GIT LAB

What is the aim of Dr. Tamara Alqudah's experiment?

What does the tension transducer do in the experiment?

What is essential to maintain the viability of the small intestine tissue in the organ bath?

What does the special software used in the experiment do?

What is the purpose of allowing the muscle to rest for 15-20 minutes before recording tension?

What is used to connect small pieces of the small intestine to a glass hook in the organ bath?

What is the role of slow waves in gastrointestinal contractions?

What is the frequency of slow waves in the ileum of humans?

What causes the appearance of spike potentials in smooth muscle cells?

What is the function of atropine in the experiment mentioned?

What is the role of muscarinic receptors in the effect of acetylcholine on intestinal smooth muscle cells?

What is the main excitatory neurotransmitter in the small intestine?

What is responsible for promoting increased contractile force in the small intestine?

What is the function of enteric neurons and parasympathetic neurons in relation to acetylcholine secretion?

What does atropine act as, with respect to acetylcholine at muscarinic receptor sites?

What is the purpose of connecting the small intestine to a tension transducer in the experiment?

What is the significance of allowing the muscle to rest for 15-20 minutes before recording tension in the experiment?

What is the primary function of atropine added to the organ bath in the experiment?

What occurs as a result of adding acetylcholine to the organ bath in the experiment?

What is the role of the glass hook in the experiment?

What is crucial to maintaining the viability of the tissue in the organ bath during the experiment?

What is the main role of the interstitial cells of Cajal (ICC) in the gastrointestinal tract?

What is the specific effect of atropine on the contractile force of the small intestine?

What leads to the appearance of spike potentials in smooth muscle cells?

What is responsible for promoting increased contractile force in the small intestine?

What is the specific function of acetylcholine in the small intestine?

What determines the maximum frequency at which contraction can occur at a particular site in the gastrointestinal tract?

What is the specific effect of slow waves on the contraction of smooth muscle fibers in the small intestine?

The tension transducer in the experiment converts the mechanical signal generated by the contraction of the small intestine to an electric signal.

The small pieces of the small intestine are hanged vertically by a thread to a glass hook in the organ bath.

Acetylcholine promotes the modification of contractions in the small intestine.

The software used in the experiment is capable of displaying a simple graph of tension versus time.

The viability of the tissue is maintained by warm, oxygenated buffer in the organ bath.

Atropine has no effect on the contraction of the small intestine.

Acetylcholine promotes increased contractile force in the small intestine primarily by increasing the frequency of slow waves.

Slow waves are undulating changes in the resting membrane potential that occur at the same frequency throughout the entire gastrointestinal tract.

The primary function of atropine added to the organ bath in the experiment is to promote increased contractile force in the small intestine.

The slow wave potential needs to rise above -40mV for the spike potentials to appear in smooth muscle cells.

The rhythm of gastrointestinal contractions is mainly determined by the frequency of spike potentials.

The interstitial cells of Cajal (ICC) are believed to act as electrical pacemakers for smooth muscle cells in the gastrointestinal tract.

The primary excitatory neurotransmitter in the small intestine is norepinephrine.

Stimulation by stretch, acetylcholine, and some GI hormones, leads to the appearance of spike potentials in smooth muscle cells.

The increase in contractile force in the small intestine due to acetylcholine is mediated through nicotinic receptors.

Atropine acts as a competitive antagonist of acetylcholine at nicotinic receptor sites in the small intestine.

Atropine is added to the organ bath before acetylcholine in the experiment.

The primary excitatory neurotransmitter in the small intestine is acetylcholine.

The increase in contractile force in the small intestine due to acetylcholine is mediated through nicotinic receptors.

Atropine has no effect on the contraction of the small intestine.

The software used in the experiment is not capable of displaying a simple graph of tension versus time.

The interstitial cells of Cajal (ICC) are believed to act as electrical pacemakers for smooth muscle cells in the gastrointestinal tract.

The slow waves in the small intestine are determined mainly by the frequency of the 'slow waves'.

The frequency of slow waves in the small intestine is 12/minute in the duodenum and 8-9/minute in the ileum.

Acetylcholine promotes increased contractile force in the small intestine due to an increase in the number of spikes, not in the frequency of slow waves.

Atropine acts as a competitive antagonist of acetylcholine at the muscarinic receptor in the small intestine.

The increase in contractile force in the small intestine due to acetylcholine is mediated through nicotinic receptors.

The primary excitatory neurotransmitter in the small intestine is norepinephrine.

The role of muscarinic receptors in the effect of acetylcholine on intestinal smooth muscle cells is essential for promoting increased contractile force.

Slow waves need to rise above -40mV for spike potentials to appear in smooth muscle cells.

Atropine has no effect on the contraction of the small intestine.

The rhythm of gastrointestinal contractions is mainly determined by the frequency of spike potentials.