IJAR.2016.518
Type of Article: Original Research
Volume 5; Issue 1 (March 2017)
Page No.: 3567-3571
DOI: https://dx.doi.org/10.16965/ijar.2016.518
OCCLUSION OF MIDDLE CEREBRAL ARTERY CAUSING THE CEREBRAL EDEMA IN PRIMATES, A STUDY BY SPECIFIC GRAVITY METHOD
K. S. Satheesha *1, Suresh Rao 2, Ravi Bhaskar 3.
*1 Professor, Department of Anatomy, Srinivas Institute of Medical Sciences and Research Centre Mukka, Mangalore Karnataka, India.
2 Senior Lecturer & Head, Anatomy & Cell Biology Unit, Faculty of Medical Sciences, The University of West Indies.
3 Tutor, Department of Anatomy, Srinivas Institute of Medical Sciences and Research Centre Mukka, Mangalore Karnataka, India.
Address for Correspondence: Dr. K. S. Satheesha, Professor, Department of Anatomy, Srinivas Institute of Medical Sciences & Research Centre, Mukka, Mangalore India. Phone: +91 8762886608, E-Mail: s67in2003Yahoo.com
ABSTRACT
Aim: To check if there is any relation between the compromise of microcirculatory perfusion, infarct location and edema of cerebrum after occluding the middle cerebral artery and to find out if any reperfusion remedy, which can be applied to minimize the infarction and cerebral edema.
Materials and Method: The present study included 24 adult monkeys which were procured from the non-forest areas. The cerebral edema was assessed by the specific gravity method.
Results: It was observed that, after the permanent occlusion of the MCA for 30min, 4 and 12h, there was insignificant risein the quantity of water of the cerebral hemisphere, when compared to sham operated monkeys. There was no contralateral variation in the water content with the occlusion of one cerebral hemisphere for 30min, 4,12h. At 24h, there was an insignificant increase in the contralateral cerebral hemisphere.
Conclusion: We opine that, it is the quantity of the infarct rather than the occurrence or absenteeism ofthe reperfusion, which is responsible for the development of cerebral edema. This study supports the clinician opinion, which reports that the brain edema will not trigger after the thrombolysis and recanalization of the obstructed artery.
Key words: Cerebral edema, Ischemia, Specific gravity, Perfusion, MCA.
REFERENCES
- Walcott BP, Kahle KT, Simard JM. Noveltreatment targets for cerebral edema. Neurotherapeutics 2012;9:65-72.
- Thrane AS, RangrooThrane V, NedergaardM. Drowning stars: Reassessing the role ofastrocytes in brain edema. Trends Neurosci2014;11:620-628.
- Simeone FA, Frazer G, Lawner P. Ischemicbrain edema: comparative effects ofbarbiturates and hypothermia. Stroke 1979;10: 8-12.
- O’Brien JR, Finch W, Clark E.A comparisonof an effect of different anti-inflammatorydrugs on human platelets. J ClinPathol1970;23:522-5.
- Satheesha K S, Ravi Bhaskar,Shakunthala R Pai. Cerebral edema in middle cerebral artery occlusion: astudy in primates by wet weight: dry weight method. International Journal of Advances in Health Sciences (IJHS) 2015;l2(5):576-581.
- Sandritter WJ. TTC als reduction sindiFujimot et al., 1976 and Ito, 1976 rzurmakroskopischen diagnosis des firschenherqinfarkets. Vern DschGesPathol. 1958;41:1650.
- Little JR: Implanted device for middle cerebral artery occlusion in conscious cats. Stroke.1977;8:258-260.
- Garcia JH, Mitchem HL, Briggs L. Transient focal ischemia in subhuman primates : Neuronal injury as a function of local cerebral blood flow. J NeurophatholExp Neurol.1983;42:44-60.
- KatzmanGlobelU, Klein B, Schrock H, Kuschinsky W: Lack of capillary recruitment in the brains of awake rats during hypercapnia. J Cereb Blood flow Metab.1989;9: 491-499.
- Satheesha KS, Somesh MS, Pai SR, Patil GV. Estimation of the infarct size on occlusion of the middle cerebral artery in primates. Journal of Clinical and Diagnostic Research 2012;6:1105-1108.