ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miyamoto, T.-A.
Right arrow Articles by Miyamoto, K.-J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miyamoto, T.-A.
Right arrow Articles by Miyamoto, K.-J.

Ann Thorac Surg 2000;70:1764-1765
© 2000 The Society of Thoracic Surgeons


Correspondence

Prevention of post-hypothermic circulatory arrest temporary neurologic deficits

Tadaomi-Alfonso Miyamoto, MDa, Koho-Julio Miyamoto, MD, PhDb

a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku,, Kitakyushu-shi, Fukuoka 802-8555, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa, Japan

To the Editor

Ergin and colleagues are to be congratulated for their article [1]. Temporary neurological dysfunction is reminiscent of neurologic dysfunction observed in the early days of cardiac surgery with surface-induced or even cardiopulmonary bypass perfusion-induced hypothermia, and must be unquestionably an entirely different entity from embolic complications.

Anoxic or hypoxic injury, alone or aggravated by the reperfusion injury, must be the basis of temporary neurologic dysfunction. Involvement of the most hypoxia-sensitive brain area, the hippocampus, supports this view. We concur with Reich’s reply to our letter to the editor, which appeared in J Thorac Cardiovasc Surg, Sept 1999 [2], concerning the initial portion of this study, that "the older population is different from young patients ... [and] is indeed more vulnerable to hypoxia or ischemia."

This vulnerability makes avoiding deleterious effects of protective strategies that much important. Nollert and associates demonstrated development of hypoxia during the early phases of hypothermia well before the induction of hypothermic circulatory arrest in spite of increased oxyhemoglobin indicative of increased hemoglobin O2 affinity by near infra-red spectroscopy [3]. Prevention of alpha-stat alkalosis and impaired O2 delivery-induced hypoxia (Bohr effect), occurring before the dissolved O2 role becomes relatively more important than that of hemoglobin as the source of O2 to the brain, below 18°C, is a crucial issue. Such hypoxia can be effectively averted by the acidosis of pH-stat strategies.

The increased chances of microembolization of normothermic hypercarbia should not be extrapolated to hypothermic circulatory arrest, which by necessity involves a period of ischemia followed by reperfusion. Flow-metabolism coupling is not disrupted during pH-stat hypothermic perfusion, nor is there evidence of increased embolic capillary occlusion by hypothermic pH-strategies at least down to 27°C [4]. We believe that, unless massive, the deleterious effects of gaseous microembolization, if it occurs, would be transient and relatively harmless if no prior hypoxia had taken place. Proper protective measures must be taken when flow is reestablished following reabsorption to avoid alkalosis-promoted Ca++ influx and too rapid or excessive bypass rewarming. The mild acidosis of pH-stat should also minimize reperfusion injury. Theoretically, microembolization and hyperoxic lipid peroxidation could be minimized by decreasing O2 flow in the oxygenator as discussed in the letter to the editor regarding McCullough’s article [5].

Nature has conferred newborns of all animal species (humans included) the ability to tolerate longer hypoxic periods than adults by providing their central nervous systems with higher contents of taurine [6].

Taurine given systemically enhances the protective effects of hypothermia [7]. Being an amino acid naturally involved with protective mechanisms, it should be effective in the older population as well without untoward effects. We believe the time has come to recognize the wisdom of nature and give pH-stat strategies and taurine a second look. Their concomitant use should maximize other protective strategies including that of memantine [8], riluzole [9], or nitric oxide generation inhibitors and may effectively cancel age as a risk factor for temporary neurological dysfunction after DHCA.

References

  1. Ergin M.A., Uysal S., Reich D.L., et al. Temporary neurological dysfunction after deep hypothermic circulatory arrest. Ann Thorac Surg 1999;67:1887-1890.[Abstract/Free Full Text]
  2. Reich D.L. Is alpha-stat management still justified for deep hypothermic circulatory arrest in adults [Letter]?. J Thorac Cardiovasc Surg 1999;118:570.[Free Full Text]
  3. Nollert G., Nagashima M., Bucerius J., et al. Oxygenation strategy and neurologic damage after deep circulatory arrest. II. Hypoxic versus free radical injury. J Thorac Cardiovasc Surg 1999;117:1172-1179.[Abstract/Free Full Text]
  4. Hindman B.J., Dexter F., Cutkomp J., Smith T., Todd M.M., Tinker J.H. Brain blood flow and metabolism do not decrease at stable brain temperature during cardiopulmonary bypass in rabbits. Anesthesiology 1992;77:342-350.[Medline]
  5. Miyamoto T.-A., Miyamoto K.-J. pH-Stat strategies protect 60-minute central nervous system ischemia at 29.5°C [Letter]. Ann Thorac Surg 2000;70:1001-1002.[Free Full Text]
  6. Huxtable R.J. Taurine in the central nervous system and the mammalian actions of taurine. Prog Neurobiol 1989;22:471-533.
  7. Ohno N., Miyamoto K.J., Miyamoto T.A. Taurine potentiates the efficacy of hypothermia. Asian Cardiovasc and Thorac Ann 1999;7:267-271.
  8. Ehrlich M., Knolle E., Ciovica R., et al. Memantine for prevention of spinal cord injury in a rabbit model. J Thorac Cardiovasc Surg 1999;117:285-291.[Abstract/Free Full Text]
  9. Lang-Lazdunski L., Heurteaux C., Vaillant N., Widmann C., Lazdunski M. Riluzole prevents ischemic spinal cord injury caused by aortic cross-clamping. J Thorac Cardiovasc Surg 1999;117:881-889.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miyamoto, T.-A.
Right arrow Articles by Miyamoto, K.-J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miyamoto, T.-A.
Right arrow Articles by Miyamoto, K.-J.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS