Faculty Collaboration Database

Oxotremorine-induced cerebral hyperemia does not predict infarction volume in spontaneously hypertensive or stroke-prone rats. Crit Care Med 2000 Jan;28(1):190-5

Date

02/10/2000

Pubmed ID

10667521

DOI

10.1097/00003246-200001000-00031

Scopus ID

2-s2.0-0033953621 (requires institutional sign-in at Scopus site)   4 Citations

Abstract

OBJECTIVES: We tested the following hypotheses: a) spontaneously hypertensive stroke-prone rats (SHR-SP) have more brain injury than spontaneously hypertensive rats (SHR) and normotensive controls (Wistar-Kyoto rats [WKY]) when exposed to transient focal ischemia; b) infarction size is not correlated with baseline blood pressure; and c) infarction size is inversely related to the cerebral hyperemic response to oxotremorine, a muscarinic agonist that increases cerebral blood flow (CBF) by stimulating endothelial nitric oxide synthase.

DESIGN: In vivo study.

SETTING: Animal laboratory in a university teaching hospital.

SUBJECTS: Adult age-matched male WKY, SHR, and SHR-SP.

INTERVENTIONS: Rats were instrumented under halothane anesthesia. Transient focal cerebral ischemia was produced for 2 hrs with the intravascular suture technique. Cerebral perfusion, estimated with laser Doppler flowmetry (LD-CBF), in response to intravenous oxotremorine, was measured in one cohort of rats to estimate endothelial nitric oxide synthase function. Infarction volume was measured at 22 hrs of reperfusion with 2,3,5-triphenyltetrazolium chloride staining.

MEASUREMENTS AND MAIN RESULTS: Infarction volume in the striatum of SHR-SP (42+/-4 mm3) was greater than in SHR (29+/-6 mm3) or WKY (1+/-1 mm3) (n = 9 rats/strain). Resting (unanesthetized) mean arterial blood pressure was similar in SHR-SP (177+/-5 mm Hg) and SHR (170+/-5 mm Hg) despite a greater infarction volume in SHR-SP (n = 4) compared with SHR (n = 5). The percentage increase in LD-CBF signal in response to oxotremorine was similar for both groups (SHR, 64%+/-22% [n = 10]; SHR-SP, 69%+/-22% [n = 8]). However, in this cohort, cortical infarction volume was less in SHR (30%+/-4% of ipsilateral cortex) than in SHR-SP (49%+/-2% of ipsilateral cortex).

CONCLUSIONS: Although SHR-SP have greater infarction volume than SHR, the mechanism of injury does not appear to be related to a difference in unanesthetized baseline mean arterial blood pressure or to an alteration in endothelium-produced nitric oxide.

Author List

Harukuni I, Takahashi H, Traystman RJ, Bhardwaj A, Kirsch JR

MESH terms used to index this publication - Major topics in bold

Animals
Brain
Brain Ischemia
Cerebral Infarction
Coloring Agents
Disease Models, Animal
Endothelium, Vascular
Hypertension
Laser-Doppler Flowmetry
Male
Muscarinic Agonists
Nitric Oxide Synthase
Nitric Oxide Synthase Type III
Oxotremorine
Predictive Value of Tests
Rats
Rats, Inbred SHR
Rats, Inbred Strains
Rats, Inbred WKY
Ultrasonography