SODIUM NITROPRUSSIDE

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Sodium nitroprusside (SNP) is a potent, rapid-acting vasodilator used to control blood pressure in various clinical situations. Its mechanism of action involves the release of nitric oxide (NO), a powerful vasodilator, which leads to smooth muscle relaxation in both arterioles and venules. The importance of sodium nitroprusside in the context of anesthesia includes:

1. Hypertensive crisis: Sodium nitroprusside can be used to manage acute hypertensive crises in the perioperative period. Its rapid onset of action and short duration make it an ideal agent for controlling severe hypertension quickly and effectively.

2. Controlled hypotension: During certain surgical procedures, it may be necessary to induce controlled hypotension to reduce blood loss and improve surgical visibility. Sodium nitroprusside can be used to achieve and maintain the desired level of hypotension, facilitating better surgical outcomes.

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The specific steps of sodium nitroprusside's mechanism of action are as follows:

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1. Upon administration, sodium nitroprusside dissociates in the bloodstream, releasing five cyanide ions and one nitroso (NO) moiety. The released NO is the active component responsible for the vasodilatory effects.

2. Nitric oxide diffuses into the smooth muscle cells in the walls of blood vessels, particularly in the arterioles and venules.

3. Within the smooth muscle cells, NO activates an enzyme called soluble guanylate cyclase (sGC). This activation leads to an increase in the production of cyclic guanosine monophosphate (cGMP).

4. The increased cGMP levels activate protein kinase G (PKG), which then phosphorylates multiple target proteins. These phosphorylation events ultimately cause a reduction in intracellular calcium levels.

5. The decrease in intracellular calcium levels leads to relaxation of the vascular smooth muscle cells, resulting in vasodilation.

 

The vasodilatory effects of sodium nitroprusside on both the arterial and venous sides of the circulation lead to reduced systemic vascular resistance and venous return. This results in decreased afterload and preload on the heart, respectively. Consequently, blood pressure is lowered, and cardiac output may be improved in certain clinical situations, such as congestive heart failure.

 

It is important to note that sodium nitroprusside's rapid onset of action and short duration make it an ideal agent for situations where rapid and precise blood pressure control is required. However, it must be used with caution due to the risk of excessive hypotension and potential cyanide toxicity.

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                                                                                  Key points about Sodium Nitroprusside

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• Direct-acting, a nonselective peripheral vasodilator that causes relaxation of arterial and venous vascular smooth muscle.

 

• The molecule is 44% cyanide by weight.

 

• Interacts with oxyhemoglobin, dissociating immediately and forming methemoglobin while releasing cyanide and nitric oxide.

 

• Nitric oxide is the active mediator responsible for the direct vasodilating effect.

 

• Toxicity includes cyanide toxicity, thiocyanate toxicity, and methemoglobinemia.

 

• Free cyanide radicals may prevent oxidative phosphorylation, precipitating tissue anoxia, anaerobic metabolism, and lactic acidosis.

 

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