The Effect Of Various Drugs On The Heart Rate Of Daphnia Magna

Like most sulphonamides, dapsone can lead to a hypersensitivity reaction that is likely cell mediated (type IV hypersensitivity reaction). T-cells are indicated because of the time delay from beginning therapy to the time of disease, approximately 4 weeks. The mechanism of T-cell response to dapsone is unknown and three mechanisms are postulated. According to the hapten model, a small inert molecule could illicit an immune response by first covalently binding directly to an intra or extra cellular protein. Where the native protein would likely be recognized as “self” and be ignored by the immune system the protein adduct could stimulate a T-cell response. This is the mechanism of the delayed hypersensitivity reactions

Acclaimed website WebMD notes that using drugs can accelerate your heart rate. You may have noticed your heart beating faster when you are high. Your heart works harder because drugs increase circulation. Therefore, they have a negative impact if you have a heart condition.

Digitalis’s mechanism of action relies on the drugs inhibition of the sodium/potassium pump (3Na+-out/2K+-in) in myocardial cells. Inhibition of the pump results in an increase in contractility of the heart via an influx of calcium ions as a direct result of a high intracellular sodium concentration and the subsequent reduction of the concentration gradient of sodium driving the sodium-calcium exchanger, which normally results in a net positive increase due to the efflux of (1Ca2+-out/3Na+-in). The reduced activity of the exchanger results in a buildup of intracellular calcium, which is taken up by the sarcoplasmic reticulum ’s calcium pump aided by the protein phospholamban. An increase in calcium-induced calcium release stored in sarcoplasmic reticulum increases the amount of calcium binding to troponin, thereby increasing cardiac

In this experiment, the purpose was to identify the effect of sedatives and stimulants on the circulatory system on the ghost shrimp and the black worm. We used caffeine as our stimulant and ethanol as our sedative. The shrimp was placed on a wet petri dish, where it was covered. After letting the shrimp rest for a few minutes, we placed it under the lowest light of a dissecting microscope. Then we located the heart, counted the number of beats in 10 seconds and multiplied it by 6 to acquire the beats-per-minute. In the next trial we dropped 0.5 mL of .0005 M caffeinated solution on the shrimp and waited 2 minutes before we measured the bpm. After the bpm was recorded, the shrimp was washed with spring water. The same procedure was performed

For this experiment students sought to demonstrate how cardiac function was regulated. Students made hypothesizes for clamping, drug injections, and stimulation with effects of arterial pressure and heart rate in mind. Students performed various tests in order to fully obtain results for this experiment which included the injection of drugs and their effects, using and removing a clamp and that effect, and finally used an electrical simulation machine in order to stimulate nerves to test that effect. The main hypothesizes depended on each treatment and each prediction was made specifically to fit a certain set of conditions. These various tests were performed to obtain a better understanding of cardiac function and its physiological aspects. Understanding cardiac function is not only very important to science but very important to the

The sympathetic noradrenergic system plays major roles in tonic and reflexive changes in cardiovascular tone. Adrenaline is a major determinant of responses to metabolic or global challenges to homeostasis. Adrenaline responses to stressors are more closely linked to responses of the hypothalamic‐pituitary‐adrenocortical system than of the sympathetic nervous system. The sympathetic noradrenergic system is active even when the individual is at rest and maintains tonic levels of cardiovascular performance. Adreno receptors in the membranes of effector cells determine the physiological and metabolic effects of catecholamine. Beta‐adrenoceptors mediate stimulatory effects of catecholamine on the rate and force of the heartbeat; stimulation of

“Strong vagal stimulation can decrease the strength of the heart muscle contraction by 20 to 30 percent” (Hall, 2011 p.120). In a study done on canines under anesthesia, sympathetic stimulation was inhibited when concurrent vagal activity was present and cardiovascular effects seen included heart rate reduction by inhibition of the sympathetic nervous system and by direct hyperpolarization of sinus nodal cells. Vagal parasympathetic activation was shown to predominate over sympathetic activation (Levy & Zieske, 1969). This response is known as “accentuated antagonism” (Olshansky et al. 2008). In the Contemporary Review of Cardiovascular Medicine and Parasympathetic Nervous System and Heart Failure published by Dr. Brian Olshansky and his colleagues at the University of Iowa, epidemiological data is examined that “indicates that the resting heart rate, a measure of vagus nerve function, predicts mortality” (Olshansky et

Given the example that a patient just received an overdose of Ca +2, this will cause the heart rate to go up dramatically. If sodium ions are introduced, this will help with the influx of calcium ions by balancing everything. Certain drugs that act as calcium channel blockers are extremely useful since they reduce electrical conduction within the heart and inhibit the force of muscle cell

For frogs, the mean mass specific heart rate experienced higher rates when exposed to Epinephrine (df=18 t-stat=-13.28; p<0.01) (Figure 1). The frog’s contraction strength mean experienced no increase when exposed to Epinephrine (df=18 t-stat=0.11; p=0.917) (Figure 1). Under Nicotine, the frog’s

Hearts were treated with the CaM kinase inhibitor KN-93 or the inactive analog KN-92 (0.5 μM) for 10 min before clofilium exposure. Early afterdepolarizations (EADs) were largely suppressed by KN-93 compared to KN-92. There were little differences in parameters favoring EADs such as monophasic action potential duration or heart rate in KN-93- or KN-92-treated hearts. CaM kinase activity in situ increased 37% in hearts with EADs compared to hearts without EADs. This increase in CaM kinase activity was prevented by pretreatment with KN-93.

The cardiovascular system is the body’s way of circulating blood and the essential biomolecules that make living possible. Blood is pumped throughout the body by the heart, the heart receives oxygenated blood from the lungs via the pulmonary vein and distributes it using the various arteries and capillaries (Farley et al.). A main constituent for the cardiovascular system and a heavily relied upon factor for measuring the heart’s work is heart rate. Heart rate is a numerical value that quantifies the number of times the heart contracts which means opening and closing the valves that are responsible for the blood movement (Mariaconsuelo et al.). Contractions in terms of heart rate are referred to as “beats” thus the numerical value is beats per minute (BPM). Heart rate can be affected by numerous factors such as physical stress, chemicals introduced into the bloodstream through the environment, as well as naturally produced chemical compounds produced by the body in response to a need. To determine what exactly happens inside the body when these numerous factors come into play we set up various experiments that will give us a measurable outcome.

Nicotine was dissolved in methanol and cotinine was dissolved in 100% alcohol to make standard solutions (0.1 M). The standard solutions were diluted in sterile phosphate-buffer saline to the anticipated solution. For the contraction and relaxation test, both carbachol and arterenol were dissolved in deionized water and fresh solutions were made for every set of experiment. Porcine ages were 6-month-old male and female pigs weighing about 110 kg from a local abattoir. Hearts were taken from porcines and were

Background and objectives: The Atenolol (AT) due to its effect of reduction in cardiac output (CO) could be expected to decrease the clearance of drugs. The objective was to know the effect of reduced CO induced by AT on its own excretion parameters.

The focus of this essay is on targets and receptors in the treatment of conditions of the cardiovascular system. In the heart we have Adrenergic receptors. These are a type of g protein couple receptors that are targets of the catecholamines .Catecholamines are hormones produced by the adrenal glands the main ones being Dopamine, Epinephrine(adrenaline) and norepinephrine .The types of adrenergic receptors are alpha,beta 1 and beta 2.Alpha receptors are located on the arteries. When they are stimulated by epinephrine or norepinephrine , the arteries constrict. This has the effect of increasing blood pressure and the blood flow returning to the heart.

Other substances such as acetylcholine is released to decrease the rate at which a heart beats (Biopac systems Inc., 2014). Other substances such as epinephrine are used to increase the heart rate drastically if the organism is frightened making it more aware and active. Caffeine also increases heart rates as it stimulates the central nervous system (Biopac systems Inc., 2014).