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Anesth Analg 2002;95:1162-1168 © 2002 International Anesthesia Research Society
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Abstract |
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The administration of a volatile anesthetic shortly before a prolonged ischemic episode exerts protective effects against myocardial infarction similar to those of ischemic preconditioning. A second window of preconditioning (SWOP) against myocardial infarction can also be elicited by brief episodes of ischemia when this occurs 24 h before prolonged coronary artery occlusion. Whether remote exposure to a volatile anesthetic also causes delayed myocardial protection is unknown. We tested the hypothesis that the administration of isoflurane 24 h before ischemia produces a SWOP against infarction. Barbiturate-anesthetized dogs (n = 25) were instrumented for measurement of hemodynamics, including aortic and left ventricular (LV) pressures and LV +dP/dtmax, and subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size and coronary collateral blood flow were assessed with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. Two groups of dogs received 1.0 minimum alveolar anesthetic concentration isoflurane for 30 min or 6 h that was discontinued 30 min (acute) or 24 h (delayed) before ischemia and reperfusion, respectively. A control group of dogs did not receive isoflurane. Infarct size was 27% ± 3% of the LV area at risk in the absence of pretreatment with isoflurane. Acute, but not remote, administration of isoflurane reduced infarct size (12% ± 1% and 31% ± 3%, respectively). No differences in hemodynamics or transmural myocardial perfusion during or after occlusion were observed between groups. The results indicate that isoflurane does not produce a SWOP when administered 24 h before prolonged myocardial ischemia in vivo.
IMPLICATIONS: Isoflurane mimics the beneficial effects of ischemic preconditioning by protecting myocardium against infarction when it is administered shortly before a prolonged ischemic episode. However, unlike ischemic preconditioning, isoflurane does not produce a second window of protection 24 h after administration in dogs.
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Introduction |
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A brief episode of myocardial ischemia occurring shortly before prolonged coronary artery occlusion protects myocardium against infarction. This phenomenon is known as "ischemic preconditioning" (IPC) (1). The immediate protective effects of this brief ischemic episode are limited to <2 h in IPC (2,3), but a delayed window of protection emerges after 24 h (4,5) that may persist for an additional 72 h after the initial ischemic stimulus (6). For example, repetitive episodes of myocardial ischemia decrease myocardial infarct size to a similar extent when sustained coronary artery occlusion is initiated immediately or 24 h, but not 3 or 12 h, after brief ischemia in a canine model (5). This second window of preconditioning (SWOP) (4,7) may also be produced by heat stress (4,8) and is mimicked by a variety of chemically distinct drugs, including adenosine subtype 1 (A1) receptor agonists (9), nitric oxide (NO) donors (10),
1-opioid receptor agonists (11), and adenosine triphosphate-dependent potassium (KATP) channel openers (12). Volatile anesthetics, including isoflurane, reduce myocardial infarct size when administered before ischemia and reperfusion in experimental animals (13–15) through a signal transduction cascade that is remarkably similar to the pathways identified in IPC and SWOP. This anesthetic-induced preconditioning is mediated by A1 receptors (16), inhibitory guanine nucleotide binding proteins (17), protein kinase C (18), and KATP channels (13,19,20). We tested the hypothesis that exposure to isoflurane 24 h before ischemia and reperfusion mimics the beneficial effects of SWOP and protects against myocardial infarction in vivo.
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Methods |
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All experimental procedures and protocols used in this investigation were reviewed and approved by the Animal Care and Use Committee of the Medical College of Wisconsin. Furthermore, all activities conformed to the Guiding Principles in the Care and Use of Animals of the American Physiologic Society and were in accordance with the Guide for the Care and Use of Laboratory Animals (National Academy Press, Washington, DC, 1996).
The experimental protocol is illustrated in Figure 1. In one group, mongrel dogs of either sex were fasted overnight before the administration of isoflurane. A peripheral IV catheter was inserted, and fluid deficits were replaced with 500 mL of 0.9% saline. Maintenance fluids were continued at 3 mL · kg-1 · h-1 for the duration of each experiment. After inhaled induction and tracheal intubation, anesthesia was maintained with 1.0 minimum alveolar anesthetic concentration (MAC) (end-tidal concentration) isoflurane for 6 h on the day before acute experimentation. End-tidal concentrations of isoflurane were measured at the tip of the endotracheal tube by an infrared anesthetic analyzer that was calibrated with known standards before and during experimentation. The canine MAC of isoflurane used in this investigation was 1.28% (21). Anesthesia was discontinued and emergence allowed to occur after the administration of isoflurane. Each dog was then housed overnight before experimentation on the following day.
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Implantation of instruments has been described in detail (19). Briefly, dogs that had been pretreated with isoflurane on the day before experimentation and those that had not were anesthetized with sodium barbital (200 mg/kg) and sodium pentobarbital (15 mg/kg) and ventilated with positive pressure with an air and oxygen mixture after tracheal intubation. Arterial blood gas tensions were maintained within a physiological range by adjustment of tidal volume and respiratory rate. Temperature was maintained with a heating blanket. A 7F, dual micromanometer-tipped catheter was inserted into the aorta and left ventricle (LV) for measurement of aortic and LV pressures and the maximum rate of increase of LV pressure (+dP/dtmax). Heparin-filled catheters were inserted into the left atrial appendage and the right femoral artery for the administration of radioactive microspheres and withdrawal of reference blood flow samples, respectively. A heparin-filled catheter was also inserted into the right femoral vein for fluid administration. A 1-cm segment of the left anterior descending coronary artery (LAD) was isolated immediately distal to the first diagonal branch, and a silk ligature was placed around the vessel for production of coronary artery occlusion and reperfusion. Hemodynamics were continuously monitored on a polygraph and digitized by using a computer interfaced with an analog-to-digital converter.
Baseline systemic hemodynamic data were recorded 90 min after instrumentation was completed and calibrated. In one group of experiments, dogs (25 ± 2 kg) that had received isoflurane for 6 h on the day before experimentation were subjected to a 60-min LAD occlusion followed by 3 h of reperfusion. A second group of dogs (23 ± 1 kg) received isoflurane (1.0 MAC) for 30 min after completion of instrumentation and stabilization of the experimental preparation, which was then discontinued 30 min before LAD occlusion and reperfusion. A final group of dogs (24 ± 1 kg) was studied that had not been pretreated with isoflurane. Regional myocardial blood flow was measured under steady-state baseline conditions, during LAD occlusion, and after 60 min of reperfusion. Dogs that developed intractable ventricular fibrillation and those with a subendocardial coronary collateral blood flow more than 0.15 mL · min-1 · g-1 were excluded from the analysis (22).
At the end of each experiment, myocardial infarct size was measured as previously described (23). Briefly, the LV area at risk for infarction (AAR) was separated from the normal area (stained with Patent blue dye), and the 2 regions were incubated at 37°C for 20 to 30 min in 1% 2,3,5-triphenyltetrazolium chloride in 0.1 M phosphate buffer adjusted to pH 7.4. After overnight storage in 10% formaldehyde, infarcted and noninfarcted myocardium within the AAR were carefully separated and weighed. Infarct size was expressed as a percentage of the AAR.
Carbonized plastic microspheres (15 ± 2 µm [SD] in diameter) labeled with 141Ce, 103Ru, or 95Nb were used to measure regional myocardial perfusion as previously described (20). Transmural tissue samples were selected from the ischemic region (distal to the LAD occlusion) and were subdivided into subepicardial, midmyocardial, and subendocardial layers of approximately equal thickness. Samples were weighed and placed in scintillation vials, and the activity of each isotope was determined. Similarly, the activity of each isotope in the reference blood flow sample was assessed. Myocardial blood flow was calculated as Qr x Cm x Cr-1, where Qr is the rate of withdrawal of the reference blood flow sample (mL/min), Cm is the activity (cpm/g) of the myocardial tissue sample, and Cr is the activity (cpm) of the reference blood flow sample. Transmural myocardial blood flow was calculated as the average of subepicardial, midmyocardial, and subendocardial blood flows.
Statistical analysis of data within and between groups was performed with analysis of variance for repeated measures, followed by the Student-Newman-Keuls test. Changes within and between groups were considered statistically significant when the P value was <0.05. All data are expressed as mean ± SEM.
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Results |
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Twenty-five dogs were instrumented to obtain 24 successful experiments. One dog pretreated with isoflurane 24 h before experimentation was excluded from the overall analysis because the subendocardial collateral blood flow exceeded 0.15 mL · min-1 · g-1. However, this dog was included in the analysis of the relationship between coronary collateral blood flow and myocardial infarct size.
No differences in hemodynamics were observed between experimental groups during LAD occlusion or after 3 h of reperfusion (Table 1). Isoflurane decreased heart rate, mean arterial, and LV systolic pressures and LV +dP/dtmax. Hemodynamics returned to baseline values within 30 min after discontinuation of isoflurane. LAD occlusion and reperfusion produced similar increases in LV end-diastolic pressure and decreases in LV +dP/dtmax in all experimental groups.
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The LV AAR was similar between groups (control, 37% ± 2%; isoflurane-acute, 39% ± 2%; and isoflurane-delayed, 39% ± 3%). Myocardial infarct size expressed as a percentage of the AAR was 27% ± 3% (n = 8) in dogs that had not been pretreated with isoflurane (Fig. 2). Acute exposure to 1.0 MAC isoflurane reduced infarct size to 12% ± 1% (n = 8) and shifted the relationship between coronary collateral blood flow and infarct size downward (P < 0.05) as compared with control experiments (Fig. 3). Thus, the extent of infarction was less after the administration of isoflurane for any degree of collateral perfusion. In contrast, a 6-h administration of isoflurane the day before experimentation did not affect infarct size (31% ± 3%; n = 8) or alter the collateral blood flow/infarct size relation as compared with dogs that had not received isoflurane (Fig. 3). No differences in myocardial blood flow were observed between groups during LAD occlusion and reperfusion (Table 2).
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Discussion |
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Protection against infarction by IPC displays an important temporal dependence between the preconditioning stimulus and the onset of the prolonged ischemic event. The heart remains resistant to infarction during this time period, after which myocardial protection no longer occurs. This acute memory phase extends between five minutes and two hours after the preconditioning stimulus in rabbits (3) and dogs (1,5). Curiously, a second period of protection reoccurs after 24 hours (4,5) that lasts an additional 48 to 72 hours (6) before myocardial preservation is no longer observed. We have previously demonstrated that isoflurane protects the myocardium from irreversible ischemic injury and, further, that this isoflurane-induced protection is characterized by an acute memory phase extending at least 30 minutes after the volatile anesthetic has been discontinued. Whether isoflurane is capable of producing a second window of protection when administered 24 hours before the onset of ischemia is unknown. A SWOP by anesthetics may be important because previous anesthetic exposure could protect against the perioperative myocardial infarction that usually occurs 24–48 hours after anesthesia and surgery. The results of this investigation confirm our previous findings indicating that isoflurane exerts protective effects against infarction with an acute memory period of 30 minutes, independent of alterations in systemic hemodynamics or coronary collateral blood flow (13). The results further demonstrate that prolonged administration of isoflurane 24 hours before a 60-minute LAD occlusion and 3 hours of reperfusion does not precondition myocardium against infarction. These data indicate that isoflurane does not produce a SWOP in dogs.
Previous studies indicate that a critical threshold must be attained by a preconditioning stimulus for protection to occur (3,24). Thus, the failure of the prolonged pretreatment with isoflurane to cause delayed preconditioning against ischemic damage may have resulted because the preconditioning stimulus did not reach the necessary threshold level. We have recently reported that acute exposure to end-tidal concentrations of isoflurane between 0.25 and 1.25 MAC for only 30 minutes followed by a memory period of 30 minutes are effective in reducing infarct size in an identical canine model (25). Thus, it appears likely that a prolonged (six-hour) pretreatment with 1.0 MAC isoflurane would represent an adequate stimulus for the production of an anesthetic-induced SWOP. Nevertheless, we did not examine longer isoflurane pretreatment periods or shorter intervals between isoflurane exposure and the onset of ischemia in this investigation. The minimal stimulus required for acute preconditioning with isoflurane may be lower than that for a possible anesthetic-induced SWOP, but previous studies have indicated that ischemic stimuli of similar intensity are capable of producing both IPC and SWOP (5,6).
The SWOP has been repeatedly described in rats (11,26) and rabbits (27), but evidence for SWOP in larger mammals, particularly swine, has been less convincing (28–30). Thus, the inability of isoflurane to produce delayed preconditioning in canine myocardium may be attributed to these species differences. Nevertheless, canine myocardium can be preconditioned by ischemia (5) or monophosphoryl lipid A (31,32) 24 hours before coronary artery occlusion. The beneficial effect of late preconditioning by monophosphoryl lipid A was also mediated by KATP channel activation in dogs (33). These data suggest that pharmacological agents are capable of mimicking the beneficial actions of SWOP in canine myocardium. Thus, it is conceivable that the administration of volatile anesthetics, including isoflurane, that also activate KATP channels may be capable of producing SWOP in dogs.
Bolli et al. (27,34) have repeatedly demonstrated that SWOP is mediated by inducible NO synthase and triggered by endothelial NO synthase (35) in rabbits. The administration of NO donors also produces SWOP (10,36). An important link between NO and KATP channels in SWOP has been inferred, because late preconditioning produced by the selective mitochondrial KATP channel opener diazoxide is abolished by both KATP channel antagonists and inhibition of NO production (12). Inhibition of the excitatory neurotransmitter-stimulated NO/guanylate cyclase signaling pathway by volatile anesthetics may play a role in the mechanism of general anesthesia (37), but there is little evidence to support the hypothesis that volatile anesthetics directly modulate NO production or function in neural (38) or cardiac tissue. Crystal et al. (39,40) have demonstrated that NO does not mediate isoflurane-induced alterations in coronary vasomotor activity or myocardial contractility. Furthermore, the production and release of NO also do not appear to be substantially affected by volatile anesthetics (41). Given the central role of NO in the mechanism of SWOP and the relative lack of effect volatile anesthetics appear to exert on NO-mediated physiologic actions, our results indicating that isoflurane does not produce SWOP were not entirely unanticipated.
These results should be interpreted within the constraints of several potential limitations. The area of the LV at risk for infarction and coronary collateral blood flow are important determinants of myocardial infarct size. No differences in these variables were observed between experimental groups that would account for our results. Acute administration of isoflurane reduced major determinants of myocardial oxygen consumption, but systemic hemodynamics returned to baseline values immediately before coronary artery occlusion. Thus, it is highly unlikely that the acute hemodynamic effects of isoflurane were responsible for observed differences in infarct size between groups. Nevertheless, coronary venous oxygen content was not measured, and myocardial oxygen consumption was not directly quantified in this investigation; therefore, alterations in myocardial oxygen metabolism during and after the administration of isoflurane cannot be completely excluded as factors involved in the reduction of infarct size. We did not determine other temporal relationships between the timing of the administration of isoflurane before prolonged coronary artery occlusion and reperfusion and myocardial infarct size. A protective effect may have occurred with isoflurane pretreatment earlier or later than 24 hours. SWOP has been reported in rabbits 48 and 72 hours after an ischemic stimulus (6). However, all previous studies describing the time course of SWOP, including those in dogs, have provided compelling evidence that myocardial protection occurs 24 hours after the initial preconditioning stimulus. We did not perform positive control experiments using ischemia as a delayed preconditioning stimulus. However, another investigation performed in a canine model demonstrated that infarct size was markedly decreased 24 hours after preconditioning with 4 five-minute occlusions and reperfusions (5). These results suggest that the failure of isoflurane to produce SWOP was not due to the absence of a delayed preconditioning effect in dogs. In addition, experiments were performed in barbiturate-anesthetized dogs, and the presence of this baseline anesthetic may have altered the results. However, SWOP elicited by ischemia (5) or pharmacological agonists (31,33) has previously been demonstrated in the presence of barbiturate anesthesia. Thus, it is unlikely that an interaction between isoflurane and barbiturate anesthesia accounts for the experimental results.
In summary, these results confirm that isoflurane acutely preconditions myocardium against infarction with a memory phase of 30 minutes, independent of alterations in systemic hemodynamics or transmural myocardial perfusion. However, prolonged administration of isoflurane 24 hours before ischemia and reperfusion does not protect myocardium from irreversible ischemic injury.
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Acknowledgments |
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Supported in part by grants HL 03690 (JRK), HL 63705 (JRK), HL 54280 (DCW), AA 12331 (PSP), and GM 08377 (DCW) from the US Public Health Service, Bethesda, MD.
The authors thank David A. Schwabe, BSEE, for technical assistance and Mary Lorence-Hanke, AA, for assistance in the preparation of this manuscript.
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References |
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|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
- Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986; 74: 1124–36.
[Abstract/Free Full Text] - Murry CE, Richard VJ, Jennings RB, Reimer KA. Myocardial protection is lost before contractile function recovers from ischemic preconditioning. Am J Physiol 1991; 260: H796–804.
[Abstract/Free Full Text] - Van Winkle DM, Thornton JD, Downey DM, Downey JM. The natural history of preconditioning: cardioprotection depends on duration of transient ischemia and time to subsequent ischemia. Coron Artery Dis 1991; 2: 613–9.[Web of Science]
- Marber MS, Latchman DS, Walker JM, Yellon DM. Cardiac stress protein elevation 24 hours after brief ischemia or heat stress is associated with resistance to myocardial infarction. Circulation 1993; 88: 1264–72.
[Abstract/Free Full Text] - Kuzuya T, Hoshida S, Yamashita N, et al. Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia. Circ Res 1993; 72: 1293–9.
[Abstract/Free Full Text] - Baxter GF, Goma FM, Yellon DM. Characterisation of the infarct-limiting effect of delayed preconditioning: timecourse and dose-dependency studies in rabbit myocardium. Basic Res Cardiol 1997; 92: 159–67.[Web of Science][Medline]
- Yellon DM, Baxter GF. A "second window of protection" or delayed preconditioning phenomenon: future horizons for myocardial protection? J Mol Cell Cardiol 1995; 27: 1023–34.[Web of Science][Medline]
- Pell TJ, Yellon DM, Goodwin RW, Baxter GF. Myocardial ischemic tolerance following heat stress is abolished by ATP-sensitive potassium channel blockade. Cardiovasc Drugs Ther 1997; 11: 679–86.[Web of Science][Medline]
- Baxter GF, Yellon DM. ATP-sensitive K+ channels mediate the delayed cardioprotective effect of adenosine A1 receptor activation. J Mol Cell Cardiol 1999; 31: 981–9.[Web of Science][Medline]
- Takano H, Tang XL, Qiu Y, et al. Nitric oxide donors induce late preconditioning against myocardial stunning and infarction in conscious rabbits via an antioxidant-sensitive mechanism. Circ Res 1998; 83: 73–84.
[Abstract/Free Full Text] - Fryer RM, Hsu AK, Eells JT, et al. Opioid-induced second window of cardioprotection: potential role of mitochondrial KATP channels. Circ Res 1999; 84: 846–51.
[Abstract/Free Full Text] - Ockaili R, Emani VR, Okubo S, et al. Opening of mitochondrial KATP channel induces early and delayed cardioprotective effect: role of nitric oxide. Am J Physiol 1999; 277: H2425–34.
- Kersten JR, Schmeling TJ, Pagel PS, et al. Isoflurane mimics ischemic preconditioning via activation of KATP channels: reduction of myocardial infarct size with an acute memory phase. Anesthesiology 1997; 87: 361–70.[Web of Science][Medline]
- Cason BA, Gamperl AK, Slocum RE, Hickey RF. Anesthetic-induced preconditioning: previous administration of isoflurane decreases myocardial infarct size in rabbits. Anesthesiology 1997; 87: 1182–90.[Web of Science][Medline]
- Cope DK, Impastato WK, Cohen MV, Downey JM. Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology 1997; 86: 699–709.[Web of Science][Medline]
- Kersten JR, Orth KG, Pagel PS, et al. Role of adenosine in isoflurane-induced cardioprotection. Anesthesiology 1997; 86: 1128–39.[Web of Science][Medline]
- Toller WG, Kersten JR, Gross ER, et al. Isoflurane preconditions myocardium against infarction via activation of inhibitory guanine (Gi) nucleotide binding proteins. Anesthesiology 2000; 92: 1400–7.[Web of Science][Medline]
- Toller WG, Montgomery MW, Pagel PS, et al. Isoflurane-enhanced recovery of canine stunned myocardium: role for protein kinase C? Anesthesiology 1999; 91: 713–22.[Web of Science][Medline]
- Kersten JR, Schmeling TJ, Hettrick DA, et al. Mechanism of myocardial protection by isoflurane: role of adenosine triphosphate-regulated potassium (KATP) channels. Anesthesiology 1996; 85: 794–807.[Web of Science][Medline]
- Kersten JR, Lowe D, Hettrick DA, et al. Glyburide, a KATP channel antagonist, attenuates the cardioprotective effects of isoflurane in stunned myocardium. Anesth Analg 1996; 83: 27–33.[Abstract]
- Steffey EP, Howland D Jr. Isoflurane potency in the dog and cat. Am J Vet Res 1977; 38: 1833–6.[Web of Science][Medline]
- Gross GJ, Auchampach JA. Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs. Circ Res 1992; 70: 223–33.
[Abstract/Free Full Text] - Warltier DC, Zyvoloski MG, Gross GJ, et al. Determination of experimental myocardial infarct size. J Pharmacol Methods 1981; 6: 199–210.[Web of Science][Medline]
- Goto M, Liu Y, Yang XM, et al. Role of bradykinin in protection of ischemic preconditioning in rabbit hearts. Circ Res 1995; 77: 611–21.
[Abstract/Free Full Text] - Kehl F, Krolikowski JG, Mraovic B, et al. Is isoflurane-induced preconditioning dose related? Anesthesiology 2002; 96: 675–80.[Web of Science][Medline]
- Yamashita N, Hoshida S, Taniguchi N, et al. A "second window of protection" occurs 24 h after ischemic preconditioning in the rat heart. J Mol Cell Cardiol 1998; 30: 1181–9.[Web of Science][Medline]
- Takano H, Manchikalapudi S, Tang XL, et al. Nitric oxide synthase is the mediator of late preconditioning against myocardial infarction in conscious rabbits. Circulation 1998; 98: 441–9.
[Abstract/Free Full Text] - Qiu Y, Tang XL, Park SW, et al. The early and late phases of ischemic preconditioning: a comparative analysis of their effects on infarct size, myocardial stunning, and arrhythmias in conscious pigs undergoing a 40-minute coronary occlusion. Circ Res 1997; 80: 730–42.
[Abstract/Free Full Text] - Schwarz ER, Fleischhauer J, Montino H, et al. Infarct size reduction by ischemic preconditioning is a monophasic, short-lived phenomenon in anesthetized pigs. J Cardiovasc Pharmacol Ther 1998; 3: 63–70.
- Jaberansari MT, Baxter GF, Muller CA, et al. Angiotensin-converting enzyme inhibition enhances a subthreshold stimulus to elicit delayed preconditioning in pig myocardium. J Am Coll Cardiol 2001; 37: 1996–2001.
[Abstract/Free Full Text] - Yao Z, Auchampach JA, Pieper GM, Gross GJ. Cardioprotective effects of monophosphoryl lipid A, a novel endotoxin analogue, in the dog. Cardiovasc Res 1993; 27: 832–8.
[Abstract/Free Full Text] - Elliott GT, Mei DA, Gross GJ. Monophosphoryl lipid A attenuates myocardial stunning in dogs: role of ATP-sensitive potassium channels. J Cardiovasc Pharmacol 1998; 32: 49–56.[Web of Science][Medline]
- Mei DA, Elliott GT, Gross GJ. KATP channels mediate late preconditioning against infarction produced by monophosphoryl lipid A. Am J Physiol 1996; 271: H2723–9.
[Abstract/Free Full Text] - Qiu Y, Rizvi A, Tang XL, et al. Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits. Am J Physiol 1997; 273: H2931–6.
- Xuan YT, Tang XL, Qiu Y, et al. Biphasic response of cardiac NO synthase isoforms to ischemic preconditioning in conscious rabbits. Am J Physiol 2000; 279: H2360–71.[Web of Science]
- Hill M, Takano H, Tang XL, et al. Nitroglycerin induces late preconditioning against myocardial infarction in conscious rabbits despite development of nitrate tolerance. Circulation 2001; 104: 694–9.
[Abstract/Free Full Text] - Zuo Z, Tichotsky A, Johns RA. Inhibition of excitatory neurotransmitter-nitric oxide signaling pathway by inhalational anesthetics. Neuroscience 1999; 93: 1167–72.[Web of Science][Medline]
- Rengasamy A, Ravichandran LV, Reikersdorfer CG, Johns RA. Inhalational anesthetics do not alter nitric oxide synthase activity. J Pharmacol Exp Ther 1995; 273: 599–604.
[Abstract/Free Full Text] - Crystal GJ, Kim SJ, Salem MR, et al. Nitric oxide does not mediate coronary vasodilation by isoflurane. Anesthesiology 1994; 81: 209–20.[Web of Science][Medline]
- Crystal GJ, Gurevicius J. Nitric oxide does not modulate myocardial contractility acutely in in situ canine hearts. Am J Physiol 1996; 270: H1568–76.
[Abstract/Free Full Text] - Fujita S, Roerig DL, Chung WW, et al. Volatile anesthetics do not alter bradykinin-induced release of nitric oxide or L-citrulline in crystalloid perfused guinea pig hearts. Anesthesiology 1998; 89: 421–33.[Web of Science][Medline]
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