Cytoplasm Changes

The second experiment sought to determine whether calcium entry is via L-type calcium channels, therefore, verapamil (10-5 M) was used to block these channels. The tissue was then stimulated using 0.2ml of Ach (10-5 M) and K+-depolarising solution.

First he had tachycardia which is when the heart rate is abnormally high. Because of the tachycardia, there is less time for the heart to pump blood to the other parts of the body. Since not enough blood is going to the heart, body and the brain, he lost consciousness.

Because the PCO2 levels are too high the body is not getting the adequate amount of oxygen. This means the oxygen-carrying hemoglobin is not working properly do to the excessive amounts carbon dioxide causing respiratory acidosis.

MH alters the calcium channel in the sarcoplasmic reticulum (SR) and this allows large quantity of calcium to be released from the SR creating hyper-action in skeletal muscle; this reaction increases oxygen consumption and increased heat production that ultimately leads to a hypermetabolic state after the inhaled Halothane has triggered the condition (Knies). The continuous elevation of calcium also causes excessive stimulation of anaerobic glycolytic metabolism. This creates respiratory and metabolic acidosis, rigidity (muscle contractions), and hyperkalemia (elevated potassium) and can ultimately lead to death

Hypoxaemia can result when there is inequality in alveolar ventilation and pulmonary perfusion (V/Q mismatch). V/Q mismatch is the most common cause of hypoxia in critically ill patients. It is caused by intrapulmonary shunting of blood resulting from airspace filling or collapse. Findings include dyspnea and tachypnea. Diagnosis is by ABGs and chest x-ray. Treatment usually requires mechanical ventilation.

* The type of proteins in the cell membrane that was involved in homeostatic imbalance of his heart cells were ATP. There was no ATP, so it affected the pumps in the membrane. The calcium levels rose, and it caused proteases to spill into the interior of the cell, attacking the cytoskeleton. This caused the lysosome enzymes to digest the plasma membranes and membranes of the organelles.

An increase in calcium inside muscle cells activates processes that generate heat and production of excess acid, leading to a continual increase in body temperature and then acidosis.

Bath application of BMS-191011 at a concentration of 20 μM strongly reduced the calcium transients. This effect was associated with bursts of bAPs (100 Hz) recorded from Fmr1−/y dendrites without affecting those recorded from wild-type dendrites. This treatment decreased dendritic calcium transients of Fmr1−/y neurons to baseline levels of wild-type neurons [3]. In normoxia, BMS-191011 significantly induced cell death. This effect was indicted by the increases in propidium iodide (PI) uptake by 9.4 ± 2.4 and 16.8 ± 2.1% at 12 and 24 h treatments, respectively. At 12 h and then 24 h, the cellular [ATP] was decreased to 83.4 ± 3.1 and further to 72.3 ± 2.8%. During hypoxia, these effects were increased by ~2-fold in all time points and measurements. PI uptake was increased to 15.1 ± 1.8 at 12 h and then 40.7 ± 1.7% at 24 h. Cellular [ATP] was decreased to 77.8 ± 1.9 at 12 h and then to 43.3 ± 3.4% at 24 h [4].

For example, cellular swelling occurs due to cellular hypoxia, which damages the sodium-potassium membrane pump; as well as fatty change it can impair cellular function and damage the cell ability of adequately metabolize fat. Both situations are reversible when the causes are eliminated. In contrast, irreversible cell injury is the cell death with continuing damage, the injury becomes irreversible, which the cell cannot recover and dies. There are two types of cell death necrosis and apoptosis. When damage to membranes is severe, enzymes leak out of lysosomes, enter the cytoplasm, and digest the cell, resulting in necrosis ( McCance & Huether, 2014). Necrosis is the major pathway of cell death in many commonly encountered injuries, for example resulting from ischemia, exposure to toxins, various infections, and

1) The primary causation of this system results from a property of hemoglobin known as the Bohr effect. This property of hemoglobin causes the protein to lose its affinity, or rather more readily give up, oxygen in the presence of a lower pH level (more acidic) in the surrounding fluid. Due to the fact that active tissues increase their basal metabolic rate, they produce more CO2 than do resting tissue during cellular respiration. This CO2 escapes the higher concentration gradient of the interior of the cell into the lower concentration outside of the cell. Upon escaping the interior of the cell, the CO2 combines with the water present in the blood plasma creating carbonic acid (H2CO3).

In most tissues of the body, ATP production primarily occurs through mitochondrial oxidative phosphorylation of reduced intermediates, which are in turn derived from substrates such as glucose and fatty acids. In order to maintain ATP homeostasis, and cellular function, the mitochondria requires a constant supply of fuels and oxygen. In many individuals at altitude, tissue oxygen levels fall and the cell must meet this hypoxic challenge to maintain energetic and limit oxidative stress. Varying on protocols, the body can adapt to the lack of oxygen which can be increasing the mass of red blood cells and haemoglobin or changes in muscle metabolism. Depending very much on the protocols used, the body may adapt to the relative lack of oxygen in one

Cerebrovascular Accident or stroke as most might recognize it, is a condition in which brain tissues does not get enough blood flow or oxygen. Cerebrovascular Accident has been around for quite some time. It dates back about thousands of years ago and was discovered by a man named Hippocrates. Hippocrates was a Greek physician who lived during the Classical Era of Greece. During this time little was known of the brains anatomy and its functions. For the Greeks it was called apoplexy. Apoplexy causes was a mystery until a man by the name Jacob Wepfer, a Swedish pathologist, postulated that apoplexy was caused because of excessive bleeding in the

Cellular hypoxemia is resultant of inadequate amounts of oxygen being delivered to the cells or the inability of the cells to use the oxygen. This can be caused by ischemia, respiratory disease, vasoconstriction, vascular obstruction, edema, or anemia. Hypoxemia may result in power failure in the cell resulting in cell death. As the oxygen tension in the cell increases, anaerobic metabolism begins building up lactic acid and reducing pH levels causing biochemical reactions, chromatin clumping, and cell shrinkage. The leakage of intracellular enzymes into extracellular fluid is an indicator of cell injury or death (Grossman & Mattson Porth, 2014). This is evident with the edema Maria is

This induced state of hypothermia is essential to protect tissue from ischemia and reperfusion injury. If you recall from earlier, ischemia is a deficiency of blood supply due to vasoconstriction. Reperfusion injury is the damage to tissue caused when blood supply returns to tissue after a period of ischemia. Inducing hypothermia stops the process of ischemia from affecting the other tissues in the body. This allows for the regeneration of ATP in the body when blood flow is restored. “Induced hypothermia generates a state of metabolic depression that preserves cellular energy when oxygen and substrates are limited (Alam, 2009)”. Hypothermia constricts the activity of the sodium-potassium adenosine triphosphatase (Na+/K+ ATPase pump) pump. The inactivation of this pump conserves ATP in the cell, suppressing the need for oxygen (Alam,2009).

Various contributing mechanisms have been identified, including the negative inotropic effects of different circulating factors, especially cytokines (TNFα, IL-1β and IL-6), lysozyme c and endothelin-1, disturbances of intracellular calcium trafficking within cardiac myocytes, alterations of myocardial microvascular blood flow, mitochondrial abnormalities and autonomic dysfunction [71-73]. There are various effects which may be responsible for the toxic actions of peroxynitrite on the heart, including myocardial cell death, either by caspase-3-dependent apoptosis [74], or PARP mediated necrosis [75]. A direct correlation linking the degree of myocardial PARP activation and the severity of cardiac functional alterations has been established in humans with septic shock [76]. Myocardial contractility can also be impaired by peroxynitrite due to disturbance in regulatory mechanism of intracellular calcium through the inactivation of SERCA2A [77], by altering different myofibrillar proteins including actin, myosin [78] and alpha-actinin [79], by interrupting myofibrillar energetics through inactivation of the myofibrillar isoform of creatine kinase [80] and by activating matrix metalloproteinases [81], which promotes contractile failure by cleaving key sarcomeric proteins including troponin and myosin light chain