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Ann Thorac Surg 1995;59:1107-1112
© 1995 The Society of Thoracic Surgeons

Retrograde Cerebral Perfusion During Profound Hypothermia and Circulatory Arrest in Pigs

Baylor College of Medicine, The Methodist Hospital, Houston, Texas

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The purpose of this study was to evaluate the use of retrograde cerebral perfusion via the superior vena cava during profound hypothermia and circulatory arrest (CA) in pigs. In three groups of 5 pigs each, group A (control) underwent cardiopulmonary bypass and normothermic CA for 1 hour, group B underwent cardiopulmonary bypass, profound hypothermia, and CA (15°C nasopharyngeal) for 1 hour, and group C underwent the same procedure as group B plus retrograde cerebral perfusion. In group A none awoke. In group B, 2 of 5 did not awake and 3 of 5 awoke unable to stand, 2 with perceptive hind limb movement and 1 moving all extremities. In group C all awoke, 4 of 5 able to stand and 1 of 5 unable to stand but moving all limbs. In neurologic evaluation group B had significantly lower Tarlov scores than group C (p = 0.0090). Group B mean wake-up time, plus or minus standard error of the mean, was 124.6 ± 4.6 minutes versus 29.2 ± 5.1 in group C (p = 0.0090). In group B late phase CA cerebral blood flow dropped 30.9% ± 4.8%, but in group C it rose 24.7% ± 9.3% (p = 0.0007, pooled variance t test, two-tailed). In group B late phase CA brain oxygenation decreased 46.0% ± 13.9% but it increased 26.1% ± 5.4% in group C (p = 0.0013). This difference was reduced somewhat during rewarming (B, -21.2% ± 14.9%; C, 16.4% ± 4.7%; p = 0.043). Group B rewarming jugular venous O₂ saturation was 30.8% ± 2.5% versus 56.0% ± 4.4% in group C (p = 0.0011). We conclude that in pigs retrograde cerebral perfusion combined with profound hypothermia during CA significantly reduces neurologic dysfunction, providing superior brain protection.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 1112.

The use of cardiopulmonary bypass, profound hypothermia, and circulatory arrest during surgical treatment of aneurysms of the ascending aorta and transverse arch, as well as in surgical treatment of congenital heart disease, is now widely accepted. However, a safe period of circulatory arrest is not well established [1].

The most devastating complications to the brain of prolonged circulatory arrest are stroke and perioperative death. Our previous report regarding the use of cardiopulmonary bypass, profound hypothermia, and circulatory arrest in patients with arch aneurysms showed that ischemic time greater than 45 minutes is associated with a higher risk of stroke; greater than 65 minutes, with a higher incidence of mortality [2].

Three primary mechanisms cause neurologic injury after cardiac and aortic operations: first, the ``mechanical'' injury that occurs from embolism, second, the alternations in blood flow distribution leading to reperfusion injury, and finally, all environmental, pharmacologic, and patient-related factors influencing the postoperative state of surgical patients [3]. In brain ischemia, the role of metabolic products, mainly free radicals, in the induction of cellular damage (especially brain edema and brain–blood barrier permeability changes) has been well described [4, 5].

Adjunct methods to extend safe circulatory arrest have included cerebroplegia [6] and antegrade perfusion of the cerebral circulation via the innominate arteries [7]. Agents such as barbiturates, isoflurane, lidocaine in large doses, or diphenylhydantoin have been tried [8]. There have been many experimental studies on the effect of hypothermic circulatory arrest time on cerebral function [8–12].

Retrograde cerebral perfusion (RCP) was introduced to extend the safe period of hypothermic circulatory arrest [13]. Clinical studies found RCP via the superior vena cava to be a valuable tool [13, 14]. It is a simple adjunct method, easily combined with the techniques of profound hypothermia and circulatory arrest. Apart from the possible benefits of oxygenating the brain, providing metabolic substrates, removing toxic metabolites, and keeping the brain cold, it may also protect the brain against reperfusion injury and extend the period of time for safe circulatory arrest [13, 14, 15].

Although preliminary application of RCP in humans was very encouraging, we chose to conduct a more detailed animal study: (1) to further validate, on an experimental basis, the application of RCP combined with profound hypothermia in the prevention of permanent brain damage during circulatory arrest, thus extending the period of ischemia to the brain before neurologic dysfunction occurs, (2) to establish an animal model for further studies of retrograde brain perfusion using different protective agents, and (3) to evaluate the clinical and neurophysiologic function of the animal after RCP via the superior vena cava during profound hypothermia and circulatory arrest.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The animal experiment was conducted with the approval of our institution's animal care and use committee, and the animals received humane care in compliance with the ``Guide for the Care and Use of Laboratory Animals'' published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Fifteen pigs, mean weight of 33 kg (range, 31.4 to 34 kg), were divided into three groups of 5 pigs each. Group A, as the control group, underwent 1 hour of normothermic circulatory arrest after placement on cardiopulmonary bypass. Group B underwent total cardiopulmonary bypass, profound hypothermia to a nasopharyngeal temperature of 15°C, and 1 hour of circulatory arrest. Group C treatment was the same as group B, plus RCP via the superior vena cava for 1 hour during circulatory arrest.

Anesthesia protocol included intramuscular injections of azaperone (2 mg/kg) and atropine (20 mg/kg) 30 minutes before the operation, and then anesthesia induced with nitrous oxide (4 L/min) and 50% oxygen (2 L/min), halothane (1% to 2%), and thiopentone (25 mg) maintained with nitrous oxide (3 L/min), 50% oxygen (1 to 5 L/min), and halothane (0.5% to 1%) with assist ventilation. Muscle relaxation was achieved with vecuronium bromide (0.25 mg/kg) given intravenously. For a constant temperature record, probes were inserted in the nasopharynx and esophagus. Baseline measurements of the hemodynamics, hematology, and arterial blood gas levels were obtained before induction of cardiopulmonary bypass.

Technique and Cardiopulmonary Bypass
The chest was entered through a bilateral thoracotomy. Cannulas were inserted into the left femoral artery and vein for pressure measurements and blood sampling and into a superficial leg vein to provide access for fluid administration. A fiberoptic oxygen saturation catheter was introduced into the internal jugular vein to monitor trend changes in oxygenation. Probes for cerebral blood flow measurement and brain tissue oxygenation were placed intracranially through a skin incision, and sequential temporal bone bore and baseline measurements were obtained.

The BioMedicus pump (Medtronic BioMedicus, Minneapolis, MN) was primed with 1,800 mL of lactated Ringer's solution and 5,000 units of heparin. The pig was given a bolus of 10,000 units of heparin. After full heparinization (300 U/kg) and after cannulation of the descending aorta and the superior and inferior venae cavae, cardiopulmonary bypass was begun. The left ventricle was decompressed using an 18-gauge catheter inserted directly into the left ventricle. Additional fluids were added accordingly. Nasopharyngeal and myocardial temperatures were monitored. In control group A the temperature of the animals was kept normothermic, whereas in groups B and C, the pigs were cooled until the nasopharyngeal temperature fell to 15°C.

At 15°C, with the pupils of the animal fixed and dilated, the circulation was arrested for 1 hour by interruption of the arterial inflow. In all animals cardioplegic solution was infused into the ascending aorta to protect the heart during the arrest period. During circulatory arrest, group C animals were placed in a head-down position and administered RCP via the superior vena cava for 1 hour. After 1 hour, RCP and circulatory arrest were stopped and with the animal still in the head-down position, cardiopulmonary bypass was restarted via the descending thoracic aorta.

Rewarming in group B and C animals was started after circulatory arrest until animal temperature returned to 37°C. Before rewarming, the acid-base and glucose levels of the perfusate were corrected and recirculated in the oxygenator. Once the animal was rewarmed to about 37°C, bypass was terminated slowly by raising the venous pressure until the heart began to eject, and then the flow was reduced slowly until the circulation was supported totally by the heart. Cannulas were then removed, chest tubes for appropriate lung expansion were placed, and surgical wounds were closed. Anesthesia was discontinued slowly and the animals were kept on the ventilator until fully awake and then extubated.

Subsequently, each animal was evaluated by a neurologist who was blinded to the particular treatment of each animal. Neurologic status was graded by a modified Tarlov score: 0, no voluntary movement; 1, perceptible movement of limbs; 2, good movement but unable to stand; and 3, able to stand and walk.

The animals then were sacrificed and the brains were removed. After 10% formaldehyde fixation of the tissue, 5-mm sections from the left cerebrum (coronal section through temporal lobe) and midbrain were cut and processed conventionally with paraffin wax, and stained with hematoxylin and eosin to demonstrate nuclear morphology.

Cerebral Blood Flow Measurement
Laser Doppler flowmetry continuously measured cerebral blood flow using a quantitative method that employs small fiberoptics (0.84 mm) to illuminate and sample reflected low-power laser light in a small volume of tissue. Laser Doppler flowmetry relies on detection of a Doppler shift in radiation caused by red blood cell movement in the microvessels. Information about red blood cell velocity and density per unit volume in a local microvascular bed is derived with a microcomputer. The product of blood velocity and blood volume is proportional, but not identical, to the local perfusion rate. The main advantage of laser Doppler flowmetry is its ability to sample changes in microcirculatory flow continuously using a relative atraumatic modality, i.e., low energy laser light. It can be used clinically for monitoring perfusion of epidural, cortical, and subcortical regions. The disadvantages of the method are that current laser Doppler flowmetry technique requires some tissue exposure for surface measurements and is therefore invasive. The method is motion sensitive and is affected by ambient light conditions. In addition, laser Doppler flowmetry is unable to report flow directly in conventional units so direct comparisons with published results derived by other techniques could not be drawn. Results were expressed as percentage changes from the baseline obtained before the thoracotomy [16, 17].

Brain Tissue Oxygenation
Dual wavelength spectroscopy is based on the ability of different forms of hemoglobin to absorb light of different wavelengths. Oxygenated hemoglobin absorbs light in the red spectrum and deoxygenated hemoglobin absorbs light in the near-infrared spectrum. The surface oximeter used in our experiment for continuous on-line monitoring had only two wavelengths of light (dual) [18]. The results were expressed as percentage changes from the baseline obtained before the thoracotomy.

Jugular Venous Oxygen Saturation
Saturation was measured by a fiberoptic catheter that was introduced into the internal jugular vein and monitored trend changes in oxygen saturation. The results of jugular venous oximetry were expressed as percentage changes in oxygenation as compared to the baseline.

Arterial Blood Gases
Samples were drawn into heparinized syringes, placed immediately on ice, and analyzed at 37°C for pH, oxygen tension, and carbon dioxide tension. Oxygen saturation was measured in all stages of the experiment using a catheter probe that was inserted through the superior vena cava to the jugular vein.

Statistical Methods
Data are reported as mean, plus or minus standard error of the mean. Measurement data were compared between experimental groups with the pooled variance t test. The mean difference between groups and the corresponding 95% confidence limits also were computed. Tarlov scores were compared with the Wilcoxon rank sum test. All tests were two-tailed. Given the large number of comparisons, the p values should be interpreted carefully. The primary hypothesis concerns the differences in Tarlov scores.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The data were tabulated according to the phase of the procedure: (1) before cardiopulmonary bypass, (2) cooling phase, (3) profound hypothermia and circulatory arrest, (4) warming phase, and (5) after cardiopulmonary bypass.

Neurologic Complications
No (0/5) animals in control group A awoke. Mean wake-up time for group B pigs, plus or minus standard error of the mean, was 124.6 ± 4.6 minutes. Two (2/5) group B animals did not awake, but all (5/5) animals in group C awoke within a mean time of 29.2 ± 5.1 minutes (p < 0.0001, pooled variance t test).

Of the 3 pigs that awoke in group B (3/5), 2 had perceptible hind limb movement (Tarlov score 1). The remaining pig moved all limbs but was unable to stand (Tarlov score 2). Four (4/5) animals in group C were able to stand (Tarlov score 3) and 1 of 5 moved all extremities but awoke unable to stand (Tarlov score 2). Comparing Tarlov scores for group A versus C, the p value was 0.0039 and for group B versus C, the p value was 0.0090 (Wilcoxon rank sum).

Cerebral Blood Flow Measurement
Cerebral blood flow measurement by laser Doppler flowmetry was recorded in five stages and is shown as a percent change from the baseline in Table 1. There was a marked drop in cerebral blood flow from the baseline in group B during the cooling time that continued during circulatory arrest. Reduced flow persisted through the early and late rewarming period and after weaning from cardiopulmonary bypass. In group C we observed a similar drop in flow, although to a lesser degree, during the cooling period and circulatory arrest, but there was an improvement in the flow in the late rewarming period that continued after the pigs were weaned from cardiopulmonary bypass.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
There have been many experimental studies on the effect of hypothermic circulatory arrest time on cerebral function. Profound hypothermia reduces the brain metabolic rate [6, 15, 19] and preserves stores of high-energy phosphates [8, 10]. There is an obligatory requirement even during hypothermic circulatory arrest, and the brain will continue to consume oxygen until it depletes the high-energy phosphate storage and adenosine triphosphate, and with this depletion brain damage ensues [3, 8, 11]. This leads to postischemic impaired cerebral microcirculation, known as the no-reflow phenomenon [20], or the development of ``misery perfusion'' characterized by uncoupled changes of flow and metabolism [21].

Neither clinically nor experimentally has a safe period of hypothermic circulatory arrest to the brain been established [2]. Adjunct methods to extend safe circulatory arrest have included the use of cerebroplegia [6] and antegrade perfusion of the cerebral circulation via the innominate arteries [7]. Agents such as barbiturates, isoflurane, lidocaine in large doses, or diphenylhydantoin, which can reduce the hypothermic cerebral metabolic rate and thus reduce lactate levels, have been tried [8].

Retrograde cerebral perfusion was introduced clinically and tested experimentally to oygenate the brain as well to keep the arteries filled with blood and clear debris from the brachiocephalic arteries. The early clinical results showed better brain protection during circulatory arrest and profound hypothermia. In our current experiment our aim was to validate the impact of RCP in conjunction with profound hypothermia and circulatory arrest on the neurologic function of the brain.

The clinical results reflected the beneficial effect of RCP on the brain during hypothermic circulatory arrest, most likely due to RCP supplying the brain with substrates as well as removing byproducts and debris from the cerebral circulation. These results were supported by the documentation of cerebral blood flow, oxygenation of the brain, and jugular venous oxygen saturation and confirm that the brain during hypothermic circulatory arrest continues to be active metabolically, leading to brain damage if ischemia persists beyond a safe period.

In this study RCP was not compared with antegrade cerebral perfusion, but further experimental models comparing these methods are warranted. In future experiments the animals will be kept alive longer to evaluate better the histologic findings with the clinical outcome of each animal. Because of the brevity of the current study pathologic evaluation produced inconclusive evidence of cerebral damage.

In conclusion, RCP during hypothermic circulatory arrest offers superior brain protection to the techniques of profound hypothermia and circulatory arrest in pigs.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We gratefully acknowledge Amy Wirtz Newland for editorial assistance.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Presented at the Forty-first Annual Meeting of the Southern Thoracic Surgical Association, Marcos Island, FL, Nov 10–12, 1994.

Address reprint requests to Dr Safi, 6550 Fannin, Suite 1603, Houston, TX 77030.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Safi, H. J. Articles by Yawn, D. H. Search for Related Content PubMed PubMed Citation Articles by Safi, H. J. Articles by Yawn, D. H.