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Related Concept Videos

Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

527
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...
527
Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

3.5K
Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial...
3.5K
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics01:11

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics

716
All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...
716
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

2.7K
Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
2.7K
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

814
Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
814
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

2.5K
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
2.5K

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Related Experiment Videos

The minimal functional sequence of protamine.

Jun Feng Liang1, Victor C Yang, Yekaterina Vaynshteyn

  • 1Department of Chemistry and Chemical Biology, Stevens Institute of Technology, Hoboken, NJ 07030, USA.

Biochemical and Biophysical Research Communications
|September 6, 2005
PubMed
Summary
This summary is machine-generated.

Researchers developed low molecular weight protamine peptides that effectively neutralize heparin with reduced toxicity. These findings suggest safer clinical applications for protamine alternatives in medical procedures.

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Biotechnology

Background:

  • Protamine is widely used but causes significant side effects.
  • It is a mixture of four major peptides with varying sequences.

Purpose of the Study:

  • To obtain and identify low molecular weight protamine peptides with potent heparin neutralization abilities.
  • To evaluate the safety and efficacy of these peptides compared to native protamine.

Main Methods:

  • Enzyme digestion was used to create various low molecular weight protamine peptides.
  • In vitro and in vivo tests were conducted to assess heparin neutralization and toxicity.

Main Results:

  • Two low molecular weight protamine peptides demonstrated equal or greater heparin neutralization capacity than native protamine.
  • These identified peptides exhibited significantly lower toxicity in vivo compared to native protamine.

Conclusions:

  • Low molecular weight protamine peptides can be safely used as alternatives to native protamine.
  • The identified peptides offer a safer profile for clinical applications requiring heparin neutralization.