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CARDIOVASCULAR ANESTHESIA

Xenon Administration During Early Reperfusion Reduces Infarct Size After Regional Ischemia in the Rabbit Heart In Vivo

Benedikt Preckel, MD, DEAA^*, Jost Müllenheim, MD^*, Andrej Moloschavij, MD, Volker Thämer, MD, and Wolfgang Schlack, MD, DEAA^*

Institut für *Klinische Anaesthesiologie and Institut für Herz- und Kreislauf-Physiologie, Heinrich-Heine-Universität Düsseldorf, Germany

Address correspondence and reprint request to Benedikt Preckel, MD, DEAA, Institut für Klinische Anaesthesiologie, Heinrich-Heine-Universität, Postfach 10 10 07, D-40001 Düsseldorf, Germany. Address e-mail to benedikt{at}herzkreis.uni-duesseldorf.de

	Abstract

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The noble gas xenon can be used as an anesthetic gas with many of the properties of the ideal anesthetic. Other volatile anesthetics protect myocardial tissue against reperfusion injury. We investigated the effects of xenon on reperfusion injury after regional myocardial ischemia in the rabbit. Chloralose-anesthetized rabbits were instrumented for measurement of aortic pressure, left ventricular pressure, and cardiac output. Twenty-eight rabbits were subjected to 30 min of occlusion of a major coronary artery followed by 120 min of reperfusion. During the first 15 min of reperfusion, 14 rabbits inhaled 70% xenon/30% oxygen (Xenon), and 14 rabbits inhaled air containing 30% oxygen (Control). Infarct size was determined at the end of the reperfusion period by using triphenyltetrazolium chloride staining. Xenon reduced infarct size from 51% ± 3% of the area at risk in controls to 39% ± 5% (P < 0.05). Infarct size in relation to the area at risk size was smaller in the xenon-treated animals, indicated by a reduced slope of the regression line relating infarct size to the area at risk size (Control: 0.70 ± 0.08, r = 0.93; Xenon: 0.19 ± 0.09, r = 0.49, P < 0.001). In conclusion, inhaled xenon during early reperfusion reduced infarct size after regional ischemia in the rabbit heart in vivo.

Implications: Xenon might be a suitable volatile anesthetic in an ischemia-reperfusion situation.

	Introduction

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Xenon is a noble gas with favorable physical, chemical, and pharmacological properties to serve as an ideal anesthetic. Its anesthetic properties have been demonstrated as early as 1946 by Lawrence et al. (1) in mice. In 1951, Cullen and Gross (2) reported the first use of xenon as an anesthetic in humans. Other studies reported that xenon produces cardiovascular stability with no significant changes in myocardial contractility, as assessed by echocardiographic variables of contractility, cardiac index, blood pressure, or systemic vascular resistance (3–5). The only cardiovascular side effects observed during xenon anesthesia was a tendency to decreased heart rate accompanied by an increased variability of the cardiac rhythm (4,6). These minimal cardiovascular effects of xenon are in contrast to the other available volatile anesthetics, which can all produce marked hemodynamic side effects. In previous studies, it was demonstrated that volatile anesthetics offer specific protection against myocardial reperfusion injury. These volatile anesthetics protect the myocardium against reperfusion injury in vitro and in vivo (7–11). The minimal cardiovascular alterations caused by xenon may make it a suitable inhaled anesthetic in a myocardial ischemia-reperfusion situation. We investigated the effects of xenon on infarct size development after regional ischemia in the rabbit heart in vivo.

	Methods

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Experimental procedures complied with the "Guiding Principles in the Use and Care of Animals" approved by the Council of the American Physiological Society and with local and state regulations. The program was approved by the bioethical committee of the District of Düsseldorf.

New Zealand White rabbits (body weight 2.7–3.4 [mean 3.1] kg) were anesthetized with IV sodium thiopental (thiopentone) 15–30 mg/kg followed by -chloralose 40 mg · kg^-1 · h^-1 IV. The trachea was intubated with a Woodbridge tube (internal diameter 3.5 mm), and ventilation was controlled by using a Harvard rodent ventilator^TM (Model 683; Harvard, South Natick, MA). Ventilation frequency was set at 28–35 bpm and tidal volume at 20–25 mL to maintain end-tidal CO₂ at approximately 35 mm Hg, corresponding to an arterial PCO₂ of approximately 38 mm Hg (Datex Capnomac Ultima, Division of Instrumentarium Corp., Helsinki, Finland). Rabbits were ventilated with air containing 30% oxygen. Surface electrocardiogram (Siemens-Elema AB, Medicins and Technik, Selna, Sweden) was recorded continuously.

For measurement of aortic pressure (AOP), a 20-gauge Teflon® (DuPont, Wilmington, DE) catheter was introduced from the left carotid artery into the aortic arch and connected to a pressure transducer (Statham transducer, PD23^TM; Gould, Cleveland, OH). After cannulation of the external jugular vein, animals received a continuous infusion of normal saline 15 mL · kg^-1 · h^-1 to compensate for fluid losses. After median sternotomy and pericardiotomy, an ultrasonic flow probe was placed around the ascending aorta to measure left ventricular (LV) stroke volume minus coronary flow volume (4S ultrasonic flow probe, T208^TM; Transonic Systems Inc., Ithaca, NY). LV pressure was monitored by using a catheter tip manometer (Micro-Tip Pressure Transducer, Sensodyn S PO SF-1^TM; Braun Melsungen AG, Melsungen, Germany) introduced via the left atrium. A snare was passed around a major coronary artery for later occlusion. After completion of the preparation, the thoracotomy site was covered with plastic film to lessen evaporative and convective heat loss. Temperature was measured inside the pericardial cradle (GTH 1160, Digital Thermometer^TM; Geisinger Electronic, Germany) and maintained at 38.5 ± 0.3%°C by adjusting a heating pad and an infrared lamp.

Fifteen minutes after completion of the preparation, baseline measurements were performed and the prepared coronary artery was occluded by tightening the snare. The effectiveness of this maneuver was verified by the appearance of epicardial cyanosis and electrocardiogram changes. Ventricular fibrillation during coronary artery occlusion was treated by using electrical defibrillation (5 J, DCS261 Defibrillator^TM Piekser, Ratingen, Germany). After 30 min of occlusion, the snare was released, and reperfusion was verified by the disappearance of epicardial cyanosis. After 120 min of reperfusion, the heart was arrested by injection of potassium chloride solution into the left atrium, quickly excised, and mounted on a modified Langendorff apparatus for perfusion with ice-cold normal saline via the aortic root at a perfusion pressure of 40 cm H₂O to wash out intravascular blood. The coronary artery was then reoccluded, and the remainder of the myocardium was perfused through the aortic root with 0.2% Evans blue. This treatment identified the area at risk as unstained. The heart was then frozen, cut into 2-mm thick slices, and incubated in buffered 0.75% triphenyltetrazolium chloride solution. This stains viable myocardium red, while necrotic myocardium is unstained. The area at risk and the infarcted area were determined by using planimetry. Finally, the dry weight of each slice was measured.

Fourteen rabbits underwent the ischemia-reperfusion program without further intervention (Control); another 14 rabbits inhaled 70% xenon/30% oxygen during the first 15 min of reperfusion (Xenon). To achieve a stable concentration at the beginning of the reperfusion period, xenon inhalation was started during the last 5 min of ischemia.

LV pressure, its first derivative dP/dt, AOP, and stroke volume were continuously recorded on an ink-recorder (Recorder 2800^TM, Gould, Cleveland, OH). The data were digitized by using an analogue-to-digital converter (Data Translation, Marlboro, MA) at a sampling rate of 500 Hz and processed later on a personal computer. LV end-diastole was determined as the point when LV dP/dt started its rapid upstroke after crossing the zero line. LV end-systole was defined as the point of minimal dP/dt. Global systolic function was measured as LV peak systolic pressure (LVPSP) and the first derivative of LV pressure, LV dP/dt_max. The time constant of decrease in LV isovolumic pressure () was used as an index of LV diastolic function. Cardiac output (CO) was calculated from stroke volume and heart rate, rate pressure product from heart rate and LVPSP, and systemic vascular resistance from mean AOP and CO, assuming a right atrial pressure of 0 mm Hg in the open-chest preparation.

All data were expressed as mean ± SEM. The effects of xenon on ischemic myocardium were assessed by paired Student’s t-test. In ischemia-reperfusion experiments, statistical analysis was done by using two-way analysis of variance for time and treatment (experimental group) effects. If an overall significance between groups was found, a comparison was performed for each time point by using one-way analysis of variance for repeated measurements followed by post hoc Dunnett’s test for time effects and by Student’s t-test for treatment effects. Differences in the influence of area-at-risk size on infarct size were determined by using analysis of variance for differences between regression slopes, followed by analysis of covariance (12). All comparisons were two-tailed, and a P < 0.05 was regarded as significant.

	Results

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Twenty-eight animals were used (Control, Xenon, n = 14 each group). Two animals of each group developed ventricular fibrillation during coronary artery occlusion and were defibrillated.

By chance, the animals of the Xenon group had a 11-mm Hg higher LVPSP, accompanied by a higher rate pressure product, and a greater dP/dt_min during baseline conditions (P < 0.05). All other hemodynamic baseline values were similar in controls and xenon-treated animals (Table 1, Figure 1). Coronary artery occlusion resulted in a decrease of LVPSP by 11% and a decrease of CO by 9% of baseline in both groups (Figure 1). Xenon inhalation had no effect on heart rate, AOP, LVPSP, dP/dt, and (Table 2). CO declined during xenon inhalation, accompanied by a small increase in mean AOP, resulting in an increased systemic vascular resistance (from 461 ± 33 mm Hg· min · mL^-1 · 10^-3 to 530 ± 38 mm Hg · min · mL^-1 · 10^-3, P < 0.05).

View larger version (20K): [in this window] [in a new window]   Figure 1. Left ventricular peak systolic pressure (LVPSP), cardiac output, and heart rate during ischemia-reperfusion experiments in controls and in xenon-treated animals. Data are mean ± SEM, n = 14 in each group. * Significantly different from corresponding baseline value. Significantly different from controls at corresponding time.

Mean LV dry weight was 1.13 ± 0.08 g. The ischemic-reperfused area (area at risk) constituted 36% ± 3% and 44% ± 3% of the LV in controls and xenon-treated animals (P = 0.07, Table 3), respectively. In the control group, infarct size was 51% ± 3% of the area at risk. Infarct size was reduced in xenon-treated animals (39% ± 5% of the area at risk). In the rabbit heart, infarct size is nearly linearly dependent of the size of the area at risk (13). To correct for the confounding effect of the area at risk size, we analyzed the relationship of the area-at-risk size and the amount of infarcted tissue (Figure 2). The slope of the regression line relating infarct size and area-at-risk size was significantly reduced in the Xenon group (0.19 ± 0.09) compared with the control group (0.70 ± 0.08, P < 0.001).

View larger version (14K): [in this window] [in a new window]   Figure 2. Scatterplot of the relationship between infarct size and size of the area at risk (n = 14 in each group). The slope of the regression line was significantly smaller in xenon-treated animals (Control: y = 0.70 ± 0.08 x - 0.06 ± 0.03, r = 0.93; Xenon: y = 0.19 ± 0.09 x + 0.09 ± 0.05, r = 0.49; P < 0.001).

	Discussion

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Myocardial reperfusion injury may occur in a variety of clinical settings, for example after periods of cardiac arrest during heart surgery with cardiopulmonary bypass. In our current understanding of ischemia-reperfusion injury, reperfusion injury is clearly distinguished from the ischemic injury itself. Reperfusion injury can be defined as the additional postischemic injury that can be avoided or reversed by modification of the conditions of reperfusion (14). Volatile anesthetics offer specific actions against myocardial reperfusion injury in different experimental models (7–11). Xenon has been most recently investigated as an inhaled anesthetic in humans. Experimental studies showed hemodynamic stability during xenon administration (4,5). Only few data are available about cardiovascular effects of xenon during pathophysiological states, i.e., myocardial ischemia or cardiomyopathy. In isoflurane anesthetized dogs with experimental dilated cardiomyopathy, Hettrick et al. (15) found only minimal cardiovascular effects of xenon inhalation.

In the present study, xenon was given in the presence of regional myocardial ischemia and reperfusion. While in healthy patients, no hemodynamic changes during xenon anesthesia were reported, in the rabbit with regional myocardial ischemia, a slight reduction of CO and an increase in mean AOP was observed during xenon inhalation, resulting in an increase in systemic vascular resistance. This effect was rapidly reversible after discontinuation of xenon (Figure 1). It cannot be ruled out that these effects have been influenced by an interaction of xenon with the basal anesthetic chloralose.

The finding that a relative lack of cardiovascular side effects of a volatile anesthetic is not a predictor of its cardioprotective effects may be surprising at first, but is consistent with previous observations that antagonism of the cardiodepressant effects of halothane by noradrenaline infusion had no effect on the cardioprotection against reperfusion injury (10). Sevoflurane and desflurane had fewer hemodynamic side effects during reperfusion, but offered a similar degree of cardioprotection as enflurane (11).

There are few data available about cellular effects of xenon in different tissues. Its anesthetic and analgesic effects are related to a powerful inhibition of the N-methyl-D-aspartate receptor (16). Suppression of Ca²⁺ signals have been considered a common denominator of the effects of xenon on the cell cycle (17). There is evidence that xenon interferes with intracellular Ca²⁺ signaling by inhibiting Ca²⁺-induced Ca²⁺ influx, with no effects on the intracellular resting Ca²⁺ concentration (18). The volatile anesthetic halothane produces its protective effect against myocardial reperfusion injury by an action on the Ca²⁺-dependent Ca²⁺ release channel of the sarcoplasmic reticulum (19). Xenon’s possible target at the cardiomyocyte is not known, but influences on Ca²⁺ signals might be involved in the reduction of infarct size we observed. A recently published study, however, demonstrated that xenon does not alter the major cardiac cation currents (20). That study investigated Na⁺, L-type Ca²⁺ and the inward-rectifier K⁺ channel in the presence and absence of xenon. Although some of these channels may contribute to the development of ischemic injury (like sodium overload), their contribution to reperfusion injury is questionable. Effects of xenon on other mechanisms involved in ischemia-reperfusion injury (humoral side effects, sympathetic nervous system activity, activation of neutrophils) are not known.

We used only one concentration of xenon, and the conclusions must be limited to this concentration. For the rabbit, the exact minimal alveolar concentration (MAC) has not been determined. In dogs, the MAC of xenon is super-atmospheric at 119% (21). In humans, 71% xenon is one MAC (22). Considering the MAC values of the commonly used volatile anesthetics in humans, dogs, and rabbits, and relating these values to the MAC of xenon, it is likely that the MAC of xenon in rabbits is in the range of 120%, similar to the value in dogs. Therefore, a smaller MAC-concentration of xenon was used in the present study compared with our previous investigations of volatile anesthetics in a reperfusion situation in vivo (10,11). This makes it difficult to compare the absolute effect of xenon on hemodynamics and on infarct size reduction with the effects of the other volatile anesthetics.

We used -chloralose for basal anesthesia because it maintains nearly normal cardiovascular reflexes (23). An antiischemic effect of -chloralose has not been found, but we cannot completely exclude an interference with reperfusion injury in the present study. To exclude effects of xenon on the severity of ischemia, it was administered during early reperfusion to investigate specific actions against reperfusion injury. However, it is possible that alteration of systemic hemodynamics (reduced CO) during the first 15 min of reperfusion also had effects on infarct size. Xenon was administered for a short period directly before reperfusion to assure that the substance was present at the onset of reperfusion when mitochondrial energy production is reactivated, creating the danger of hypercontracture (24). Because xenon was administered only during the last minutes of ischemia, a potential antiischemic effect of xenon cannot have contributed to differences in infarct size. The rabbit has virtually no collateral circulation (25), and therefore, it is not necessary to assess collateral blood flow in the ischemic area. However, alterations of blood flow to different myocardial layers (endo-, mid-, epicardial) of the nonischemic area were not measured and can therefore not be excluded. The rabbit heart may have other ways of supplying oxygen to parts of the area at risk which are independent of collateral blood flow, probably by diffusion or through retrograde thebesian vein circulation (13). Consequently, there is virtually no infarction in very small areas at risk. Therefore, we analyzed the relationship between infarct size and size of the area at risk to avoid distortion of the results by unaccounted differences in size of the area at risk between groups. In this analysis, the slope of the regression line relating infarct size and area at risk size was significantly reduced in the xenon-treated animals. Therefore, the reduction of infarct size seen in the xenon group is not the result of differences of the area at risk size.

By chance, there was a small difference in LVPSP during baseline conditions, with LVPSP being higher in the xenon group. However, LV unloading has been associated with beneficial effects against myocardial reperfusion injury (26). A higher LVPSP might therefore increase infarct size, and it is unlikely that the reduction in infarct size seen in the present study is caused by the higher LVPSP during baseline in xenon-treated animals.

Because of increasing clinical use of thrombolysis, percutaneous balloon angioplasty, and coronary bypass surgery, it is of great practical interest to determine if additional therapeutic intervention during the ischemia/reperfusion period can lead to a reduction of ischemia/reperfusion injury. The effects of xenon on infarct size reduction after cardioplegic arrest or during a clinical ischemia-reperfusion situation remain to be investigated. The analgesic potency of xenon combined with its hemodynamic stability and its beneficial effects against reperfusion injury may make it a suitable anesthetic during cardiac surgery.

	Acknowledgments

 
We thank Elke Hauschildt, BTA, for excellent technical assistance. Xenon was generously supplied by Messer Griessheim, Germany.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999