BACKGROUND: Oxygen-derived free radicals are known to contribute to tissue injury during myocardial ischemia and reperfusion. Recent in vitro studies have shown that propofol has potent antioxidant properties. The present study was aimed to investigate the effects of propofol on recovery of mechanical and coronary endothelial function in a myocardial stunning model. METHODS: Thirty-five dogs were acutely instrumented under halothane anesthesia to measure aortic and left ventricular pressure, pulmonary and left anterior descending coronary artery (LAD) flow, and subendocardial segment length. After completion of the surgery, halothane was replaced by fentanyl- midazolam. Animals were then subjected to 15 min of LAD occlusion and 3 hrs of reperfusion under either intracoronary (i.c.) propofol (5 microgram/mL, n=11; 20 microgramg/mL LAD flow, n=12) or vehicle (saline, n=12) for 1 hr beginning 30 min before LAD occlusion. Percent segment shortening (%SS) and the slope of the preload recruitable stroke work (Mw), as an index of regional myocardial contractility, and peak lengthening rate (dL/dtmax) and percent post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. Coronary endothelial function was assessed by examining LAD flow response to i.c. acetylcholine (ACh, 1 microgram over I min) and i.c. sodium nitroprusside (SNP, 20 microgram over I min). The myocardial content of malondialdehyde (MDA) from LAD area was measured to evaluate lipid peroxidation. RESULTS: Despite equally severe ischemic dysfunction during LAD occlusion, recovery of %SS was significantly improved during reperfusion by either dose of propofol compared to controls. However, Mw recovered to the baseline within 60 min of reperfusion in all three groups. In addition, propofol-treated dogs showed better recovery of both indices of regional diastolic function (dL/dtmax and %PSS) as compared to controls. Ischemia-reperfusion similarly attenuated the increases in the LAD flow by ACh in all the groups, whereas it had no significant effect on these increases in LAD flow by SNP. The increase in MDA induced by ischemia and reperfusion was significantly suppressed by either dose of propofol. CONCLUSIONS: The results indicate that propofol attenuates mechanical but not coronary endothelial dysfunction in postischemic, reperfused myocardium in an open-chest canine model. The protective action of propofol against mechanical dysfunction is probably due to its effect to reduce lipid peroxidation.
Acetylcholine ; Anesthesia ; Animals ; Coronary Vessels ; Dogs* ; Endothelium* ; Free Radicals ; Halothane ; Ischemia ; Lipid Peroxidation ; Malondialdehyde ; Midazolam ; Myocardial Ischemia ; Myocardial Stunning* ; Myocardium ; Nitroprusside ; Propofol* ; Reperfusion ; Stroke ; Ventricular Pressure

BACKGROUND: The influenza is a contagious respiratory illness caused by influenza viruses. The primary target groups recommended for annual vaccination are healthcare workers and households which have frequent contact with persons at high risk and can transmit influenza to those persons at high risk. Members of these groups should be vaccinated against the flu so that they can avoid getting infected with continuously mutating influenza viruses. We assessed healthcare workers' knowledge and attitudes regarding influenza vaccination in order to help promote the vaccination rate. METHODS: This survey was carried out in two hospitals affiliated with the Catholic University School of Medicine, from December 2004 to January 2005. Of the 3,023 questionnaires distributed, 2,023 could be evaluated. RESULTS: The most frequently cited reason for receiving influenza vaccine was self-protection against influenza (55.4%). The most common reasons for not receiving influenza vaccine are personal health problems such as concurrent flu, pregnancy or breast-feeding (29.2%). There is no significant difference in the frequency of side effect between two groups receiving and not receiving vaccine. The most frequent side effect of influenza vaccination is flu-like syndrome; People receiving vaccine have more significant knowledge than those people not receiving vaccine about efficacy of flu vaccination, risk of influenza infection of healthcare workers and their need of flu vaccination. CONCLUSION: In order to promote the vaccination rate, education targeting people at high risk need to keep continuous and facilitate access to vaccination.
Delivery of Health Care* ; Education ; Family Characteristics ; Humans ; Influenza Vaccines ; Influenza, Human* ; Orthomyxoviridae ; Pregnancy ; Vaccination* ; Surveys and Questionnaires

Succinylcholine (Sch) has long been used to facilitate laryngoscopy and endotracheal intubation for general anesthesia, because of a rapid onset of intense but brief paralysis. However, exaggerated potassium (K+) release following Sch, sufficient to cause ventricular dysrhythmias and cardiac arrest, has sporadically been reported in susceptible conditions, including spinal cord injury, severe burn, massive trauma and neuromuscular disorder. And diazepam has been shown to attenuate the increase in serum K+ following Sch administration. The purpose of this study was to assess the effect of Sch on serum K+ in patients with spinal cord lesions, and to assess the effect of pretreatment with diazepam (0.05 mg/kg IV) on potassium flux. The results were as follows: 1) Baseline K+ values were not significantly different among the groups. 2) The time to peak increases in K+ was 3 minutes following Sch in all groups. 3) The magnitude of maximum increases in K' following Sch were 0.32 Eq/l, 0.63 mEq/l, 0.06 mEq/I and 1,10 mEq/I in group 1, group 2A, group 2B, and group 3, respectively. 4) Diazepam pretreatment attenuated the increases in K+ following Sch. From the above results, it can be concluded that Sch may safely be used to facilitate intubation in paraplegic patients, provided that they are normokalemic and pretreated with diazepam.
Anesthesia, General ; Burns ; Diazepam ; Heart Arrest ; Humans ; Hypnotics and Sedatives ; Intubation ; Intubation, Intratracheal ; Laryngoscopy ; Paralysis ; Potassium* ; Spinal Cord Injuries ; Spinal Cord* ; Succinylcholine*

Perioperative myocardial infarction is a major cause of morbidity and mortality in patients who undergo non-cardiac surgery, while an increasing number of patients with a coronary artery disease are presenting for surgery. In order to cope with this problem, one should first evaluate risk factors of these complications, and then manage the patient at risk to reduce or eliminate the risk factors. Risk assessment evaluates patients' co-morbidities and exercise tolerance, as well as the type of surgery to be performed, to determine the overall risk of perioperative cardiac complications. Previous or current cardiac disease, diabetes, and renal insufficiency all confer higher risks for perioperative cardiac complications. Poor exercise tolerance and high-risk surgical procedures (e.g., vascular, prolonged thoracic, or abdominal operations) also predict worse perioperative outcomes. Stress testing should be reserved for patients at moderate to high risk undergoing moderate- or high-risk surgery and those who have poor exercise capacity. After the assessment of the risk of cardiac complications, one should take measures to reduce it, including medical therapy and coronary intervention. Medical therapy using beta blockers, statins, and alpha-2 agonists may be effective to reduce perioperative risk and to obviate the need for more invasive procedures in high-risk patients. Coronary intervention should be performed for those patients who are indicated independent of the non-cardiac surgery. There appears to be no single best myocardium-protective anesthetic management, and therefore, the choice of anesthesia and intraoperative monitors is left at the discretion of the anesthesia care team.
Anesthesia* ; Coronary Artery Disease ; Exercise Test ; Exercise Tolerance ; Heart Diseases* ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Mortality ; Myocardial Infarction ; Renal Insufficiency ; Risk Assessment ; Risk Factors

No Abstract available.
Anesthetics* ; Reperfusion Injury* ; Reperfusion*

No abstract available.
Hemodynamics* ; Nitroprusside*

No abstract available.

BACKGROUND: Video-assisted thoracic surgical procedure via thoracoscopy has recently gained popularity, as it avoids a thoracotomy, reducing intraoperative blood loss, postoperative pain, respiratory dysfunction and hospital stay. However, to visualize adequately the intrathoracic structures, creation of artificial pneumothorax by carbon dioxide insufflation during thoracoscopy would cause significant hemodynamic compromise. The aim of this study was to evaluate the effect of CO2 insufflation into the pleural cavity on the hemodynamics and the arterial blood gas tension under general anesthesia. METHODS: Twenty-five patients, after intubation with single lumen endotracheal tube, underwent enflurane (1~2%) and N2O-O2 (1:1) general anesthesia. Before placement of a thoracoscope, the baseline mean arterial pressure and heart rate were obtained. Measurements were taken at 5, 10, and 20 min. after the beginning of carbon dioxide insufflation (3~5 mmHg) and 10 min. after gas evacuation. Blood gas analyses were done before, during CO2 insufflation and after CO2 evacuation. Data were analyzed using Student t-test. RESULTS: Positive-pressure CO2 insufflation (3~5 mmHg) caused a decrease of mean arterial pressure (5~7%) and an increase of airway pressure (1.5 times) and heart rate (13~20%) throughout the gas insufflation period (p<0.05). Blood gas analyses revealed no significant change. CONCLUSIONS: These results suggest that low CO2 insufflation pressures (3~5 mmHg) may cause cardiovascular depression during thoracoscopy. Therefore careful monitorings should be done during this procedure.
Anesthesia, General* ; Arterial Pressure ; Blood Gas Analysis ; Carbon Dioxide* ; Carbon* ; Depression ; Enflurane ; Heart Rate ; Hemodynamics* ; Humans ; Insufflation* ; Intubation ; Length of Stay ; Pleural Cavity ; Pneumothorax, Artificial ; Postoperative Hemorrhage ; Thoracic Surgical Procedures ; Thoracoscopes ; Thoracoscopy* ; Thoracotomy

In order to evaluate the efficacy of adenosine triphosphate (ATP) in the reduction of left ventricular afterload, we studied the hemodynamic and intrapulmonary shunt effects of intravenous ATP during ethrane-N2O anesthesia. Hemodynamic measurements and arterial and mixed venous blood gas analyses were made in ten patients before (baseline) and 10 min after. ATP infusion at 80,60,120 and 250 mcg/kg/min, respective. The results were as follows: 1) ATP produced a rapid and stable reduction in mean arterial pressure resulting from a marked decrease in systemic vascular resistance. 2) Cardiac index increased significantly by 14, 47 and 72% from baseline value after intravenous infusion of ATP at rates of 60, 120 and 250 mcg/kg/min, respectively. 3) Stroke volume index, heart rate, mean pulmonary arterial pressure, pulmonary capillary wedge pressure and central venous pressure increased significantly, whereas systemic vasular resistance and pulmonary vascular resistance decreased significantly in a dose related fashion during ATP infusion. 4) Intrapulmonary ehunt fraction increased from 5.67% to 6.73, 8.28, 9.85 and 13.38% after intra- venous infusion of ATP at rates of 30, 60, 120 and 250 mcg/kg/min, respectively. 5) Arterial oxygen tension decreased significantly after ATP infusion. These results suggest that ATP might be of value in augmentation of cardiac performance in patients with low cardiac output with high peripheral vascular resistance.
Adenosine Triphosphate* ; Adenosine* ; Anesthesia ; Arterial Pressure ; Blood Gas Analysis ; Cardiac Output, Low ; Central Venous Pressure ; Enflurane* ; Heart Rate ; Hemodynamics* ; Humans ; Infusions, Intravenous ; Lung ; Oxygen ; Pulmonary Wedge Pressure ; Stroke Volume ; Vascular Resistance

BACKGROUND: The present study was aimed (1) to assess the effects of nitric oxide (NO) synthesis inhibitor on regional myocardial function and systemic and pulmonary hemodynamics; (2) to determine whether the blockade of the cyclo-oxygenase (COX) pathway modifies these effects on the variables, and (3) to investigate the mechanism of cardiac depression following NO synthesis inhibition in an open-chest canine model. METHODS: Twenty-five dogs of either sex were acutely instrumented under 1.6% ethrane anesthesia to measure aortic, pulmonary arterial and left ventricular pressure, pulmonary (cardiac output) and left circumflex coronary flow, and subendocardial segment length. NG-nitro-L-arginine methyl ester (L- NAME) at doses of 0.3, 1.0, 3.0, or 10.0 mg/kg i.v. was administered alone (control dogs, n = 10) or in the presence of COX inhibitor, indomethacin (10 mg/kg i.v., n = 10). Seven dogs (n = 7) received phenylephrine at doses of 0.1, 0.3, 1.0, or 3.0 microgram/kg/min i.v. to compare its hemodynamic effects with those of L-NAME. The preload recruitable stroke work slope (Mw) and percent systolic shortening (%SS) as an index of regional myocardial contractility, and the maximum segment lengthening rate (dL/dt max) and percent post-systolic shortening (%PSS) as an index of regional diastolic function, were evaluated. RESULTS: L-NAME dose-dependantly attenuated both regional systolic (Mw and %SS) and diastolic functions (dL/dt max and %PSS), whereas it caused an increase of coronary flow. L-NAME dose- dependently increased systemic blood pressure and vascular resistance as well as pulmonary arterial pressure and vascular resistance. L-NAME also reduced cardiac and stroke volume indices. Pretreatment with indomethacin did not affect the regional myocardial and systemic hemodynamic responses to L-NAME, but did blunt the coronary flow and pulmonary pressure responses. The magnitude of decreases in cardiac and stroke volume indices and Mw was greater with L-NAME than with phenylephrine (P <0.05), despite the comparable blood pressure increases. CONCLUSIONS:These results suggest (1) that NO plays a significant role in cardiac function as well as in systemic and pulmonary but not coronary, vasomotor activities, and (2) that COX products are involved in pulmonary hemodynamic responses to NO synthesis inhibition. It is also suggested that the decline in cardiac output following the NO synthesis inhibition results from a direct myocardial depressant effect of the drug.
Anesthesia ; Animals ; Arterial Pressure ; Blood Pressure ; Cardiac Output ; Depression ; Dogs* ; Enflurane ; Hemodynamics* ; Indomethacin ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Phenylephrine ; Prostaglandin-Endoperoxide Synthases ; Stroke ; Stroke Volume ; Vascular Resistance ; Ventricular Pressure