Disease relevance of Rigor Mortis

• The evolution of rigor mortis was studied in cases of nitrogen asphyxia, drowning and strangulation, as well as in fatal intoxications due to strychnine, carbon monoxide and curariform drugs, using a modified method of measurement [1].
• Reconsideration of the sequence of rigor mortis through postmortem changes in adenosine nucleotides and lactic acid in different rat muscles [2].
• Tolcapone (400 mg/kg/day or 600 mg/kg/day) increased mortality after only one week treatment and induced signs of toxicity such as a rise in body temperature, stimulation of respiration and rapid onset of rigor mortis after death [3].
• Symptoms of hypothermia begin subtly with fatigue and loss of concentration, but progress to stupor, coma, and resemble rigor mortis [4].

High impact information on Rigor Mortis

• Mossy cells in epilepsy: rigor mortis or vigor mortis [5]?
• The mean luminal diameter of the fifth intercostal arteries varied from 1.4 +/- 0.3 mm at the origin to 0.9 +/- 0.2 mm at 30 cm (30% to 40% decrease in diameter due to the flaccid state and rigor mortis) [6].
• The degree of development of rigor mortis in the carcases of slaughter pigs was assessed subjectively on a three-point scale 35 minutes after they were exsanguinated, and related to the levels of cortisol, lactate and creatine kinase in blood collected at exsanguination [7].
• Elevated plasma corticosterone concentrations influence the onset of rigor mortis and meat color in broilers [8].
• Rapid post-mortem metabolism concomitant with the early onset of rigor mortis can lead to the development of pale, soft, and exudative (PSE) meat [9].

Chemical compound and disease context of Rigor Mortis

• Rigor mortis developed in all hearts after 90 minutes incubation or within 20 minutes of perfusing the heart with 50 ml of 5 mM iodoacetate in Hanks solution [10].
• Gastrocnemius muscles taken from decapitated mice at various intervals after death and from mice killed by 2,4-dinitrophenol or mono-iodoacetic acid injection to induce rigor mortis soon after death, were observed by electron microscopy [11].
• The importance of the muscle lactate level is connected to the glucose entry into the muscle cell and the rigor mortis [12].
• 4. The high mol. wt proteins titin and nebulin were highly sensitive to proteolysis during the rigor mortis period [13].

Anatomical context of Rigor Mortis

• The alterations in adenosine nucleotides and lactic acid in striated muscles of rats during Rigor mortis following death with drowning or cervical dislocation [14].
• During a subsequent further decline in ATP, the mean deformability of myocardium fell from 30 to 12% indicating the development of rigor mortis [15].

Gene context of Rigor Mortis

• The myosin content of the extracts decreased during the rigor mortis period at storage temperatures greater than 8 degrees C. 6. alpha-Actinin was very resistant to proteolysis, but could be released from Z-disc structure during post-mortem aging [13].
• The post-mortem ventricular volume is influenced to a very great degree by rigor mortis [16].
• The carcasses of them showed early rigor mortis and the higher final pH above 6 [17].
• We conclude that proteolysis of AMP deaminase is the basis of the large ammonia accumulation that occurs in skeletal muscle subjected to strong tetanic contraction or passing into rigor mortis [18].

References