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Related Concept Videos

2° Amines to N-Nitrosamines: Reaction with NaNO201:20

2° Amines to N-Nitrosamines: Reaction with NaNO2

Secondary amines react with nitrous acid to form N-nitrosamines, as depicted in Figure 1. Nitrous acid, a weak and unstable acid, is formed in situ from an aqueous solution of sodium nitrite and strong acids, such as hydrochloric acid or sulfuric acid, in cold conditions. In the presence of an acid, the nitrous acid gets protonated. The subsequent loss of water results in the formation of the electrophile known as nitrosonium ion.
1° Amines to Diazonium or Aryldiazonium Salts: Diazotization with NaNO2 Mechanism01:37

1° Amines to Diazonium or Aryldiazonium Salts: Diazotization with NaNO2 Mechanism

Nitrous acid is a relatively weak and unstable acid prepared in situ by the reaction of sodium nitrite and cold, dilute hydrochloric acid. In an acidic solution, the nitrous acid undergoes protonation when it loses water to form a nitrosonium ion—an electrophile. Nitrous acid reacts with primary amines to give diazonium salts. The reaction is called diazotization of primary amines.
Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance01:23

Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance

The elimination half-life and drug clearance of drugs following nonlinear kinetics can vary with dosage. The Michaelis-Menten parameters and drug concentration influence these factors. As the dose increases, the elimination half-life tends to lengthen, resulting in a reduction in clearance and a disproportionately larger area under the curve. The total clearance can be derived from the Michaelis-Menten equation for drugs following a one-compartment model.
A study on guinea pigs examined the...

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Decay of nitroprusside. II: In vivo.

C J Vesey1, B Sweeney, P V Cole

  • 1Anaesthetics Laboratory, St Bartholomews Hospital, West Smithfield, London.

British Journal of Anaesthesia
|June 1, 1990
PubMed
Summary

Nitroprusside (SNP) rapidly decays in the body, unlike in lab tests. This rapid nitroprusside breakdown in patients is the source of cyanide, impacting blood pressure.

Area of Science:

  • Pharmacology
  • Clinical Chemistry

Background:

  • Nitroprusside (SNP) is a potent vasodilator used clinically.
  • Observed clinical data suggest faster SNP degradation in vivo compared to in vitro settings.

Purpose of the Study:

  • To quantify plasma concentrations of SNP in patients during and after infusion.
  • To investigate the relationship between SNP decay, mean arterial pressure (MAP), and cyanide (HCN) levels.
  • To confirm the source of in vivo cyanide generation from SNP decomposition.

Main Methods:

  • Plasma SNP concentrations were measured in 20 patients post-infusion.
  • Mean arterial pressure (MAP) and plasma cyanide (HCN) concentrations were simultaneously monitored.
  • Pharmacokinetic analysis, including biphasic decay and half-life determination, was performed.

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Main Results:

  • Plasma SNP concentrations ranged from 20-243 µg/L, correlating with infusion rate (r=0.66, P<0.001).
  • SNP levels declined rapidly to a mean of 7.7 µg/L within 15 minutes.
  • SNP decay strongly correlated with a rise in MAP (r=-0.993, P<0.001) and showed biphasic elimination (T1/2α=0.89 min, T1/2β=14.3 min).
  • Plasma HCN and SNP concentrations decreased concurrently (r=0.955, P<0.001), confirming SNP as the HCN source.

Conclusions:

  • Nitroprusside exhibits rapid in vivo decay, significantly faster than observed in vitro.
  • The in vivo decomposition of nitroprusside is the primary source of cyanide generation.
  • Rapid SNP clearance is closely linked to its hypertensive effects and cyanide release.