<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>
ingestion, propulsion, mechanical or physical digestion, chemical digestion, absorption, and defecation. The first of these processes, ingestion, refers to the entry of food into the alimentary canal through the mouth.
<h2>Functions of plasmodesmata</h2>
Explanation:
- They allow the movement of cells to cells for cytoplasmic connection between different cells
- Plant cells, encompassed as they are by cell dividers, don't get in touch with each other through wide stretches of plasma film the manner in which creature cells can. Be that as it may, they do have particular intersections called plasmodesmata (solitary, plasmodesma), places where a gap is punched in the phone divider to permit direct cytoplasmic trade between two cells.
- Plasmodesmata are fixed with plasma film that is consistent with the layers of the two cells. Each plasmodesma has a string of cytoplasm stretching out through it, containing a much more slender string of endoplasmic reticulum.
- Particles beneath a specific size (the size rejection limit) move unreservedly through the plasmodesmal channel by latent dissemination. The size avoidance limit changes among plants, and even among cell types inside a plant. Plasmodesmata may specifically enlarge (extend) to permit the section of certain huge atoms, for example, proteins, in spite of the fact that this procedure is inadequately comprehended.
Enzyme. An enzyme is a biological catalyst and is almost always a protein. It speeds up the rate of a specific chemical reaction in the cell.
