Images of Vasospasm

This is a review of an interesting study from 1997 (published in Stroke) that illustrates how vasospastic arteries in a rat subarachnoid hemorrhage model looks like under the scanning electron microscope.

The researchers injected hemolysate (lysed autologous blood) into the cisterna magna of male Sprague-Dawley rats.  After ten minutes, a polymer resin casting medium was injected intravenously.  Once the resin has casted, the tissue and bones were corroded using NaOH solution, until only the vascular cast remains.  The casts were visualized under scanning electron microscope, and the following images were derived:


Basilar artery of:  A.  saline-injected control rats;  B. hemolysate-injected rats;  arrowheads = PICA;  note the narrowing and corrugation seen in the basilar artery of the hemolysate-injected rats.

Capture.JPG Other major arteries were also observed to be in vasospasm.  (note corrugation in these arteries)


Vasospasm (demonstrated as corrugation in the casted vessels) is seen in the major arteries (A) as well as the small arteries (B).


High magnification showing “corrugation” of the basilar artery.  The arrows point to nuclear indentations which correspond the the endothelial cell nucleus.  (see below0


The researchers also performed conventional SEM.  A and B are normal vessels while C and D are hemolysate-induced vasospastic blood vessels.   A and C are low magnification, B and D are high magnification.

The normal vessels (A) show that the inner surface is very smooth and the vessel wall is thin, and (B) the endothelial nuclei are clearly observed, projecting into the inner surface at regular intervals of 10-20 um.

The vasospastic vessels (C) shows that the smooth muscle layer is thicker, corrugation is observed and (D) many humps are sandwiched and flattened between hills formed by the endothelial cells.

Cast model shows corrugation, characteristic folds of endothelial cells at regular intervals and indentations of endothelial cell nuclei at each peak of those folds.  These indentations correspond to the humps seen in conventional SEM analysis.  The mechanical force of corrugation compressed the endothelial cells, flattened their nuclei and likely disturbed their function.  These physical alterations cause narrowing of the vessels, disturbs local blood flow, and may disturb blood coagulation and adhesion of WBC and platelets to the endothelium.  This may be a mechanism that explains thrombus inflammation and inflammatory response in these diseased vessels.

Their research also showed that arteries exposed to greater amount of hemolysate exhibit more severe vasospasm.


Ono, S. et al. “Three-Dimensional Analysis Of Vasospastic Major Cerebral Arteries In Rats With The Corrosion Cast Technique”. Stroke 28.8 (1997): 1631-1638.


  • Gaze deviation AWAY from hemiparesis : hemispheric lesion contralateral to hemiparetic side.
  • Gaze deviation TOWARD hemiparesis: pontine lesion, contralateral hemispheric seizure focus and contralateral thalamic lesion
  • Downward gaze deviation : midbrain tectum lesion. (Parinaud’s – accompanied by impaired pupillary reaction to light and convergence-retraction nystagmus)
  • Ocular bobbing : lesion of bilateral pontine horizontal gaze center (fast downward movements of both eyes with a slow return to primary position)



Rana, Abdul Qayyum, and John Anthony Morren. Neurological Emergencies In Clinical Practice. London: Springer, 2013. Print.

Vitamin K Cycle and Coumadin

Explanation of Vitamin K Cycle from NEJM  (N Engl J Med 2013; 369:2345-2346December 12, 2013DOI: 10.1056/NEJMe1313682)

Vitamin K plays a single role in human biology — as a cofactor for the synthesis of γ-carboxyglutamic acid. 

Importance of γ-carboxyglutamic acid?

1.  component of at least 14 proteins (factor IX, factor VII, factor X, and prothrombin, protein C and protein S)

2. critical for the physiologic function of these proteins

We do not synthesize vitamin K, we ingest it in our diet. 

Vit K Cycle:

1. vitamin K quinone reduced to the semiquinone –> cofactor required for conversion of glutamic-acid residues on the vitamin K–dependent proteins to γ-carboxyglutamic acid by vitamin K–dependent carboxylase

2.  reaction produces Vitamin K epoxide –>  converted back to vitamin K quinone by VKOR (vitamin K epoxide reductase)

Warfarin inhibits VKOR –> post-translational modification of the vitamin K–dependent blood-coagulation proteins is impaired –>  reduced function of factors 10, 9, 7, 2 leads to delayed coagulation

Simplified Diagram:

Where the Protein products come in the cycle:

A more complicated diagram to illustrate the Vit K cycle:

Illustration showing where warfarin works in the Vit K cycle: