Etiology Of Vasospasm Potential Pathogens

The principal cause of vasospasm is the periarterial subarachnoid blood clot. Several substances that have been implicated in vasospasm are gradually released from the blood clot (Table 2). Of these, the most extensively studied is oxyhemoglobin, which is widely believed to be the principal pathogen of vasospasm (17). However, it is likely that the cascade of events that eventually lead to irreversible vasoconstriction is modulated by many other factors. Studies designed to examine the importance of the different fractions of the breakdown products of whole blood have predominantly focused on the ability of these substances to cause cerebral arteries to contract, as well as the timeframe within which these substances can be measured in the cerebrospinal fluid (CSF). As we begin to unravel the intracellular events that follow SAH, we might be able to better appreciate the importance of these substances.

Figure 1 Two branches of the right middle cerebral artery in a patient 12 months after subarachnoid hemorrhage. Cerebral blood vessel (left) shows marked intimal proliferation, compared to normal (right). Source: From Ref. 21.

Table 2 Potential Spasmogens Released After Subarachnoid Hemorrhage and Their Possible Role in Vasospasm

Spasmogen or process

Possible role

Erythrocytes and contents Oxyhemoglobin and breakdown products, such as hemin, iron, bilirubin, and globin chains

Products of free radical reactions stimulated by hemoglobin oxidation Adenosine nucleotides Cytosolic proteins Erythrocyte membranes Platelet contents Serotonin Adenosine Growth factors

Leukocytes and inflammatory mediators

Leukocytes

Eicosanoids

Cytokines (interferons, tumor necrosis factor, interleukins, macrophage-derived cytokines, growth factors, chemokines, monokines) Products of the coagulation cascade Fibrin degradation products Fibrinogen Thrombin

Other serum proteins

Vasoconstriction, promotion of free radical reactions, blockage of NO vasodilatation, increase in endothelin release, blockage of perivascular nerve effects, and alteration of eicosanoid release Possible vasoconstriction

Vasoconstriction

Unknown

Lipid peroxidation

Possible vasoconstriction early after SAH

Vasoconstriction

Vasoconstriction

Vasoconstriction

Increased vasoconstriction by prostaglandins and thromboxanes, decreased vasodilatation by decreased PGI2

Increased inflammation, possible vasoactive effects

Increased vasoconstriction due to other spasmogens

Unknown

Unknown

Unknown

Abbreviations: SAH, subarachnoid hemorrhage; NO, nitric oxide. Source: Adapted from Ref. 16.

Metabolism Masterclass

Metabolism Masterclass

Are You Sick And Tired Of All The Fat-Burning Tricks And Trends That Just Don’t Deliver? Well, Get Set To Discover The Easy, Safe, Fast, And Permanent Way To Mega-Charge Your Metabolism And Lose Excess Fat Once And For All! This Weight Blasting Method Is Easy AND Natural… And Will Give You The Hot Body And Killer Energy Levels You’ve Been Dreaming Of.

Get My Free Ebook


Post a comment