A RAPIDLY growing body of evidence indicates that volatile anesthetics protect myocardium against reversible and irreversible ischemic injury. Identifying the mechanisms by which volatile agents mediate these antiischemic actions is the subject of intense research. This objective has been difficult to accomplish because volatile anesthetics also profoundly affect cardiovascular function. Volatile agents reduce arterial and coronary perfusion pressure, cause dose-related depression of myocardial contractility, produce coronary vasodilation, affect electrophysiologic function, and modify autonomic nervous system activity to varying degrees. Therefore, the antiischemic effects of volatile anesthetics may be mediated, at least in part, by favorable alterations in myocardial oxygen supply–demand relations, preservation of energy-dependent cellular functions, and increased coronary blood flow. However, it seems unlikely that changes in myocardial metabolism and coronary perfusion caused by volatile anesthetics are solely responsible for protection against ischemic damage. Instead, several endogenous signal transduction pathways, acting through the adenosine triphosphate (ATP)–sensitive potassium (KATP) channel and involving the generation of reactive oxygen species (ROS), have been implicated in mediating the antiischemic actions of volatile anesthetics. The experimental and clinical findings documenting the phenomenon of volatile anesthetic preconditioning against ischemic injury of myocardium are evaluated. Recent findings in vitro and in vivo that seek to define the intracellular mechanisms responsible for these beneficial actions are also summarized.

Mechanisms of cardioprotection by volatile anesthetics.

Cardioprotection by volatile anesthetics.

SPECIFIC AIMSThis study used an in vivo rat model of ischemia-reperfusion injury to 1) examine the potentiation of cardiac KATP channel opening by opioids and volatile anesthetics to confer protect...

https://faseb.onlinelibrary.wiley.com/doi/pdf/10.1096/fj.02-0170fje

Delta opioid agonists and volatile anesthetics facilitate cardioprotection via potentiation of KATP channel opening

1 Schröder FH. Prostate cancer: to screen or not to screen? BMJ 1993; 306 : 407–8 2 Schröder FH, Boyle P. Screening for prostate cancer – necessity or nonsense? Eur J Cancer 1993; 29A (5): 656–61 3 Bentvelsen FM, Schröder FH. Modalities available for screening for prostate cancer. Eur J Cancer 1993; 29A (6): 804–11 4 Schröder FH, Damhuis RAM. Vasectomie en prostaatkanker; toelichting en praktische adviezen. Ned Tijdschr Geneeskd 1993; 137 (10): 485–6 5 Nijs HGT, Tordoir DMR, Schuurman JH, Kirkels WJ, Schröder FH. Evaluatie van de vroege opsporing van prostaatkanker. Tijdschr Soc Gezondheidszorg 1993; 78 : 31A 6 Schröder FH. Screening for prostate cancer (letter to the editor). The Lancet 1994; 343 : 1438–9 7 Schröder FH. The European screening study for prostate cancer. Canadian J Oncol 1994; 4 (Suppl. 1): 102–5 8 Bosch JLHR, Hop WCJ, Niemer AQHJ et al. Parameters of prostate volume and shape in a community based population of men 55–74 years old. J Urol 1994; 152 : 1501–5 9 Blijenberg BG. De standaardisatie van de PSA-bepaling. Tijdschr Klin Chemie 1994; 19 : 271–4 10 Schröder FH. Detection of prostate cancer, screening the whole population has not yet been shown to be worth while (letter to the editor). 1995; 310 : 140–1 11 Denis LJ, Murphy GP, Schröder FH. Report of the consensus workshop on screening and global strategy for prostate cancer. Cancer 1995; 75 (5): 1187–207 12 Schröder FH, Denis LJ, Kirkels WJ, De Koning HJ, Standaert B. European randomized study of screening for prostate cancer: Progress report of Antwerp and Rotterdam pilot studies. Cancer 1995; 76 (1): 129–34 13 Aus G, Pileblad E, Hugosson J. Impact of competing mortality on the cancerrelated mortality in localized prostate cancer. Urology 1995; 46 (5): 672–5 14 Aus G, Hugosson J, Norlen L. Longterm survival and mortality in prostate cancer treated with non-curative intent. J Urol 1995; 154 : 460–5 15 Schröder FH. Screening, early detection, and treatment of prostate cancer: a European view. Urology 1995; 46 (Suppl. 3a): 62–70 16 Bangma CH, Blijenberg BG, Schröder FH. Prostate-specific antigen: its clinical use and application in screening for prostate cancer. Scand J Clin Laboratory Invest 1995; 55 (Suppl. 221): 35–44 17 Bangma CH, Kranse R, Blijenberg BG, Schröder FH. The value of screening tests in the detection of prostate cancer. Part I. Results of a retrospective evaluation of 1726 men. Urology 1995; 46 (6): 773–8 18 Bangma CH, Kranse R, Blijenberg BG, Schröder FH. The value of screening tests in the detection of prostate cancer. Part II. Retrospective analysis of Free/ Total Prostate-Specific Analysis ratio, age-specific reference ranges, and PSA density. Urology 1995; 46 (6): 773–8 19 Blijenberg BG, Kessler A-C, Uhl W. Multicentre evaluation of a new fully automated enzyme immunoassay for total prostate-specific antigen. Eur J Clin Chem Clin Biochem 1995; 33 (965): 973 20 Bangma CH, Hop WCJ, Schröder FH. Eliminating the need for per-operative frozen section analysis of pelvic lymph nodes during radical prostatectomy. BJU 1995; 76 : 595–9 21 Ciatto S, Bonardi R, Mazzotta A et al. Comparing two modalities of screening for prostate cancer: digital rectal examination and transrectal ultrasonography vs. prostate specific antigen. Tumori 1995; 81 : 225–9 22 Denis LJ. Prostate cancer: a continuum of controversy. Eur J Cancer 1995; 31A (5): 839–40 23 Denis LJ. Prostate cancer screening and prevention: realities and hope. Urology 1995; 46 (Suppl. 3a): 56–61 24 Denis LJ. Diagnosing benign prostatic hyperplasia versus prostate cancer. BJU 1995; 76 (Suppl. 1): 17–23 The European Randomized Study of Screening for Prostate Cancer (ERSPC) had, from the beginning in 1993, not only the goal of confirming or excluding a decrease in prostate cancer mortality as a result of screening compared with a randomized control group, but also to contribute to related issues. The secondary goals of the ERSPC were specifically a contribution to an optimization of screening regimens, including the resulting sensitivities and specificities, the relation of screening tests to tumour aggressiveness, the exploration of lead-time and the determination of the optimal re-screening interval, and the optimal age distribution in future applications of prostate cancer screening to healthcare policies. In addition to that, the effect of screening, the diagnosis of prostate cancer and the treatment of the disease on quality of life are major issues of research within the study. Data are collected to evaluate cost-effectiveness and it will soon be possible to produce estimates. In many of these side projects, modelling using the Rotterdam based microsimulation or MISCAN system has become an important tool.

https://bjui-journals.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1464-410X.2003.4698x.x

European Randomized Study of Screening for Prostate Cancer: achievements and presentation.

Background:Isoflurane reduces myocardial ischemia–reperfusion injury within hours to days of reperfusion. Whether isoflurane produces sustained cardiac protection has never been examined. The authors studied isoflurane-induced cardiac protection in the intact mouse after 2 h and 2 weeks of reperfusi

Isoflurane produces sustained cardiac protection after ischemia-reperfusion injury in mice.

In common with halogenated anaesthetics, nicorandil, a new KATP channel opener, has been shown to have cardioprotective and vasodilator effects. Recent studies have also suggested that the vasodilator and protective effects of halogenated anaesthetics are mediated partly via KATP channel opening. This study examined the effects of concurrent administration of nicorandil and isoflurane on haemodynamic state and ventricular function before, during and after 15 min of ischaemia. We studied left ventricular function in 40 anaesthetized rabbits using ultrasonomicrometry. Measurements were obtained before, during and after 15 min of regional ischaemia. Regional ventricular function was assessed in terms of systolic shortening (SS%) and preload recruitable work area (PRWA, the area beneath the regional stroke work vs end-diastolic length relationship) during reperfusion. Four groups were studied: group F (n = 10) received a bolus dose of fentanyl 100 micrograms kg-1 and then 400 micrograms kg-1 h-1 throughout; group 1 (n = 10) received 2.05% end-tidal concentration of isoflurane (1 MAC); group FN (n = 10) received fentanyl, a bolus does of nicorandil 100 micrograms kg-1 and then 25 micrograms kg-1 min-1, 15 min before occlusion; and group IN (n = 10) received isoflurane and nicorandil. Isoflurane decreased left ventricular systolic pressure and ventricular contractility (+dP/dtmax, slope of preload recruitable stroke work, and SS%). Nicorandil increased -dP/dtmax in group FN. Post-ischaemic regional left ventricular contractility in group I did not differ from that in group F, however, groups receiving nicorandil recovered to a greater extent. Group IN showed better recovery compared with all other groups when ventricular contractility was assessed by PRWA normalized to pre-occlusion values (mean 99.3 (SEM 10.5)% vs 73.4 (7.5)%, 50.2 (5.8)% and 52.4 (3.7)% at 120 min reperfusion in groups FN, I and F, respectively). Tissue ATP and lactate contents did not differ between groups. We conclude that concurrent administration of nicorandil and isoflurane enhanced post-ischaemic recovery compared with isoflurane anaesthesia or nicorandil and fentanyl administration.

Beneficial effect of concomitant administration of isoflurane and nicorandil.

Nicorandil, a new KATP channel opener, is used in clinical practice for anti-anginal therapy. It exhibits vasodilator properties as does the halogenated anaesthetic isoflurane. We have examined the cardiovascular effects of increasing concentrations of isoflurane after administration of nicorandil in 10 adult beagle dogs anaesthetized with thiopental and whose lungs were ventilated mechanically. During surgery, anaesthesia was maintained with 1.0-1.5% isoflurane. A left thoracotomy was performed and the heart suspended in a pericardial cradle. Monitoring included: ECG; aortic, left ventricular, arterial, central venous and pulmonary artery pressures; cardiac output; coronary flow; and segmental length in the apical region. After surgery, isoflurane anaesthesia was set at an end-tidal concentration of 1.05% (1 MAC) and measurements obtained; these were repeated with 1.4%, 1.75%, 2.1% and 1.05% isoflurane concentrations after appropriate stabilization periods. Nicorandil (100 micrograms kg-1 bolus, 25 micrograms kg-1 min-1 infusion) was begun and a second dose-response study of isoflurane was obtained as before. Blood samples were obtained for measurement of concentrations of nicorandil. Systolic ventricular function was assessed by systolic shortening (%SS) and preload recruitable stroke work (PRSW). Increasing isoflurane concentration produced decreases in heart rate, systolic pressure, cardiac output, %SS and PRSW. Nicorandil produced a slight decrease in systolic arterial pressure (10 and 15 mm Hg after 1.05% and 2.05% isoflurane) and a slight increase in heart rate (10 and 5 beat min-1 after 1.05% and 2.05% isoflurane). Preload, assessed by end-diastolic length, decreased. Coronary blood flow increased with infusion of nicorandil. Left ventricular function was not affected by infusion of nicorandil. We conclude that nicorandil has only minor vaso/venodilatory effects in the presence of isoflurane. Ventricular function was not altered by infusion of nicorandil.

Cardiovascular effects of concomitant administration of isoflurane and nicorandil in dogs.

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Beneficial effect of concomitant administration of isoflurane and nicorandil.

Cardiovascular effects of concomitant administration of isoflurane and nicorandil in dogs.