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Ann Thorac Surg 1995;59:651-657
© 1995 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan
Accepted for publication November 14, 1994.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentReferences |
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Thirty-six mongrel dogs weighing 9 to 16 kg were used in this study. Anesthesia was induced with intramuscularly administered ketamine hydrochloride (15 mg/kg) and intravenously administered fentanyl (30 µg/kg). After endotracheal intubation, each animal was ventilated with a volume-controlled ventilator. The respiratory variables were adjusted to maintain a stable pH (7.35 to 7.45), and carbon dioxide (35 to 45 mm Hg) and oxygen (>200 mm Hg) tension, with monitoring done by intermittent blood gas measurement. Pancuronium bromide (1 mg intravenously) was given hourly to maintain muscle paralysis, and anesthesia was maintained with intravenously administered fentanyl (3 µg • kg-1 • h-1). A catheter was placed in the superior sagittal sinus (SSS) for the withdrawal of blood samples. Catheters for measuring the femoral and carotid arterial pressure and for venous infusion were also inserted. During the experiment, the femoral and carotid arterial pressures were monitored continuously.
Blood was obtained from the common carotid artery or from the arterial line of the bypass circuit, and from the SSS catheter. The arterial samples were analyzed at 37°C to determine the pH, oxygen and carbon dioxide tensions, hematocrit, and oxygen saturation using a GME-STAT (Senkoika, Tokyo, Japan).
Somatosensory Evoked Potential Recording
Craniotomy was performed over the left temporoparietal area, the dura mater was exposed, and silver-ball recording electrodes were placed on the dura mater over the somatosensory cortex. Reference and ground electrodes were placed subcutaneously lateral and posterior to the cranial defect. Stimulating needle electrodes were inserted percutaneously over the right median nerve.
The SEPs were recorded with a CA5200A system (Serucomu, Fukuoka, Japan), and were generated using square-wave electrical pulses (0.2 ms at 2/s). The band-pass filter was set between 10 and 1,000 Hz, the recording duration at 100 ms, and the sensitivity at 120 µV. Fifty to 100 responses were averaged.
Cardiopulmonary Bypass
After the median sternotomy was done, preparations for cardiopulmonary bypass (CPB) were made (Fig 1
). After heparinization (2 mg/kg), the femoral artery and right atrium were cannulated for arterial return and venous drainage, respectively. The right and left sides of the heart were vented through the right and left ventricles, respectively. Cardiopulmonary bypass was instituted at a perfusion flow rate of 100 mL • kg-1 • min-1. When the brain had been cooled to 25°C, the SCP cannula was placed in the aortic arch. After cross-clamping of the proximal and distal sides of the aortic arch and the right and left subclavian arteries, SCP was performed for 90 minutes. During SCP, the systemic perfusion flow rate was maintained between 30 to 40 mL • kg-1 • min-1 to keep the systemic arterial pressure around 50 mm Hg.
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Experimental Protocol
The 36 dogs were divided into four groups that were subjected to different flow rates during SCP. To determine the physiologic cerebral perfusion flow rate for each dog, we measured blood flow in the brachiocephalic trunk and the proximal left subclavian artery during fentanyl anesthesia using an electromagnetic flowmeter (MVF-3200; Nippon Koden, Tokyo, Japan), after cross-clamping of the right and left subclavian arteries. The sum of the blood flow in the brachiocephalic and left subclavian arteries was defined as the physiologic flow rate (100%). The flow rate was 100% in group I (n = 10), 50% in group II (n = 10), 25% in group III (n = 8), and 0%, or no flow, in group IV (cerebrocirculatory arrest) (n = 8).
The SEPs were monitored from the beginning. Cardiopulmonary bypass was initiated at a flow rate of about 100 mL • kg-1 • min-1, and then cooling was begun (Fig 2). When the brain temperature reached 25°C as a result of core cooling, SCP was started. After 90 minutes of SCP, the dogs were gradually rewarmed to normal temperature. Blood samples for the measurement of lactate and pyruvate were drawn from the arterial line of the bypass circuit and the SSS cannula before CPB, at the initiation of SCP, at the end of SCP, and after rewarming. The oxygen saturation in SSS blood was measured before CPB and during SCP in each group. At the end of the experiment, the dogs were sacrificed and the brains fixed with 10% formalin.
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). The latency and the amplitude of the negative (N1) cortical evoked potential were determined. Latency was measured at the midpoint of the wave and amplitude was measured from the peak of the first positive deflection at P1 to the peak negative deflection at N1. Data were expressed as a percentage of the value before CPB.
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XL) [13, 14] was determined as an index of anaerobic cerebral metabolism by the following formula:
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where La, Ls and Pa, Ps are the lactate and pyruvate concentrations in arterial and SSS blood, respectively.
Histopathologic Examination
At the end of the experiment, after rewarming, saline solution and 10% formaldehyde were perfused through the aortic arch. About 500 mL of saline solution and 500 mL of fixative were flushed through each animal before the cerebrum was removed and placed in the fixative for a further 48 hours.
After fixation, 5-mm coronal slices that contained the cerebral cortex (frontal, temporal, parietal, and occipital lobes) and hippocampus, which are vulnerable to ischemia, were cut and processed conventionally with paraffin. Five-micrometer-thick sections were cut and stained with hematoxylin and eosin and Klüver-Barrera stains for examination under a light microscope.
Statistics
All the measured values are expressed as the mean ± standard deviation. Data obtained at each stage of the experiment were analyzed with the Wilcoxon signed-rank test, and data from the same stage were compared with the Mann-Whitney U test. A p value of less than 0.05 was considered to indicate significance.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Changes in the Latency and Amplitude of the Somatosensory Evoked Potentials
The precooling potential after the start of CPB was almost the same as that before it. After the commencement of core cooling, the latency gradually increased until the temperature reached 25°C. In contrast, the amplitude increased with cooling to around 30°C and then gradually decreased. There was no significant difference in the cooling time, latency, and amplitude among the four groups. In all groups, the latency was increased by 180% to 190% at 25°C and the amplitude was decreased by almost 60% versus the pre-CPB value. During SCP, the SEPs in groups I and II showed little change. However, the amplitude in group III gradually decreased and the SEPs disappeared at 10 to 30 minutes after the commencement of SCP in 7 of the 8 dogs. In group IV, the SEPs disappeared after 5 to 15 minutes in all dogs. During rewarming, there was no significant difference in the latency and amplitude between groups I and II, nor were the post-rewarming final values significantly different from the pre-CPB values in both groups. However, only 3 dogs in group III showed recovery of the SEPs to almost the same waveform as that before CPB after rewarming; the remaining 5 dogs showed no recovery. In group IV, the SEPs did not recover after rewarming in any of the dogs. The latency and amplitude data are summarized in Table 1 and the waveforms are shown in Figure 4.
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. There was no significant difference among the four groups at both the pre-CPB stage and at the 25°C stage of CPB. At the end of SCP, group IV animals had a higher value than did the animals in the other three groups, although it was not a significant increase. Additionally, no significant differences among the four groups were noted at the end of the experiment after rewarming. During the course of the experiment, a significant increase compared with the pre-CPB value also did not occur in any group.
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. None of the dogs in groups I and II showed morphologic changes of the cerebral cortex and hippocampus at the light microscopic level that were attributable to cerebral hypoxia. The 3 dogs in group III that showed recovery of SEPs also had no ischemic changes, but some of the other 5 dogs in this group showed slight ischemic damage compared with the changes observed in group IV (see Fig 5). In group IV, there were prominent acute ischemic changes in both the cerebral cortex and hippocampus. The neurons were shrunken and angular with prominent processes, the nuclei were pyknotic, and the Nissl substance in the cytoplasm had disappeared (chromatolysis) (see Fig 6). Group IV dogs thus showed severe neuronal injury and a significant increase in the number of damaged neurons compared with the dogs in group III.
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Oxygen Saturation
During SCP, the oxygen saturation was 78.8% ± 4.1%, 57.3% ± 7.8%, 41.1% ± 9.7%, and 22.9% ± 4.1% in groups I, II, III, and IV, respectively. It decreased significantly as the cerebral perfusion flow rate decreased, and the values in groups III and IV were significantly lower than the pre-CPB levels (53.8% ± 5.7%).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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The perfusion conditions during CPB, such as perfusion flow and pressure, should be determined based on whether the function of the perfused organ can be sufficiently maintained or not. The physiologic functions of the brain are affected by cerebral blood flow and cerebral metabolism, and the extent of damage very accurately reflects the overall degree of cerebral ischemia. A Toronto University group [10] reported that direct measurement of cerebral blood flow does not assess regional variations in flow, nor can it provide information about the effect of hypothermia on absolute cerebral blood flow requirements. Direct measurement of end-organ function during hypothermic bypass provides the most reliable indication of the adequacy of cerebral perfusion. Thus, evaluation of cerebral function is needed to determine the optimum cerebral perfusion flow rate. Therefore, in our experiment, we recorded SEPs [8–10, 15] as an index of cerebral function.
Somatosensory evoked potentials have many clinical uses, such as in cardiovascular procedures as a means of monitoring the central nervous system [8–10]. The results in our experiment showed that the latency was prolonged and the amplitude decreased when the brain temperature was lowered to 25°C, but the SEPs did not disappear. This implies that, even though neuronal activity is reduced and metabolism is suppressed during hypothermia, which reduce the oxygen requirement [16], the neurons are not completely static but still require some oxygen at 25°C. The Toronto University group [10] reported that what was most striking was the relatively low cerebral blood flow requirements that were needed to support evoked potentials over the clinically relevant temperature range. Further, Mizeahi and colleagues [17] reported that hypothermia-induced cerebral inactivity protects the brain during prolonged circulatory arrest. In short, because the neurons are still active at 25°C, a certain level of cerebral blood flow must be maintained. Hence, these findings suggest that, because flow rates of 100% and 50% provide sufficient perfusion to meet the oxygen requirements of the brain, and because there was no change in the SEPs during SCP, the SEPs almost completely recovered after rewarming. However, at a flow rate of 25% and at no flow, the SEPs disappeared as the rate became insufficient and the degree of ischemia greatly increased.
To maintain neural activity in the brain, it is necessary to synthesize and release a neurotransmitter using adenosine triphosphate that was produced in the presence of glucose and oxygen. Usually as the cerebral metabolism is high and the brain cannot store glucose and oxygen, a decrease in or deprivation of oxygenated blood soon leads to ischemic cerebral damage [14]. Regarding energy metabolism, the brain usually produces adenosine triphosphate by aerobic glycolysis using more than 95% of the glucose [18], but anaerobic glycolysis from glycogen to pyruvate and lactate occurs during ischemia. Because anaerobic metabolism cannot maintain cerebral function because of the low energy efficiency, the lactate-to-pyruvate ratio or excess lactate level can be used as indicators of both anaerobic metabolism and the state of cerebral ischemia [11, 12]. However, we must be careful about drawing conclusions concerning cerebral function based on these values alone, because even though the brain may have incurred neurologic damage, the increase in anaerobic metabolism may not be apparent in some cases. In other words, although increased metabolism and the resultant abnormality in the state of the cerebral energy indicate disease, a normal state of cerebral energy is not a confirmation that the brain is normal [16]. In our experiment, the excess lactate level was used as an indicator of anaerobic metabolism. However, there was no significant increase in the excess lactate level at a flow rate of 25% and even at no flow, which is equivalent to the state of complete cerebral ischemia. This contradicts the results of changes in SEPs. In short, an exhaustion of the energy store alone may not be sufficient to induce abnormal cerebral function. Other factors, such as the exposure time to ischemia, whether the pyruvate and lactate were washed out during cerebral reperfusion, and whether stored glycogen disappeared in the brain, are also important for explaining the discrepancy between function and metabolism.
We also carried out histopathologic investigations in this study. When examining the state of cerebral ischemia, the maintenance of cell structure must be considered. There are two ischemic flow thresholds involved in the mechanism of cerebral damage: the functional threshold of synaptic transmission failure and the morphologic threshold of membrane failure [19, 20]. The functional threshold is the critical level beyond which any further decrease in cerebral blood flow will cause the electrophysiologic activity to stop. Although the cerebral function is temporarily inhibited, this will not necessarily lead to irreversible structural cell damage. On the other hand, the morphologic threshold is the critical low blood flow level below which irreversible damage will occur, and it will then become impossible to maintain cell structure and the membrane ionic pump. If the blood flow continues to be below the morphologic threshold, the neurons will undergo acute ischemic necrosis, as shown by the results [14]. In the present study, at flow rates of 100% and 50%, cerebral function was normal in all dogs without any morphologic changes. Therefore, the blood flow was thought to be maintained above the functional and morphologic thresholds. At a flow rate of 25%, cerebral blood flow was shown to be sometimes below the morphologic threshold in some of the 5 dogs in which slight morphologic changes were found. However, we are not sure of this finding because the histopathologic studies were done in a nonquantitative manner. At a no-flow rate, morphologic changes occurred in all dogs, suggesting that the blood flow rate was below the morphologic threshold. Thus, histopathologic reasons require that the perfusion flow rate be kept at more than 50% for safety sake.
As already indicated, because the cerebral perfusion flow rate of over 50% is thought to be necessary for safety sake, as assessed by cerebral function and histopathologic changes, the mean carotid arterial pressure of 39.8 ± 6.2 mm Hg at a flow rate of 50% in our experiment could be considered the minimum perfusion flow pressure.
In this study, the oxygen saturation level was also measured in SSS blood. This index reflects the demand and supply balance of oxygen for the brain, so it can be used as an indirect indicator of the status of cerebrocirculatory metabolism. Our results showed an approximately greater than 60% oxygen saturation at a cerebral perfusion flow rate of over 50%, which means the value had better be maintained at more than 60% for safety reasons if it is used as an indicator. This is supported by the findings from comparison of the control value (about 54%) before CPB with the value at different flow rates during SCP, which showed that the values were higher than the control value at flow rates of 100% and 50%.
At present in our institution, for clinical use we employ a perfusion rate of about 10 mL • kg-1 • min-1 for SCP to prevent cerebral ischemia during aortic arch repair; this flow rate is considered to be within 50% to 100% of the physiologic flow rate, judging from the normal cerebral blood flow rate in human beings [21]. These observations from actual patients, in whom a distinct stroke occurred postoperatively in only 1 of 73 patients (1.3%) perfused at a rate of 10 mL • kg-1 • min-1 for SCP [6], support the results of our experiment.
Based on our findings from this study to clarify the safety of SCP, we conclude that the safe range of cerebral perfusion flow during moderate hypothermia at 25°C is more than 50% of the physiologic flow rate with a perfusion pressure (carotid arterial pressure) of about 30 mm Hg or more. In clinical cases, of course, we have to remember the differences in the cerebral arterial anatomic characteristics between human beings and dogs. However, we can hope for clinical results similar to our experimental results.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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References |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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