joint work process. The authors describe a practically applicable approach to the anesthesiological care of obesity surgery patients and recommend using a pragmatic formula for dosing the medication calculated on the basis of total body weight (TBW).

Peroxisome-proliferator-activated receptor γ mediates the second window of anaesthetic-induced preconditioning.

The second window of anaesthetic-induced preconditioning (APC) is afforded by the interplay of multiple signalling pathways, whereas a similar protective response is mediated by peroxisome-proliferator-activated receptor γ (PPARγ) agonists. However, a possible role of this nuclear receptor during APC has not been studied to date. We investigated the hypothesis that the second window of APC is mediated by the activation of PPARγ. New Zealand White rabbits (n = 48) were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. The animals received desflurane (1.0 minimal alveolar concentration), the PPARγ antagonist GW9662, as well as the combined application of both, respectively, 24 h prior to coronary artery occlusion. Infarct size was determined gravimetrically; tissue levels of 15-deoxy-(12,14)-prostaglandin J(2) (15d-PGJ(2)) and nitrite/nitrate (NO(x)), as well as PPAR DNA binding were measured using specific assays. Data are presented as means ± s.e.m. Desflurane led to a reduced myocardial infarct size (41.7 ± 2.5 versus 61.8 ± 2.8%, P < 0.05), accompanied by significantly increased PPAR DNA binding (289.9 ± 33 versus 102.9 ± 18 relative light units, P < 0.05), as well as elevated tissue levels of 15d-PGJ(2) (224.4 ± 10.2 versus 116.9 ± 14.2 pg ml(-1), P < 0.05) and NO(x) (14.9 ± 0.7 versus 5.4 ± 0.7 µm, P < 0.05). Pharmacological inhibition of PPARγ abolished these protective effects, resetting the infarct size (56.5 ± 2.9%), as well as PPAR DNA-binding activity (91.2 ± 31 relative light units) and NO(x) tissue levels (5.9 ± 0.9 µm) back to control levels. Desflurane governs a second window of APC by increasing the production of 15d-PGJ(2), subsequently activating PPARγ, resulting in a diminished myocardial infarct size by increasing the downstream availability of NO.

Propofol inhibits desflurane-induced preconditioning in rabbits.

OBJECTIVES: The authors tested the hypothesis that ischemic and desflurane-induced preconditioning are blocked by propofol. DESIGN: A prospective, randomized, vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: New Zealand white rabbits (n = 52). METHODS: Pentobarbital-anesthetized rabbits were subjected to 30 minutes of coronary artery occlusion followed by 3 hours of reperfusion. Rabbits received 0.0 (control) or 1.0 minimum alveolar concentration of desflurane (30 minutes' duration and a 30-minute memory period) or ischemic preconditioning (5 minutes of ischemia and a 30-minute memory period) in the absence or presence of propofol (10 mg/kg/h intravenously) or its vehicle (10% Intralipid emulsion; B Braun, Melsungen, Germany). The myocardial infarct size was measured with triphenyltetrazolium staining. Statistical analysis was performed with 1-way and 2-way analysis of variance when appropriate, followed by a post hoc Duncan test. Data are mean ± standard deviation. RESULTS: Myocardial infarct size was 56% ± 8% in control animals (n = 7). Desflurane significantly (p < 0.05) reduced the infarct size to 37% ± 6% (n = 7). Desflurane-induced preconditioning was blocked by propofol (65% ± 10%, n = 7) but not by its vehicle (45% ± 11%, n = 5). Propofol and its vehicle alone had no effect on the infarct size (62% ± 8% [n = 6] and 58% ± 3% [n=5], respectively). Ischemic preconditioning reduced infarct size in the absence or presence of propofol to 24% ± 7% (n = 7) and 29% ± 12% (n = 6). CONCLUSION: Desflurane-induced preconditioning markedly reduced infarct size and was blocked by propofol, whereas ischemic preconditioning was not blocked by propofol. The results suggest an important interference between propofol and anesthetic-induced preconditioning and might explain some contradictory findings in studies in humans.

Activation of adenosine-monophosphate-activated protein kinase abolishes desflurane-induced preconditioning against myocardial infarction in vivo.

OBJECTIVES: Myocardial ischemia is accompanied by a rapid activation of adenosine-monophosphate-activated protein kinase (AMPK). However, it is unclear whether this represents a potentially beneficial or detrimental event in the course of ischemic injury. The role of AMPK activation in the cardioprotective setting of desflurane-induced preconditioning has not been investigated to date. Hence, the current study was undertaken to address the role of AMPK activation during desflurane-induced preconditioning in vivo. DESIGN: A prospective randomized vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: Male New Zealand white rabbits (n = 44). INTERVENTIONS: The animals were subjected to a 30-minute coronary artery occlusion (CAO) followed by 3 hours of reperfusion. Desflurane (1.0 minimum alveolar concentration) was administered for 30 minutes and discontinued 30 minutes prior to CAO. Different groups of animals received the AMPK activator, 5-aminoimidazole-4-carboxamide-1-b-riboside (AICAR), alone or in combination with desflurane. Infarct size was determined gravimetrically; AMPK activity and myocardial glycogen content were measured using specific assays. Phosphorylation of the AMPK substrate, acetyl-CoA carboxylase, was assessed by immunoblotting. Data are mean ± standard error of the mean. RESULTS: Desflurane significantly reduced the myocardial infarct size (36.7 ± 1.9%, p < 0.05) compared with the control group (61.6% ± 3.0%), concomitant with increased myocardial tissue levels of glycogen (2.09 ± 0.07 µg, p < 0.05). Activation of the AMPK by AICAR alone did not protect against ischemic injury (65% ± 3.3), but did abolish the cardioprotection elicited by desflurane (61.8% ± 4.2%) at the same time as increasing myocardial glycogen consumption (1.42 ± 0.15 µg/mL). CONCLUSIONS: The results obtained show that the pharmacologic activation of AMPK abolishes cardioprotection elicited by desflurane.

Time course of desflurane-induced preconditioning in rabbits.

OBJECTIVES: The authors tested the hypothesis that volatile anesthetic-induced preconditioning (APC) follows a similar time pattern as that described for ischemic preconditioning and that delayed APC is mediated by nitric oxide. DESIGN: A prospective randomized vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: New Zealand white rabbits (n = 75). METHODS: Rabbits were instrumented for the measurement of systemic hemodynamics and subjected to a 30-minute coronary artery occlusion (CAO) and 3 hours of reperfusion. Desflurane (1.0 minimum alveolar concentration) was administered for 30 minutes and was discontinued 0.5 hours, 2 hours, 3 hours, 12 hours, 24 hours, 48 hours, 72 hours, and 96 hours before CAO, respectively. In 2 separate experimental groups, the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NA) was administered 72 hours after the administration of 0.0 or 1.0 minimum alveolar concentration of desflurane. The infarct size was determined gravimetrically. Data are mean +/- standard deviation. RESULTS: Desflurane significantly (p < 0.05) reduced the infarct size compared with the control (63% +/- 12%, n = 7) when administered 0.5 hours (35% +/- 5%, n = 7), 2 hours (35% +/- 9%, n = 7), 24 hours (31% +/- 8%, n = 7), 48 hours (30% +/- 11%, n = 6), and 72 hours (39% +/- 5%, n = 6) before CAO. However, when desflurane was administered 3 hours (53% +/- 9%, n = 7), 12 hours (71% +/- 6%, n = 7), or 96 hours (66% +/- 5%, n = 7) before CAO, the myocardial infarct size was not reduced. The second window (72 hours) of preconditioning was abolished by the NOS inhibitor L-NA (52% +/- 16%, n = 7). L-NA alone had no effect on infarct size (64% +/- 11%, n = 7). CONCLUSIONS: Desflurane induces a first (0.5-2 hours) and second window of preconditioning (24-72 hours) in the rabbit model of acute myocardial infarction. The second window of APC is mediated by nitric oxide.

Estrogen receptor alpha interacts with 17beta-hydroxysteroid dehydrogenase type 10 in mitochondria.

Estrogen receptor alpha (ERalpha) is present in the nucleus, the cytosol and in mitochondria. The rat ERalpha ligand binding domain was employed as bait in a bacterial two-hybrid screening of a human heart cDNA library to detect novel protein-protein interaction partners of ERalpha in the heart. 17beta-Hydroxysteroid dehydrogenase type 10 (17beta-HSD10), which converts potent (17beta-estradiol) to less potent estrogens (estrone), co-localized with 17beta-HSD10 in the mitochondria of rat cardiac myocytes. GST pull-down experiments confirmed the interaction of ERalpha and 17beta-HSD10. These findings suggest that the ERalpha estrogen receptor might be involved in regulating intracellular estrogen levels by modulating 17beta-HSD10 activity.

Desflurane-induced postconditioning is mediated by beta-adrenergic signaling: role of beta 1- and beta 2-adrenergic receptors, protein kinase A, and calcium/calmodulin-dependent protein kinase II.

BACKGROUND: Anesthetic preconditioning is mediated by beta-adrenergic signaling. This study was designed to elucidate the role of beta-adrenergic signaling in desflurane-induced postconditioning. METHODS: Pentobarbital-anesthetized New Zealand White rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion and were randomly assigned to receive vehicle (control), 1.0 minimum alveolar concentration of desflurane, esmolol (30 mg x kg(-1) x h(-1)) for the initial 30 min of reperfusion or throughout reperfusion, the beta2-adrenergic receptor blocker ICI 118,551 (0.2 mg/kg), the protein kinase A inhibitor H-89 (250 microg/kg), or the calcium/calmodulin-dependent protein kinase II inhibitor KN-93 (300 microg/kg) in the presence or absence of desflurane. Protein expression of protein kinase B, calcium/calmodulin-dependent protein kinase II, and phospholamban was measured by Western immunoblotting. Myocardial infarct size was assessed by triphenyltetrazolium staining. RESULTS: Infarct size was 57 +/- 5% in control. Desflurane postconditioning reduced infarct size to 36 +/- 5%. Esmolol given during the initial 30 min of reperfusion had no effect on infarct size (54 +/- 4%) but blocked desflurane-induced postconditioning (58 +/- 5%), whereas esmolol administered throughout reperfusion reduced infarct size in the absence or presence of desflurane to 42 +/- 6% and 41 +/- 7%, respectively. ICI 118,551 and KN-93 did not affect infarct size (62 +/- 4% and 62 +/- 6%, respectively) but abolished desflurane-induced postconditioning (57 +/- 5% and 64 +/- 3%, respectively). H-89 decreased infarct size in the absence (36 +/- 5%) or presence (33 +/- 5%) of desflurane. CONCLUSIONS: Desflurane-induced postconditioning is mediated by beta-adrenergic signaling. However, beta-adrenergic signaling displays a differential role in cardioprotection during reperfusion.

Differential role of Pim-1 kinase in anesthetic-induced and ischemic preconditioning against myocardial infarction.

BACKGROUND: Ischemic preconditioning (IPC) and anesthetic-induced preconditioning against myocardial infarction are mediated via protein kinase B. Pim-1 kinase acts downstream of protein kinase B and was recently shown to regulate cardiomyocyte survival. The authors tested the hypothesis that IPC and anesthetic-induced preconditioning are mediated by Pim-1 kinase. METHODS: Pentobarbital-anesthetized male C57Black/6 mice were subjected to 45 min of coronary artery occlusion and 3 h of reperfusion. Animals received no intervention, Pim-1 kinase inhibitor II (10 microg/g intraperitoneally), its vehicle dimethyl sulfoxide (10 microl/g intraperitoneally), or 1.0 minimum alveolar concentration desflurane alone or in combination with Pim-1 kinase inhibitor II (10 microg/g intraperitoneally). IPC was induced by three cycles of 5 min ischemia-reperfusion each, and animals received IPC either alone or in combination with Pim-1 kinase inhibitor II (10 microg/g intraperitoneally). Infarct size was determined with triphenyltetrazolium chloride, and area at risk was determined with Evans blue (Sigma-Aldrich, Taufkirchen, Germany). Protein expression of Pim-1 kinase, Bad, phospho-Bad, and cytosolic content of cytochrome c were measured using Western immunoblotting. RESULTS: Infarct size in the control group was 47 + or - 2%. Pim-1 kinase inhibitor II (44 + or - 2%) had no effect on infarct size. Desflurane (17 + or - 3%) and IPC (19 + or - 2%) significantly reduced infarct size compared with control (both P < 0.05 vs. control). Blockade of Pim-1 kinase completely abrogated desflurane-induced preconditioning (43 + or - 3%), whereas IPC (35 + or - 3%) was blocked partially. Desflurane tended to reduce cytosolic content of cytochrome c, which was abrogated by Pim-1 kinase inhibitor II. CONCLUSION: These data suggest that Pim-1 kinase mediates at least in part desflurane-induced preconditioning and IPC against myocardial infarction in mice.

Desflurane-induced cardioprotection against ischemia-reperfusion injury depends on timing.

OBJECTIVES: The authors tested the hypothesis that desflurane-induced cardioprotection depends on the timing of application and whether desflurane-induced postconditioning is mediated by nitric oxide. DESIGN: A prospective randomized vehicle-controlled study. SETTING: A university research laboratory. SUBJECTS: New Zealand White rabbits (N = 56). INTERVENTIONS: Rabbits were instrumented and subjected to a 30-minute coronary artery occlusion (CAO) and 3 hours of reperfusion. Animals were randomized to 8 groups (n = 7) and received 0.0 or 1.0 minimum alveolar concentration desflurane for 30 minutes before CAO (PRE), during CAO (ISCH), after CAO (POST), before and after CAO (PRE + POST), or continuously for 90 minutes starting 30 minutes before CAO (PRE + ISCH + POST). In 2 separate experimental groups, the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (L-NA) was administered before reperfusion in the presence or absence of desflurane. Data are mean +/- standard deviation. RESULTS: Infarct size was 68% +/- 14% in control experiments. Desflurane significantly (p < 0.05) reduced infarct size in the PRE (43% +/- 9%) and POST groups (49% +/- 12%) but not in the ISCH group (69% +/- 9%). The PRE + ISCH + POST and PRE + POST groups produced similar reductions in infarct size to 47% +/- 12% and 43% +/- 9%, respectively. L-NA alone had no effect on infarct size (61% +/- 9%) but blocked postconditioning completely (L-NA + POST, 68% +/- 10%). CONCLUSIONS: Desflurane induces pre- and postconditioning but does not confer cardioprotection during ischemia in rabbits. The combination of pre- and postconditioning or continuous application does not provide additional cardioprotection. Furthermore, desflurane-induced postconditioning is mediated by nitric oxide.

Desflurane-induced preconditioning has a threshold that is lowered by repetitive application and is mediated by beta 2-adrenergic receptors.

OBJECTIVE: An optimal administration protocol to induce a maximal effect of anesthetic preconditioning has not been evaluated to date. In this study, desflurane preconditioning was characterized with respect to its threshold, dose dependency, and continuous versus repetitive application. Furthermore, the role of beta(2)-adrenergic receptors in anesthetic preconditioning was tested. DESIGN: A randomized controlled study. SETTING: Laboratory study in a University hospital. SUBJECTS: New Zealand white rabbits in vivo. INTERVENTIONS: Systemic hemodynamics were continuously measured. Rabbits were subjected to 30 minutes of coronary artery occlusion and 3 hours of reperfusion. Animals received desflurane continuously for 30 minutes at 0.5, 1.0, or 1.5; desflurane for 90 minutes at 0.5 or 1.5 MAC; or repetitively for three 10-minute periods at 0.5, 1.0, or 1.5 MAC before coronary occlusion. The beta(2)-adrenergic receptor blocker ICI 118,551 (0.2 mg/kg) or saline placebo was given in the absence or presence of 1.0 MAC desflurane. Myocardial infarct size was measured with triphenyltetrazolium staining. MEASUREMENTS AND MAIN RESULTS: Myocardial infarct size was 61% +/- 5% in control experiments. Desflurane, administered continuously at 0.5 MAC for 30 minutes (52% +/- 4%) or 90 minutes (56% +/- 8%) had no effect, whereas 0.5 MAC of desflurane given repetitively reduced infarct size to 36% +/- 7%. Desflurane administered continuously for 30 minutes at 1.0 or 1.5 MAC reduced infarct size to 35% +/- 5% and 39% +/- 4%, respectively. Repetitive application at 1.0 MAC (37% +/- 6%) or 1.5 MAC (29% +/- 4%) and continuous administration of 1.5 MAC for 90 minutes (32% +/- 6%) did not result in further infarct size reduction. ICI 118,551 did not affect infarct size (53% +/- 2%) but abolished desflurane preconditioning (51% +/- 5%). CONCLUSION: beta(2)-Adrenergic receptors mediate desflurane-induced preconditioning. Desflurane-induced preconditioning has a threshold that can be lowered by repetitive administration.

Validation of the GlideScope video laryngoscope in pediatric patients.

BACKGROUND: GlideScope laryngoscopy provides a glottic view equal or superior compared to Macintosh laryngoscopy for endotracheal intubation in adult patients. Data evaluating GlideScope laryngoscopy in pediatric patients are lacking. This study compared intubation times of GlideScope laryngoscopy vs Macintosh laryngoscopy in pediatric patients. METHODS: Sixty ASA I-III patients, aged 10 years or less, were included in this study. Prior to intubation, airway characteristics were measured, and all patients were given an airway class by a separate anesthesiologist using a Macintosh laryngoscope. Patients were then randomly assigned for endotracheal intubation using a Macintosh laryngoscope or the GlideScope, and intubation time was measured. All blades were investigated for blood traces as a surrogate of laryngeal injury. RESULTS: Demographic data and airway characteristics were not statistically significant different between groups. GlideScope intubation time (14 +/- 5 s) was not different from Macintosh intubation time (13 +/- 5 s). Blood traces were not observed on Macintosh or GlideScope blades. CONCLUSION: The GlideScope video laryngoscope is equally suitable to facilitate orotracheal intubation in pediatric patients compared to the Macintosh laryngoscope with respect to intubation time and laryngeal trauma.

[Anaesthesia for major vascular surgical procedures]. / Anästhesie für grosse gefässchirurgische Eingriffe.

Vascular surgery carries a high perioperative risk for the patients, because of the high incidence of coexisting diseases with an increased risk of cardiovascular complications. Based on preoperative findings, anaesthetic technique, monitoring and postoperative management are planned. For risk optimization the anaesthetist should have a high theoretical and practical experience in the used anaesthetic techniques and a profound knowledge of the pathophysiological characteristics of the vascular procedures.