Analysis of Dr. Teppema and Dr. Dahan's Work

Dr. Teppema and Dr. Dahan illustrated through their experiment that Hypoxia often caused the denervation of carotid bodies. This means that the affected carotid bodies did not harbor the ability to release neurotransmitters. The denervation would lead to the loss of the ability to detect an action potential by the carotid bodies. This action potential, or rather a difference in the voltage between the membrane of the intracellular and extracellular environment is what would originally cause the reaction by the chemoreceptive cells. If the action potential persists or grows without a restoration of the potential back to a restoration potential, that would lead to the loss of regulation to an extreme. This would directly affect the working state of the Hypoxic Drive by further disabling it and its consistency in performance. This would play a rather large role in the secondary development of the Hypoxic Drive under the carbon dioxide chemoreceptor driven respiratory system.  The scientists, Dr. Teppema and Dr. Dahan in fact displayed the concept that peripheral chemoreceptors in rats and other organisms were agents of decline in Hypoxic Ventilatory response. They charted the relative Hypoxic Ventilatory response over time in controlled experiments and marked the marginal decline of the response. This contends to the idea that the Hypoxic Drive has a tendency to lose its clutch on regulation. This is a grand reason for carbon dioxide regulation to peak and since it is a favorable trait to organisms, it would ideally grow as a genotype.

 

The image above is actually a representation of action potentials that are crucial to the body and the levels at which they operate.

Results of Experiment 1 and Analysis

For further evidence, the two scientists raised rat offsprings in a 10% oxygen environment. Because oxygen sensing is done within protein and potassium channels in organisms as well, the scientists found out that there were signs of blunted and reduced hypoxic ventilatory response. The potassium channel sensors failed to recognize the Hypoxic conditions. (Teppema and Dahan 2010, p 686) This strongly suggests the innate viability of the Hypoxic Drive to function fully within organisms. It displays that through natural selection and acclimatization of organisms to the environment, the Hypoxic Drive is left undeveloped within organisms at first, allowing Carbon Dioxide sensation to be active from the start. This vastly helps “hatch the egg” to see the answer as to why the Hypoxic Drive is a secondary respiratory drive in humans. The experimental reports relay that the carotid bodies of rats contained the ability to open and close potassium channels. It is known that potassium serves to increase perfusion and also help the electrical network of organism’s bodies. (McCutcheon, p 340-341) Teppema and Dahan noted that the channels were inactive in an environment where there were low peripheral oxygen levels. The Hypoxic Drive did not regulate so the Potassium levels remained minimal. However, when there was interaction with carbon dioxide, the Potassium channels were able to transport potassium ions through the channels. This suggests that the Hypoxic Drive is not integrated well within the body contributing to the minimalized aid it provides to the body compared to carbon dioxide regulation.


Above is a sample picture of the primary potassium channels used to 
infuse and control cellular disposition and permeability to potassium ions.

How Were Experiments for Hypoxic Drive Results?

Teppema and Dahan conducted studies mainly on mammalian organisms such as rats and rabbits. In the experiment, the neonatal organisms were exposed to a regular amount of gasses in the air. The O₂ and CO₂ reactions that occurred within the organisms were noted. After such reactions continued for one to two weeks in the neonatal organisms, the organisms were subject to hypoxia. The hypoxic ventilatory response that was initiated by the carotid bodies was blunted according to the scientists. This is important because it is the first sign of how the natural environment has created organisms accustomed to carbon dioxide control and minimal oxygen regulation. If the oxygen controls were blunted, then that means the Hypoxic Drive should be interpreted as a drive that is not meant to be put into effect till later in the maturation period of organisms.



Above is a picture of one of the mechanical devices that were used
to control the intake and output of ventilation for the organic 
substances and organisms upon which tests were run such as rats and 
rabbits. The rabbits required bigger chambers. The machine has a tight
air lock so as to maintain a very thorough experimental unit and system
that is well isolated.

Introduction to Experimenters and Results of Tests on Hypoxic Drive

Luc J Teppema and Albert Dahan (Teppema and Dahan 2010), two major physiological scientists conducted a study on the Hypoxic Drive and ventilatory response. The importance of their study is that the study delineates the effects of the Hypoxic Drive and chemoreceptors and also how they function in reality. The point in the making is that there are genetic conditions and also physiological conditions and naturally selective reasons as to why the Hypoxic Drive was dropped into a secondary slot. The experiments described will allow for the research question to be seen through an experimental point of view. Though experimentation was not used for this extended essay, scientists who have legitimately performed experiments in regards to the Hypoxic Drive and their conclusive data will be referenced here.

The three diagrams above show some of the experimental results that Teppema and Dahan recovered from their studies. In the diagrams, they map the points at which hypoxia is induced and how it affects chemical substance concentrations in experimental bodies within that period of time in minutes.

One thing to notice is that there are no peripheral oxygen chemoreceptors in framework of chemoreception that pertains to the medulla oblongata. Thus, there would not be a direct route for neurotransmission of peripheral oxygen chemoreceptors as do the carbon dioxide chemoreceptors located by the medulla oblongata which is connected to the brain. Overall, the chemoreceptors are the integral components that relate to both respiratory systems. Knowledge of how chemoreceptors function and work with action potentials, their processing, monitoring, limitations, and also the points at which they activate reflexes and respiratory neurotransmissions allows for a three dimensional view to be established as to how the body uses the two respiratory drives. Chemoreceptors are the materials that delegate the power of the Hypoxic Drive and how effective it is.


Above is a picture of the way neurotransmission is induced by blood CO2 levels. 

Carbon Dioxide Regulation by Normal Respiration

Going back to the carbon dioxide regulation, the Medulla Oblongata, a sector of the brain that controls autonomous reactions in the body, is responsible for monitoring the carbon dioxide levels and pressure. Once the medulla oblongata sees retention of carbon dioxide past normal pressures, the medulla oblongata activates respiratory reflex loops. This will in turn lead to inspiration to restore the balance or homeostatic conditions of the arterial blood gasses. The chemoreceptors that are controlled by the Medulla oblongata are indeed Carbon dioxide chemoreceptors. It is generally stated that since the medulla oblongata is bathed in carbon dioxide, it is able to use the carbon dioxide chemoreceptors within that specific area to easily monitor the transitory carbon dioxide levels. The medulla oblongata tracks the gas levels in order to make sure that acidity will be controlled. Acidity in the body is important because of the sole reason that the acids and bases in the body retain the ability to control all metabolic activities in the body. (A.C.F.A.S.P. 2009, p 2)

Note that the information here pertains to the normal Carbon Dioxide regulation and not through Chemoreception of peripheral chemoreceptors. There is a big difference as there is a Medulla Oblongata for normal CO2 regulation

Here is a picture of the Human upper body. The Medulla Oblongata is just under the brain and is where the regulation occurs with our primary carbon dioxide regulatory system( respiratory system).

Carotid Body Function and Unique Characteristics

Once the chemoreceptors pick up the trace of O₂ deprivation, they release neurotransmitters. These neurotransmitters in turn set off a chain of reactions that cause the body to release stored ATP and AMPK that will allow for the body to restore functions. (Wyatt, Mustard, and others, p 282) In essence, ATP and AMPK are the compounds in our body that are essential to body functions and processes that occur throughout every microcell of our body. (Khakh and Burnstock) The carotid body sensing is significantly different from normally used Carbon dioxide chemoreceptors. Carbon dioxide chemoreceptors are located in brain stem, coronary arteries and in carotid bodies as well. However, the major difference between the carbon dioxide chemoreceptors and the oxygen chemoreceptors is that the carbon dioxide chemoreceptors react to changes on a far more optimized level in the sense that they induce major alveolar ventilation with sensation of extraneous levels of carbon dioxide within the body. (Dean and Nattie 2010) The point in the making is that oxygen chemoreceptors can pick up the slightest drops; however, they do not introduce or rather initialize or catalyze a reaction until the oxygen pressure drops below an approximated 60 torr. The problem with an oxygen pressure below 60 torr is that the pressure is dubbed as Hypercapnic respiratory failure which is detrimental to the cellular functions of the body and the brain itself.




Above is a picture of AMPK and its uses within the body. The main elemental nature of AMPK is that it provides the power for protein synthesis which esentially drives the cellular functions of the body.