Of rigor mortis

A decrease in the concentration of ATP in the sarcoplasm (eg, by excessive usage during the cycle of con-traction-relaxation or by diminished formation, such as might occur in ischemia) has two major effects (1) The Ca ATPase (Ca + pump) in the sarcoplasmic reticulum ceases to maintain the low concentration of Ca + in the sarcoplasm. Thus, the Interaction of the myosin heads with F-actin is promoted. (2) The ATP-depen-dent detachment of myosin heads from F-actin cannot occur, and rigidity (contracmre) sets in. The condition of rigor mortis, following death, is an extension of these events. 

Postmortem findings include dark-tarry blood discharge from body orifices, absence of rigor mortis, hemorrhage of the mucous membranes, bloating, and rapid decomposition of the carcass. 

Varetto, L. and Curto, O. (2005). Long persistence of rigor mortis at constant low temperature. Forensic Sci. Int. 147, 31-34. 

Before the influence of freezing was studied, it was necessary to determine whether postmortem (p.m.) storage of muscle at temperatures above freezing (+4°C) influenced the subcellular distribution of the enzymes investigated. As is well known, storage of muscle p.m. results in drastic changes such as development of rigor mortis and a decline in pH from above 7 to about 5.5. 

Based on model studies with bovine spleen catheptic enzymes, West et al. (96) have suggested that cathepsins may be involved in the onset of rigor mortis by degrading the sarcoplasmic reticulum resulting in decreased binding capacity for Ca2 The free Ca2+ would then be free to initiate rigor mortis. 

The stiffness of rigor mortis is evidently due to the disappearance of ATP (see Bate-Smith and Bendall, 1947, 1949), and whenever the rapid phase of ATP breakdown (which is the cause of the disappearance of ATP) takes place in conditions (pH > 6) under which actomyosin is capable of contracting at all, rigor is accompanied by contracture. 

A. Acute exposure causes irritation of the skin, eyes, and upper respiratory tract. Systemic absorption may cause headache, vomiting, weakness, and lethargy. Profound sweating, hyperthermia, tachycardia, tachypnea, convulsions, and coma are associated with severe or fatal poisonings. Pulmonary edema may occur. Death is usually caused by cardiovascular collapse or hyperthermia. After death an extremely rapid onset of rigor mortis is frequently reported. Dinitrophenol may also induce methemoglobinemia, liver and kidney failure, and yellow-stained skin. 

Bate-Smith, E. C. 1948. The physiology and chemistry of rigor mortis, with special reference to the aging of beef. Advances in Food Research 1, 1. 

E. C. Bate-Siuth, The Physiology and Chemistry of Rigor Mortis, with Special Reference to the Aging of Beef. 1... 

The onset of rigor mortis occurs in beef muscle within 10-24 h in pork, 4-18 h and in chicken, 2-4 h. 

Lesions include an empty stomach, cyanosis, rapid onset of rigor mortis, and a flaccid, pale heart. 

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