Biology 3602A/B Lecture Notes - Lecture 14: Heart Valve, Pulmonary Valve, Sinoatrial Node

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blushcicada362

5 Aug 2016

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We can change the amt of ca that goes into the heart cells that cause it to contract (dynamics) Or we can change the sensitivity of those ca elements to ca (response) We can do this by endocrine responses, nerve responses, or drugs. One of the drugs is digoxin, which inhibits na-k-atpase in the cell, causing a buildup of. Na, but cell wants to get rid of na so it gets na out by putting ca in -- thus stronger contractions. The effect of sympathetic neurotransmitters such as norepinephrine increasing heart rate (chronotropic effect) but also can have an ionotropic effect by sensing sensitivity of contractile elements to ca. Norepinephrine or epinephrine binds to b1 receptor, activating ac, activating pka. In (7) pathway, pka can (p) myosin, one of the contractile filaments; by (p) this, makes it more sensitive to ca. So get more ca in or change sensitivity to increase contractile strength.

Related Questions

Please answer the question after reading the paragraph.

We have a global health challenge in our hands today, and that is that the way we currently discover and develop new drugs is too costly, takes far too long, and it fails more often than it succeeds. It really just isn't working, and that means that patients that badly need new therapies are not getting them, and diseases are going untreated. We seem to be spending more and more money. So for every billion dollars we spend in R&D, we're getting less drugs approved into the market. More money, less drugs. Now we have a whole pipeline of different organ chips that we are currently working on in our labs. Now, the true power of this technology, however, really comes from the fact that we can fluidically link them. There's fluid flowing across these cells, so we can begin to interconnect multiple different chips together to form what we call a virtual human on a chip. Now we're really getting excited.We're not going to ever recreate a whole human in these chips, but what our goal is is to be able to recreate sufficient functionality so that we can make better predictions of what's going to happen in humans. For example, now we can begin to explore what happens when we put a drug like an aerosol drug. Those of you like me who have asthma, when you take your inhaler, we can explore how that drug comes into your lungs, how it enters the body, how it might affect, say, your heart. Does it change the beating of your heart? Does it have a toxicity? Does it get cleared by the liver? Is it metabolized in the liver? Is it excreted in your kidneys? We can begin to study the dynamic response of the body to a drug. Organs on chips could also change the way we do clinical trials in the future. Right now, the average participant in a clinical trial is that: average. Tends to be middle aged, tends to be female. You won't find many clinical trials in which children are involved, yet every day, we give children medications, and the only safety data we have on that drug is one that we obtained from adults. Children are not adults. They may not respond in the same way adults do. There are other things like genetic differences in populations that may lead to at-risk populations that are at risk of having an adverse drug reaction. Now imagine if we could take cells from all those different populations, put them on chips, and create populations on a chip. This could really change the way we do clinical trials. And this is the team and the people that are doing this. We have engineers, we have cell biologists, we have clinicians, all working together. We're really seeing something quite incredible at the Wyss Institute. It's really a convergence of disciplines, where biology is influencing the way we design, the way we engineer, the way we build. It's pretty exciting.

Question: For years, technology and medicine have joined together to pave the way or even solve some of the worldâs greatest issues in healthcare. These issues include but are not limited to incurable diseases and disorders like AIDS and cancer. According to Geraldine Hamilton however, we as a population are spending too much money to develop drugs and solutions to these issues, only to be at a deficit with the drugs actually produced. She believes that one of the keys is how we test these drugs and finding more efficient ways to do so. As a result, she suggests the use of organs on chips, an innovation created and pioneered by her lab. The use of organs on chips could change the way new drugs are released and tested, thus possibly furthering the process of creating solutions to healthcareâs problems. Where is the fine line between technology and human innovation? Is human innovation gradually becoming depending on technology? (At least two paragraphs, a paragraph is at least 5 sentences long.)

receptor	Agonist	antagonist


a1	Norephinephrine	Phenylephrine
a2	Phenoxybenzamine	Prazosin
B1	Clonidine	Yohimbine
	Norephinephrine	Propranolol
	Epinephrine	Metoprolol
	Isoproterenol
	Dobutamine
B2	Epinephrine	Proranolol
	Norepinephrine	Butoxamine
	Isoproterenol
	Albuterol


Nicotinic	Ach	Curare
	Nicotine
		Hexamethonium
Muscarinic	Ach	Atropine

Assume all the chemicals in the table are available to you.

You are given a piece of smooth muscle tissue, you stimulate it with Norepinephrine and find the muscle responds with contractions. Your hypothesis is that the muscle contraction is caused by the activation of Î±1 adrenergic receptors. Now you need to design an experiment protocol to test your hypothesis.

Background knowledge: The figure below is an experiment setup, the red tissue in the organ bath is the smooth muscle tissues. In this kind of experiment smooth muscle tissue is minimally stretched vertically by two hooks or clips in the organ bath filled with physiological saline solution (PSS). Agonist is added to the PSS to challenge the muscle tissue, muscle contraction is sensed by a force transducer at the top and force is recorded by a computer. Adding antagonist before adding agonist blocks agonist action. PSS may or may not be changed, it depends on your purposes, e.g. if you want to block a type receptors, then you do not want change PSS after you add antagonist to the PSS. Your correct step is that you add antagonist to PSS, wait some time, and add agonist, you keep both antagonist and agonist in the PSS so that you can judge if the receptor blockage by antagonist abolish the agonist action.

The key to this assignment is that you eliminate possible cross-activities of agonists. Cross-activity means an agonist activate more than one types of receptors, you need block each type of the receptor in order to see what type of the receptor is activate to cause contraction. This muscle tissue can have both Î± and Î² receptor types and their subtypes, you need to demonstrate convincingly that you only stimulate Î±1 receptors.

Write an experimental protocol to demonstrate your work, for each step in the protocol you write the chemical(s) you add, why you add, what result you are expecting to see e.g. contract, relax, no response. If the step is to wash the tissue with fresh PSS, then you do not need to indicate the responses.

Here is an example of the answer.

step	chemical added	response
1.	epinephrine, activate alpha and beta receptors,	blood vessel ring contract slightly.
2.	wash with PSS
3.	alpha receptor antagonist and norepinerphine, block NE activating alpha receptor.	blood vessel ring should not contract.
4.	wash with PSS
5.	â¦	â¦
6.	â¦	â¦

Discuss your protocol to show the relation between activation of Î±1 receptors and the vascular smooth muscle contraction.Design the experiemnt and its conclusion/ results.

Consider the following abstracts about intervention to improve memory, one real, and one fictitious:

Memory enhancement in healthy older adults using a brain plasticity-based training program: A randomized, controlled study
Mahncke HW et al. PNAS August 15, 2006 vol. 103 no. 33 12523-12528
Normal aging is associated with progressive functional losses in perception, cognition, and memory. Although the root causes of age-related cognitive decline are incompletely understood, psychophysical and neuropsychological evidence suggests that a significant contribution stems from poorer signal-to-noise conditions and down-regulated neuromodulatory system function in older brains. Because the brain retains a lifelong capacity for plasticity and adaptive reorganization, dimensions of negative reorganization should be at least partially reversible through the use of an appropriately designed training program. We report here results from such a training program targeting age-related cognitive decline. Data from a randomized, controlled trial using standardized measures of neuropsychological function as outcomes are presented. Significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25) were documented in the group using the training program. Memory enhancement appeared to be sustained after a 3- month no-contact follow-up period. Matched active control and no-contact control groups showed no significant change in memory function after training or at the 3-month follow-up. This study demonstrates that intensive, plasticity-engaging training can result in an enhancement of cognitive function in normal mature adults.

Memory enhancement in healthy older adults using genetic modification also protects against Alzheimerâs Disease.1
I M Genius, Prestigious Journal 1 (1): 1-10
Inserting extra copies of the gene NR2B, which encodes the NMDA receptor, leads to improved memory and also prevents onset of Alzheimerâs Disease. Two chemical signals are needed to trigger this nerve cell receptor, which means that it plays a key role in forming associations. For instance, if you touch a flame, the visual signal and pain signal arrive to the brain at roughly the same time, activating NMDA receptors and creating a memory. Healthy adults were given extra copies of the gene and these were rigged so that genesâ activity would increase over time as the adults aged. Earlier studies had revealed that in young animals, NMDA receptors are activated even by signals that arrive somewhat far apart, facilitating learning. As an animal ages, though, the signals must travel more in step to trip NMDA receptors and cement memories. Adults treated with the NR2B gene had significant improvements in assessments directly related to the training tasks and significant generalization of improvements to nonrelated standardized neuropsychological measures of memory (effect size of 0.25). In addition, adults treated with the genes showed lower levels of onset of Alzheimerâs Disease compared with matched controls.

For discussion

Are these interventions therapy or enhancement? (Is age-related loss of memory a disease?)

Are there morally significant differences between the methods (cognitive training versus genetic

modification)?

What are the potential harms and benefits from using these interventions?

What are your views on the moral permissibility of the interventions?

How would your responses change if the interventions were for increasing muscle mass and performance in elite athletes?

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Biology 3602A/B Lecture Notes - Lecture 14: Heart Valve, Pulmonary Valve, Sinoatrial Node

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