Trees take in carbon dioxide to build their tissues , which releases oxygen for us in the process.
<span>Rhabdomyolysis constitutes a common cause of acute renal failure and presents paramount interest. A large variety of causes with different pathogenetic mechanisms can involve skeletal muscles resulting in rhabdomyolysis with or without acute renal failure. Crush syndrome, one of the most common causes of rhabdomyolysis presents increased clinical interest, particularly in areas often involved by earthquakes, such as Greece and Turkey. Drug abusers are another sensitive group of young patients prone to rhabdomyolysis, which attracts the clinical interest of a variety of medical specialties.
We herein review the evidence extracted from updated literature concerning the data related to pathogenetic mechanisms and pathophysiology as well as the management of this interesting syndrome.
Keywords: Rhabdomyolysis, acute renal failure, myoglobin, crush syndrome
The first case of the crush syndrome, which constitutes one of the main causes of rhabdomyolysis, was reported in Sicily in 1908, after an earthquake1,2. In 1930, in the Baltic area, an epidemic of myoglobinuria was observed due to consumption of contaminated fish. Interest in rhabdomyolysis and crash syndrome was stimulated during the World War II particularly after the bombing in London, where the victims developed acute renal failure and myoglobinuria1.
Rhabdomyolysis is a rupture (lysis) of skeletal muscles due to drugs, toxins, inherited disorders, infections, trauma and compression3. Lysis of muscle cells releases toxic intracellular components in the systemic circulation which leads to electrolyte disturbances, hypovolemia, metabolic acidocis, coagulation defects and acute renal failure due to myoglobin4.
The skeletal muscle consists of cylindrical myofibrils, which contain variant structural and contraction proteins. Actin and myosin, arranged in thin and thick filaments respectively, form the repeated functional units of contraction, the sarcomeres5. The sarcoplasmic reticulum constitutes an important cellular calcium storage. It is structurally connected to the t-tubules, that are formed by invaginations of the muscle cell plasma membrane, the sarcelemma, around every fibril (Figure 1). After the sarcelemma depolarization, the stimulation arrives, through the t-tubules junctions, at the sarcoplasmic reticulum, inducing the calcium ions release and triggering muscle contraction6.</span>
Clinical death is the medical term for cessation of blood circulation and breathing, the two necessary criteria to sustain human and many other organisms' lives.
It occurs when the heart stops beating in a regular rhythm, a condition called cardiac arrest.
Brain injuries start to accumulate almost immediately after Clinical Death.
Full recovery of the brain after more than 3 minutes of clinical death at normal body temperature is rare.
Usually brain damage or later brain death results after longer intervals of clinical death even if the heart is restarted and blood circulation is successfully restored.
Although loss of function is almost immediate, there is no specific duration of clinical death at which the non-functioning brain clearly dies.
The most vulnerable cells in the brain, CA1 neurons of the hippocampus, are fatally injured by as little as 10 minutes without oxygen.
However, the injured cells do not actually die until hours after resuscitation.
Brain failure after clinical death is now known to be due to a complex series of processes called Reperfusion Iinjury that occur after blood circulation has been restored, especially processes that interfere with blood circulation during the recovery period.
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~Alkka♥
Answer:
species richness is the number of species in an ecosystem
