BL2016 Tissue to Organisms Physiology & Pharmacology Assignment Sample
Here’s the best sample of BL2016 Tissue to Organisms Physiology & Pharmacology Assignment.
Introduction
Pharmacology is the study of how drugs interact with our bodies. Knowing where medications come from and how they’re used in medicine are essential. Tissue-organ baths, organ perfusion devices, and Ussing chambers are utilised in in vitro pharmacological research.
Discussion
Atrial and ventricular myocytes, as well as the fast-conducting Purkinje system in the ventricles, all exhibit non-nodal action potentials, also known as “rapid response” action potentials. Here, the action potentials are demonstrated to exhibit a real resting potential as well as a rapid depolarization and a protracted plateau phase. In the sinoatrial and atrioventricular nodes, “nodal action potentials,” or “slow response action potentials,” are the most common type of action potential. Because of their automaticity, or pacemaker activity, these action potentials depolarize of their own own. Unlike non-nodal, quick reaction action potentials, their depolarization phase is longer and they have a shorter action potential duration (Diekman and Wei, 2021). Certain ion channels in non-nodal tissue are blocked by antiarrhythmic medications, altering the fast reaction action potentials there. Drugs that inhibit the rapid sodium channels in the brain, such as quinidine, slow the rate of depolarization. A drug called verapamil affects the action potential’s plateau phase, while diltiazem affects the rising phase.
Depolarization and repolarization of many cells in the body can be caused by either external processes (such as motor nerve stimulation of skeletal muscle or cell-to-cell depolarization in the heart) or internal, spontaneous causes (e.g., cardiac pacemaker cells). When it comes to cardiac action potentials, the existence or absence of spontaneous pacemaker activity as well as the rate at which they depolarize set the stage for three main categories. Typical of atrial and ventricular myocytes are non-pacemaker action potentials, or “quick response” action potentials, due of the rapid depolarization of these myocytes. As a result of the slower rate of depolarization, pacemaker cells produce “slow reaction” action potentials that are also known as spontaneous action potentials. The heart’s sinoatrial and atrioventricular nodes often include them. Unlike regular atrial and ventricular myocytes (rapid response, non-pacemaker cells), the ventricle’s His-Purkinje system’s specialised conducting cells display spontaneous depolarization, making them a third form of action potential (Hu et al., 2020).
The heart’s contraction is triggered by depolarizing it every beat. This electrical activity is transported throughout the body and may be seen on the skin. The ECG is based on this idea. ECG machines use electrodes on the skin to capture and show this activity. In order to do an ECG, the patient’s body is fitted with 10 electrical cables: one for each limb and six for the chest. The ECG’s distinct waves depict the atria and ventricle’s depolarization and repolarization sequence. When atrial depolarization begins, this gap shows the time it takes for ventricular depolarization to follow. Ventricular depolarization is depicted by the QRS complex. The interval between QRS complexes can be used to compute the ventricular rate (Tse et al., 2021).
Conclusion
There are structural and functional abnormalities at the molecular, cellular, and tissue and organism levels that cause cardiac arrhythmias. Because of these flaws, the membrane potential becomes unstable, resulting in aberrant excitations and impulse transmission.
Reference
Hu, N., Xu, D., Fang, J., Li, H., Mo, J., Zhou, M., Li, B., Chen, H.J., Zhang, T., Feng, J. and Hang, T., 2020. Intracellular recording of cardiomyocyte action potentials by nanobranched microelectrode array. Biosensors and Bioelectronics, 169, p.112588.
Mahapatra, C. and Manchanda, R., 2020. Modelling VAS Deferens Smooth Muscle Electrophysiology: Role of Ion Channels in Generating Electrical Activity. Biophysical Journal, 118(3), pp.259a-260a.
Tse, G., Li, K.H.C., Cheung, C.K.Y., Letsas, K.P., Bhardwaj, A., Sawant, A.C., Liu, T., Yan, G.X., Zhang, H., Jeevaratnam, K. and Sayed, N., 2021. Arrhythmogenic mechanisms in hypokalaemia: Insights from pre-clinical models. Frontiers in Cardiovascular Medicine, 8.
Uzelac, I., Ji, Y.C., Hornung, D., Schröder-Scheteling, J., Luther, S., Gray, R.A., Cherry, E.M. and Fenton, F.H., 2017. Simultaneous quantification of spatially discordant alternans in voltage and intracellular calcium in Langendorf-perfused rabbit hearts and inconsistencies with models of cardiac action potentials and ca transients. Frontiers in physiology, 8, p.819.
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