title: Insular lesion evokes autonomic effects of stroke in normotensive and hypertensive rats.
abstract: OBJECTIVE
  Increases in sympathetic activity and frequency of myocardial damage occur after middle cerebral artery occlusion (MCAO) in Wistar rats, while MCAO in the spontaneously hypertensive rat (SHR) decreases sympathoadrenal activity. Autonomic changes have been suggested to result from damage to the insular cortex (IC).
  
  
  METHODS
  A lesion of the IC was made using the excitotoxin D,L-homocysteic acid (DLH; 1 mol/L), in urethane-anesthetized Wistar rats and SHRs. Mean arterial pressure (MAP), heart rate, renal sympathetic nerve discharge (SND), ECG, and plasma catecholamines were measured in 14 SHRs and 14 Wistar male rats after a 500-nL injection of DLH or phosphate-buffered saline (PBS) into the IC.
  
  
  RESULTS
  Histological examination showed that DLH resulted in neuronal damage throughout the IC. DLH injection initially elevated MAP (at approximately 10 minutes after injection) in Wistar rats but not in SHRs. At 4 hours after the DLH injection, there was a secondary, longer-term increase in MAP in the Wistar rats. MAP decreased in the SHRs after IC lesion such that at 6 hours, lesioned SHRs had a MAP that was significantly lower than that of sham-lesioned SHRs. SND initially increased (at 10 minutes) after DLH injection in Wistar rats. In the SHRs, SND decreased significantly from the initial values, by 3 hours after DLH injection. Plasma catecholamine levels were not significantly changed as a result of IC lesion in the Wistar rats or the SHRs. Heart rates increased in all animals, with no differences between groups. There were no changes in the ECG or in the frequency of cardiac myocytolysis in either strain (sham or lesioned animals).
  
  
  CONCLUSIONS
  IC lesion in the SHR and Wistar rat therefore appears to result in autonomic changes similar to that seen after MCAO. Unlike MCAO, however, the autonomic changes do not appear to be sufficient to produce myocardial damage.
authors.affiliation: Department of Stroke and Aging, John P. Robarts Research Institute, London, Ontario, Canada.
authors.forename: K S
authors.initials: KS
authors.lastname: Butcher
authors.forename: D F
authors.initials: DF
authors.lastname: Cechetto
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001927:Brain Diseases / Q000139:chemically induced; D002539:Cerebral Arterial Diseases / Q000503:physiopathology; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000473:pathology / Q000503:physiopathology*; D004562:Electrocardiography / Q000187:drug effects; D004837:Epinephrine / Q000097:blood; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006710:Homocysteine / Q000009:adverse effects / Q000031:analogs & derivatives; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects / Q000294:innervation; D008297:Male; D009206:Myocardium / Q000473:pathology; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D006710:Homocysteine; C007956:homocysteic acid; D009638:Norepinephrine; D004837:Epinephrine