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Anesth Analg 2000;91:1333-1338
© 2000 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Recovery from Myocardial Stunning Is Faster with Desflurane Compared with Propofol in Chronically Instrumented Dogs

Andreas Meißner, MD, Thomas P. Weber, MD, Hugo Van Aken, MD, PhD, Kai Zbieranek, BSc, and Norbert Rolf, MD, PhD

Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität, Münster, Germany

Address correspondence and reprint requests to Hugo Van Aken, MD, PhD, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin der Westfälischen Wilhelms-Universität Münster, Albert-Schweitzer-Str. 33, D-48149 Münster, Germany.


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Volatile anesthetics exert a protective role in myocardial ischemia. An increase in sympathetic tone might exert deleterious effects on the ischemic myocardium. The use of the volatile anesthetic desflurane in myocardial ischemia is controversial because of its sympathetic activation. We compared propofol and desflurane on myocardial stunning in chronically instrumented dogs. Mongrel dogs (n = 8) were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure, rate of rise of left ventricular pressure, and myocardial wall-thickening fraction (WTF). An occluder around the left anterior descending artery (LAD) allowed the induction of reversible LAD-ischemia. Two experiments were performed in a cross-over fashion on separate days: 1) Induction of 10 min of LAD-ischemia during desflurane anesthesia and 2) Induction of 10 min of LAD-ischemia during propofol anesthesia. Both anesthetics were discontinued immediately after completion of ischemia. WTF was measured at predetermined time points until complete recovery from ischemic dysfunction occurred. Both anesthetics caused a significant decrease of WTF in the LAD-perfused myocardium. LAD-ischemia led to a further significant decrease of LAD-WTF in both groups. During the first 3 h of reperfusion, WTF was significantly larger in the desflurane group. Mean arterial pressure and heart rate were greater during ischemia and the first 10 min of reperfusion in the desflurane group compared with the propofol group. Recovery from myocardial stunning in dogs was faster when desflurane was used at the time of ischemia as compared with propofol anesthesia. The mechanism for this difference is unclear, but sympathetic activation by desflurane was not a limiting factor for ischemic tolerance in chronically instrumented dogs.

Implications: The use of the volatile anesthetic desflurane during cardiac ischemia is controversial because of its effect of sympathetic activation. In chronically instrumented dogs, recovery from myocardial stunning was faster when desflurane was used for anesthesia during ischemia compared with propofol.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Volatile anesthetics exert a protective role in myocardial ischemia (1,2). The application of desflurane to patients with coronary artery disease, however, is controversial because of its hemodynamic effects on the pulmonary circulation (3) and its activation of sympathetic outflow (4). This activation is a transient phenomenon after rapid increases of the inspiratory concentration in young, healthy individuals without any premedication (5). The blockade of sympathetic efferent activity improves functional recovery after myocardial ischemia (6) and decreases infarct size (7). Therefore, the application of desflurane might lead to a deterioration of functional recovery via deleterious sympathetic activation, although there are broad species differences for sympathetic stimulatory effects of desflurane. Additionally, an effect on myocardial catecholamine stores has been described for rats (8) and humans (9).

However, volatile anesthetics are advocated for use in cardiac surgery, and desflurane might offer advantages because of its pharmacokinetic properties. Currently, an IV technique with propofol in conjunction with opioids is commonly used in cardiac anesthesia. Postischemic reversible contractile dysfunction, termed myocardial stunning, is an important phenomenon after cardiac surgery. The effects of desflurane on myocardial stunning have not been investigated. We investigated the hypothesis that desflurane, like other volatile anesthetics, improves recovery from myocardial stunning as compared with propofol in chronically instrumented dogs.


   Methods
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 Abstract
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 Methods
Results
 Discussion
 References
 
The experimental protocol was approved by the District Government of Münster, and all experiments were performed according to the Helsinki Declaration. After overnight fasting, eight mongrel dogs (either sex; weight, 20–26 kg) were premedicated IM with 15 mg of piritramide and ketamine 5 mg/kg. Animals were anesthetized IV with propofol 5 mg/kg. After tracheal intubation, anesthesia was maintained with isoflurane in a mixture of oxygen and air. Cefamandole 30 mg/kg was given as a prophylactic perioperative antibiotic.

Details of the instrumentation have been described elsewhere (10). Briefly, a left thoracotomy in the fifth intercostal space was performed under aseptic conditions. Under direct vision, the descending aorta and the left atrium were cannulated by using 18-gauge catheters for measurement of pressures, injection of microspheres, and withdrawal of blood. A pressure microtransducer was inserted into the left ventricle through an apical stab wound for measurement of left ventricular pressure (LVP) and rate of rise of LVP (LVdP/dt) (11). Pulsed Doppler blood flow velocity probes were fitted around the left anterior descending (LAD) and the left circumflex (Cx) coronary arteries. For measurement of regional myocardial wall-thickening fraction, 10-MHz pulsed Doppler crystals were sutured to the myocardium of the LAD and Cx perfused areas. Proximal to the Doppler flow probe, a hydraulic occluder was positioned around the LAD for the induction of reversible ischemic episodes in the LAD-perfused myocardium. After closure of the thorax, all leads were tunneled subcutaneously and exited from the body between the scapulae.

Experiments were performed only after complete recovery from the instrumentation and when blood gas values and hemodynamic variables had returned to normal. After the instrumentation, the animals were trained daily to get accustomed to the experimental environment and to lie quietly in a cage when connected to the data acquisition system.

Aortic and left atrial pressures were measured by using disposable pressure transducers. Pressures, flow velocities, and wall-thickening signals were processed by using a six-channel pulsed Doppler system. The left ventricular micromanometer was calibrated to the pressures measured in the aorta and left atrium. The LVP signal was electronically differentiated. All signals were recorded on an eight-channel thermal writing polygraph.

All animals underwent the two experimental conditions in a cross-over fashion, randomized (four animals successfully received their first coronary artery occlusion under desflurane-anesthesia and three animals underwent the first ischemic episode using propofol). Blood flow was determined for each state by using colored microspheres. The number of determinations was limited to four because of the availability of five colors. Because multiple stun maneuvers may induce extensive development of coronary collaterals and thus may preclude the induction of postischemic dysfunction, the number of ischemic episodes was restricted to two in each animal.

Desflurane anesthesia was induced by using a mask after the application of 0.2 mg of fentanyl as bolus IV to avoid excessive sympathetic stimulation. After an adequate level of anesthesia had been achieved, the trachea was intubated. Anesthesia was maintained with desflurane in a mixture of oxygen in air. The desflurane concentration was measured by using a gas-monitor and kept constant at 1.2 minimum alveolar concentration, which is 7.2 vol% in dogs (12). The minute volume and oxygen:air ratio was adjusted to achieve a PaCO2 of 35–45 mm Hg and a PO2 of 90–120 mm Hg. Propofol anesthesia was induced by bolus injection followed by a continuous infusion of 30 mg · kg-1 · h-1 after the application of 0.2 mg of fentanyl. The ventilator was adjusted to the same values as used during desflurane anesthesia.

The following experiments were performed in succession for each of the two conditions: 1. Measurement of baseline values in the awake state, the induction of desflurane anesthesia, measurement of values during steady-state desflurane anesthesia (at least 20 min after the intubation), and the induction of 10 min of LAD-ischemia. The regional wall-thickening fraction (WTF) was followed until complete recovery had occurred. 2. Measurement of baseline values in the awake state, the induction of propofol-anesthesia, measurement of values during steady-state propofol anesthesia (at least 20 min after the intubation), followed by the induction of 10 min of LAD-ischemia. Regional WTF was recorded as above.

All variables were measured continuously after release of the hydraulic occluder. The dose of propofol and desflurane was chosen as the infusion rate or inspiratory concentration to prevent movement to incision of the skin. Because of a different pharmacokinetic profile in dogs, the dose of propofol is 30 mg · kg-1 · h-1, which achieves a plasma concentration of 6 µg/mL (13). The concentration of desflurane was also taken from previous findings in laboratory animals (12). An experimental period from 20 to 60 min after ischemia was ended by awakening the dogs.

A second ischemic episode (either for Experiment 1 or 2) was induced only when regional myocardial function of the LAD-perfused area had completely recovered; the minimal time interval between the two experiments was 72 h. The second experiment was performed only when baseline values deviated less than 5% from the baseline values of the previous experiment.

Regional myocardial blood flow was measured with colored microspheres. For each determination, 9 x 106 microspheres suspended in a volume of 3 mL was injected into the left atrium. The reference blood sample was withdrawn from the aortic catheter at a rate of 10 mL/min. After the animals had been killed, the heart was dissected and tissue samples were obtained from the Cx- and the LAD-perfused left ventricle. LAD samples were taken from the immediate vicinity of the LAD wall-thickening probe. Only samples from animals with severe ischemic dysfunction as determined by the LAD wall-thickening probe were included. Samples were further divided into the subendocardial, subepicardial, and midmyocardial layers. Measurement of microspheres in the tissue samples was performed as described previously (14,15). Measurement of regional myocardial blood flow to the above-mentioned regions was performed four times during the two experiments: during desflurane anesthesia without ischemia, during desflurane anesthesia 5 min after the induction of ischemia, during propofol anesthesia without ischemia, and during propofol anesthesia 5 min after the induction of ischemia.

Data were analyzed by using repeated measures two-way analysis of variance. The analysis of each time point was determined by Bonferroni-corrected Student’s t-test whenever appropriate; P < 0.05 was considered significant. Data are presented as mean ± SEM.


   Results
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 Methods
 Results
Discussion
 References
 
One of the eight instrumented dogs had to be excluded from the study because the balloon occluder ruptured during the induction of the second ischemic episode.

Both propofol and desflurane anesthesia decreased mean arterial pressure and tended to increase heart rate (Table 1). No change was noted in left atrial pressure. The induction of ischemia did not change the mean arterial pressure but increased heart rate and left atrial pressure. During reperfusion, the heart rate increased and mean arterial pressure reached a maximum at approximately the 15th min. The animals were then awakened from anesthesia, after which the heart rate recovered by the 30th min.


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  		Table 1. Hemodynamic Variables During Ischemia and Reperfusion
 
The induction of anesthesia in both experiments led to a decrease of LVdP/dt as compared with baseline. Ischemia led to a further decrease in LVdP/dt, which returned to baseline values by the 15th min of reperfusion.

The induction of anesthesia led to a significant reduction of WTF in both experimental conditions. The degree of WTF reduction during ischemia was not different between the two anesthetics. The WTF of the LAD-perfused region is shown in Figure 1. The induction of ischemia led to an immediate decrease of WTF to negative values within seconds. During desflurane anesthesia, WTF recovered to positive values within the first minute, and during propofol-anesthesia, positive values were reached after a reperfusion period of 5 min. Recovery of WTF in desflurane anesthetized dogs was significantly faster than in propofol anesthetized dogs during the first 3 h of reperfusion.



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  		Figure 1. Wall-thickening fraction (WTF) of the left anterior descending-perfused area as percentage of control values during the reperfusion period (n = 7). Two-way analysis of variance P < 0.01. Data are presented as mean values ± SEM. *P < 0.05 versus baseline. #P < 0.05 versus propofol.

 
Regional myocardial blood flow was decreased in the ischemic region from 1.15 ± 0.32 mL · g-1 · min-1 to 0.24 ± 0.23 mL · g-1 · min-1 during desflurane anesthesia and from 1.36 ± 0.28 mL · g-1 · min-1 to 0.26 ± 0.18 mL · g-1 · min-1 during propofol anesthesia. In the Cx artery perfused region, blood flow was unchanged during baseline and ischemia: 1.35 ± 0.24 mL · g-1 · min-1 and 1.48 ± 0.3 mL · g-1 · min-1 during desflurane anesthesia; 1.26 ± 0.23 mL · g-1 · min-1 and 1.23 ± 0.34 mL · g-1 · min-1 during propofol anesthesia.


   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This study shows a beneficial effect of desflurane on the recovery from myocardial stunning in chronically instrumented dogs compared with propofol-anesthetized animals. Because of a preclusion by our ethical committee, we were only allowed to compare the actual findings with already published data in awake dogs (6). Comparing the effects of desflurane with awake animals (6) without any intervention, the volatile anesthetic enhances the recovery, whereas propofol delays the recovery from stunning (see Table 2) compared with the awake state.


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  		Table 2. Wall-Thickening Fraction After Ischemia and Reperfusion
 
Chronically instrumented dogs are a well established model for myocardial stunning; the phenomenon of a reversible contractile dysfunction was also first described in dogs (16). This model avoids the confounding influence of acute surgical trauma, baseline anesthesia, and temperature on recovery from stunning. Studies in open- and closed-chest animals have shown conflicting results about the role of oxygen radicals in stunning (17). Dogs in this study were eligible for the study only when they had fully recovered from the instrumentation. No pathologies were detectable, and hemodynamics and blood gas variables were within the normal range.

Desflurane and propofol were applied in concentrations that prevent movement during skin incision. Both anesthetics cause dose-dependent decreases in arterial blood pressure as a result of decreased myocardial contractility and reduced peripheral vascular resistance (18).

For propofol, protective effects in myocardial ischemia have been suggested by several in vitro models. In ischemic isolated rat hearts, functional and metabolic recovery was enhanced when propofol was infused before ischemia and during reperfusion, or only during reperfusion compared with controls without propofol application (19). Similarly, intracoronary propofol enhanced recovery of regional myocardial function in dogs (20). The latter setting may promote artifactual results, because propofol was injected directly into the coronary arteries and systemic effects were not present. In both studies, the protective effects were related to attenuation of lipid peroxidation by propofol. In comparison with other IV anesthetics, propofol did not show advantages on recovery rates from stunning. In comparison with fentanyl, recovery from 10 minutes of ischemia was not different in acutely instrumented dogs if propofol or fentanyl was continuously infused (21). In ischemic dog myocardium, impairment of regional function was more pronounced after an IV bolus of propofol compared with control or collateral-dependent areas (22). As in this study, which compared volatile anesthetics, propofol did not produce the cardioprotective effect of inhaled anesthetics in in situ and in vitro rabbit hearts (23). It appears that propofol does not significantly affect reperfusion injury.

Protective effects of inhaled anesthetics have been described for halothane and isoflurane first by Warltier et al. (1) and subsequently for enflurane and sevoflurane (23). Desflurane has not been investigated in the in vivo setting. The cardioprotective effects of inhaled anesthetics may depend on adenosine receptors and protein kinase C, mechanisms closely related to ischemic preconditioning (23). Inhaled anesthetics might protect against ischemic injury by influencing adenosine triphosphate-dependent potassium-channels (2).

Another important effect of inhaled anesthetics is the decrease in coronary vascular resistance that has also been described for desflurane (18). In a canine model of multivessel coronary artery obstruction, desflurane did not redistribute blood flow away from collateral-dependent myocardium; hence, it did not produce coronary "steal" (24). Whether myocardial blood flow and with special respect to reperfusion was changed in this study cannot be answered because determinations of myocardial blood flow were not made during reperfusion. Bolli et al. (25) have demonstrated that the effect is not at the level of the greater coronary vessels but on the microvasculature, a mechanism possibly independent of myocardial stunning.

Focusing on the effects of desflurane, Murray and Luney (26) reported an unexpected increase in immediate postoperative mortality when desflurane was used in patients with a history of coronary artery disease. In another group of patients with ischemic heart disease, a significant increase of pulmonary artery pressure and pulmonary capillary wedge pressure was reported when desflurane was used instead of isoflurane (3).

A blockade of sympathetic activity improves recovery from myocardial stunning (6) or myocardial ischemia (27). The sympathetic activation driven by an increased concentration of desflurane in the bronchial system is of concern, whereas increases in systemic blood levels do not affect sympathetic activity (28). Sympathetic activation can be avoided by appropriate premedication (29). This modulating effect has been shown for fentanyl, esmolol, and clonidine. We have chosen fentanyl in this study because it attenuates heart rate and mean arterial blood pressure increases. In addition, the vagally mediated increase in heart rate that occurs in dogs after propofol is also attenuated by fentanyl (30).

One important effect of desflurane is the release of intramyocardial catecholamine stores, which has been shown for rats (8) and recently for humans (9). Catecholamine stores might interfere with preconditioning, an effect during myocardial ischemia, however, which has to be elucidated.

In summary, desflurane improves recovery from myocardial stunning in this setting of chronically instrumented dogs. As this study shows an improvement compared with propofol and the awake state, comparisons with other inhaled anesthetics are desirable to further determine the role of desflurane in myocardial reperfusion injury.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication August 23, 2000.




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Lippincott, Williams & Wilkins 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 HighWire Press