Related Experiment Video

Updated: Oct 3, 2026

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
07:03

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage

Published on: January 17, 2013

Docosahexaenoic acid inhibits blood viscosity in stroke-prone spontaneously hypertensive rats

S Kimura1, M Tamayama, M Minami

  • 1Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Japan.

Research Communications in Molecular Pathology and Pharmacology
|September 8, 1998
PubMed

Increased blood viscosity facilitates the formation of thrombosis. This is an important risk factor in the occurrence of cerebral infarctions. The present study was undertaken to elucidate whether docosahexaenoic acid (DHA) inhibits blood viscosity, hematocrit and fibrinogen in the disease animal model, stroke-prone spontaneously hypertensive rats (SHRSP). An attempt was also made to clarify the effect of DHA on blood pressure in SHRSP. Blood viscosity, hematocrit and fibrinogen in non-treated SHRSP increased significantly when compared with levels in age-matched non-treated Wistar Kyoto rats (WKY). SHRSP rats which were administered DHA for 5 weeks displayed significant decreases in blood viscosity, hematocrit and fibrinogen when compared with the values in non-treated SHRSP. The blood pressure of DHA-treated SHRSP was significantly lower than that of non-treated SHRSP. A positive correlation existed between blood pressure and blood viscosity. These findings suggest that decreased blood viscosity induced by DHA appears to be associated with the reduction of thrombosis formation and hypotensive action in SHRSP.

More Related Videos

Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke06:36

Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke

Published on: June 5, 2019

Real-Time Monitoring and Modulation of Blood Pressure in a Rabbit Model of Ischemic Stroke09:00

Real-Time Monitoring and Modulation of Blood Pressure in a Rabbit Model of Ischemic Stroke

Published on: February 10, 2023

Related Concept Videos

Regulation of Stroke Volume01:27

Regulation of Stroke Volume

The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...