[Postmortem changes in serum potassium and sodium levels of persons who died of combined injuries of the head, trunk and limbs].
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The dielectric properties of the bovine brain grey and white matter in the frequency range from 20 kHz to 100 MHz were measured at different times following animal death. Changes in the dielectric parameters versus time are interpreted in terms of the reduction of the cell volume fraction that results from either cell disintegration or cell size reduction. Good agreement between the computer fitted parameters and the values calculated from the Maxwell-Wagner model of the static dielectric constants was found. At frequencies above 1 MHz the changes of the dielectric properties are less pronounced, confirming earlier observations made by other investigators for different species.
Four monoamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA), were determined in the cerebrospinal fluid (CSF) of cadavers, whose causes of death had been suicidal hanging (SH) or ischemic heart failure (IHF). The concentration of DOPAC increased in parallel with the increment of the postmortem interval (PMI) (r = 0.626), whereas the concentrations of HVA, MHPG and 5-HIAA did not. The correlation coefficient was further increased by considering each cause of death separately: i.e., SH, r = 0.761; IHF, r = 0.705. These findings suggest the possible usefulness of the DOPAC level in CSF for estimating PMI.
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The possibility that gamma-hydroxybutyrate (GHB), a metabolite of gamma-aminobutyric acid (GABA), may play a role in the CNS has recently come to attention. We describe here a sensitive and specific mass fragmentographic technique that allows the measurement of picomole amounts of GHB in single rat brain areas. Moreover, we show that GHB can accumulate postmortem, an effect that is blocked by the use of microwave irradiation to kill the animals. To understand further the relationship between GABA and GHB formation, we treated rats with drugs known to interfere with GABA metabolism at different levels and concomitantly measured GABA and GHB in cerebral cortex and cerebellum. Isoniazide, which blocks the formation of GABA, also decreases GHB. Blockers of the catabolism of GABA, such as aminooxyacetic acid and gamma-acetylenic GABA, increase GABA levels and decrease those of GHB. Sodium dipropylacetate increases both GABA and GHB, supporting the hypothesis that this effective antiepileptic drug also blocks in vivo the enzyme that converts succinic semialdehyde to succinic acid.
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Postmortem (pm) manipulations of brain tissue of decapitated mice produced a maximum decline in 5-HT and a maximum rise in 5-HIAA of 20 and 40%, respectively. The pm treatments included freezing and thawing, mincing, and leaving over. Microwave irradiation or pretreatment of the animals with the enzymatic inhibitors NSD 1015 or pargyline suppressed the pm effects. The possible role of pm effects in the initial accumulation of 5-HT and decline of 5-HIAA in the brain following administration of pargyline was studied. Out data suggest that, when MAO inhibitors are used, 5-HT turnover might be overestimated by pm changes.
Autolytic changes in the guinea pig cochlear nucleus were studied by means of light- and transmission electron microscopy from 5 min. up to 5 h post mortem. Hyperchromasy and shrinking of neurons was observed already after 5 min. in areas, where the neurons have a high number of primary afferent nerve endings (Kane 1973). A second mode of post mortem degeneration was found. It was characterized by a swelling of the cell, which showed a diminished stain-ability. This lytic swelling seemed to be less rapid and probably less harmful in the beginning. The cochleae were examined by scanning electron microscopy. In contrary to known damaging agents (like noise or antibiotics) the outer haircells showed hardly any changes in the surface structures up to 1 hour in the basal coil, while lytic protrusions were observed in outer and inner haircells already after 5 min. in the apical parts. Post mortem changes in the cochlea and in the nucleus cochlearis show two different modes of autolytic degeneration.
Detailed toxicological studies were undertaken on two suicides by amitriptyline overdose, one with salicylate also. In the first case, 10 initial blood samples taken 21 h after body discovery and an estimated 28 1/2 h after overdose had drug concentration (mg/L) ranges of 2.5-12 for amitriptyline (AM), 0.7-3.1 for nortriptyline (NOR), and 81-244 for salicylate (SAL). Ten blood samples taken 42 h later showed corresponding ranges of 1-39 AM, 0.6-7.0 NOR, and 86-310 SAL. Sample haemoglobin concentrations (range, 8.7-23.5 g/dl) did not correlate with drug concentrations. Postmortem increase in pulmonary vein AM concentration occurred more rapidly than in the pulmonary artery, likely reflecting relative ease of diffusion across the vessel walls from lung (AM, 60 mg/kg). In nine tissue samples, drug concentrations (mg/kg) were highest in the liver: AM, 301; and SAL, 670. Considerable drug residue was present in gastric contents, duodenal contents, and seven sequential small bowel contents. In both cases, sanguineous putrefactive pleural fluid showed higher AM concentrations on the left than on the right (2.0 vs 1.4 and 23 vs 16), likely reflecting diffusion from gastric drug residue. The detailed case data illustrate the intensity and complexity of postmortem drug diffusion from reservoirs in solid organs, such as the lungs, and unabsorbed gastric residue, into the blood and putrefactive fluids.
The changes in 16 cerebral metabolites produced by cardiac arrest and subsequent room temperature autolysis were studied using high-resolution proton nuclear magnetic resonance spectroscopy. Biopsies of rabbit cerebral cortex, cerebral white matter, and cerebellum were quantitatively analyzed for acetate, alanine, gamma-aminobutyric acid, creatine, glutamate, glycine, inositol, lactate, N-acetylaspartate, phosphocreatine, succinate, taurine, and threonine. Of these, N-acetylaspartate and the total creatine pool are the best candidates for use as concentration reference standards linking in vitro to in vivo 1H nuclear magnetic resonance measurements. Both changed little immediately after death, and they varied in a distinctive way among cortex, white matter, and cerebellum.
BACKGROUND: The human temporal bone preparation is a common model for research of physical processes of the ear canal and middle ear. In the past decade only a few reports were published discussing changes of the vibration behaviour of the tympanic membrane, as well as the ear canal resonance, during the time between death and preparation of the temporal bone. The aim of our study is to verify whether measurements at the temporal bone of dead humans can be really applied to the in vivo situation. METHODS: We investigated whether changes of the ear canal resonance and the vibration of the tympanic membrane depend on temperature and time after death. In a female human body we defined the resonance of the outer ear and the impedance of the tympanic membrane using a tympanometer and a real ear measurement system during nine hours post mortem. RESULTS: We were able to prove that before the preparation of the temporal bone none of the parameters changed significantly. CONCLUSIONS: In conclusion, the method of preserving the bone after its preparation is decisive for the validity of measurements at the isolated (post mortem) human temporal bone.
The autopsy on an body recovered from the water showed evidence of drowning and, in addition, the occurrence of extensive intramuscular bleeding on the neck, in the area of the shoulder girdle and the upper arms. There was a suspicion that criminal violence had been used, and the police carried out extensive investigations; these were inconclusive. The subsequent histological examination of the affected musculature revealed "reactive" changes throughout which corresponded to post mortem damage. The case presented here serves to illustrate the usefulness of muscle histology for differentiating between the occurrence of intramuscular bleeding before and after death; the corresponding histological criteria are outlined.
1. Studies were performed in porcine left circumflex coronary arteries to determine the time course of changes in their responses to smooth muscle and endothelial cell agonists following death. 2. The pigs were kept at room temperature for 3, 6, 12 and 24 hr after death before removing the arteries, and the responses compared with fresh arteries. Rings of the arteries were mounted in organ chambers filled with modified Krebs-Ringer solution for isometric tension recording. 3. Fresh rings with endothelium relaxed with stretching, whereas 3- and 6-hr rings developed an increase in tension and often rhythmic activity. In 3-hr rings, there were diminished contractile responses to KCl and serotonin. The contractile responses to prostaglandin F2 alpha were depressed at 3 and 6 hr. 4. At 6 hr, rings from six of 14 pigs failed to contract and the responses of the other eight to histamine and serotonin but not to KCl or acetylcholine, were depressed compared to fresh rings. 5. 6 hr after death endothelium-mediated relaxations to bradykinin and calcium ionophore A-23187 were depressed while endothelium-mediated as well as direct smooth muscle relaxation by adenosine diphosphate did not change. 6. These studies indicate that caution must be observed in interpreting the findings in autopsy specimens examined as early as 3 hr after death.
The molecular species of 1,2-diacyl-sn-glycerol (DAG), phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), and phosphatidylinositol 4,5-bisphosphate (PIP2) from brains of adult rats (weighing 150 g) were determined. The DAG, isolated from brain lipid extracts by TLC, was benzoylated, and the molecular species of the purified benzoylated derivatives were separated from each other by reverse-phase HPLC. The total amount and the concentration of each species were quantified by using 1,2-distearoyl-sn-glycerol (18:0-18:0) as an internal standard. About 30 different molecular species containing different fatty acids at the sn-1 and sn-2 positions of DAG were identified in rat brains (1 min postmortem), and the predominant ones were 18:0-20:4 (35%), 16:0-18:1 (15%), 16:0-16:0 (9%), and 16:0-20:4 (8%). The molecular species of PC, PE, PS, and PI were determined by hydrolyzing the lipids with phospholipase C to DAG, which was then benzoylated and subjected to reverse-phase HPLC. PIP and PIP2 were first dephosphorylated to PI with alkaline phosphatase before hydrolysis by phospholipase C. The molecular species composition of phosphoinositides showed predominantly the 18:0-20:4 species (50% in PI and approximately 65% in PIP and PIP2). PS contained mainly the 18:0-22:6 (42%) and 18:0-18:1 (24%) species. PE was mainly composed of the 18:0-20:4 (22%), 18:0-22:6 (18%), 16:0-18:1 (15%), and 18:0-18:1 (15%) species. In PC the main molecular species were 16:0-18:1 (36%), 16:0-16:0 (19%), and 18:0-18:1 (14%). Studies on postmortem brains (30 s to 30 min) showed a rapid increase in the total amount (from 40-50 nmol/g in 0 min to 210-290 nmol/g in 30 min) and in all the molecular species of DAG. Comparatively larger increases (seven- to 10-fold) were found for the 18:0-20:4 and 16:0-20:4 species. Comparison of DAG species with the molecular species of different glycerolipids indicated that the rapid postmortem increase in content of DAG was mainly due to the breakdown of phosphoinositides. However, a slow but continuous breakdown of PC to DAG was also observed.
In September 1989 an old motor car was accidentally discovered in a lake, 50 meters below the water surface. The automobile contained the torso of an adult woman with extensive adipocere formation and the skeletonized body of a man. Forensic and criminalistic investigations lead to the identification of the deceased persons. In the year 1939 the persons together had committed suicide. The corpses were immersed for fifty years.
The activity of calcium pumping adenosine triphosphatase (Ca2+-ATPase) in cardiac sarcoplasmic reticulum plays a pivotal role in myocardiac contraction-relaxation. The Ca2+-ATPase activity is controlled by phosphorylation and dephosphorylation of a sarcoplasmic reticulum protein "phospholamban" in response to neurotransmitters and drugs. To clarify the role of Ca2+-ATPase in the development of cardiac rigor mortis, we examined the changes of cardiac rigidity and cardiac sarcoplasmic reticulum Ca2+-ATPase activity up to 5 h after the decapitation of rats. Fifteen minutes after decapitation, the rats showed a cardiac rigidity on left ventricles. After 30 min, rigidity was obvious over the whole heart. After 1 h, the rigidity reached a high degree which was maintained for the rest of the observation period. On the other hand, the Ca2+-ATPase activity controlled by phosphorylation and dephosphorylation of phospholamban did not change for the whole observation period (5 h). Another Ca2+-ATPase activity representing the total amount of Ca2+-ATPase in sarcoplasmic reticulum gradually decreased. The data suggest that no significant phosphorylation or dephosphorylation of phospholamban occurs for a short time, at least for 5 h, after death and that the Ca2+-ATPase tends to relax the myocardium against the development of cardiac rigor mortis.
Microdialysis combined with a solid-phase radioimmunoassay was used to monitor changes in extracellular opioid peptide levels in the rat globus pallidus/ventral pallidum as a result of terminal brain ischemia. Ischemia was induced by anesthetic overdose or by severance of blood vessels supplying the brain. In control animals the recovered immunoreactivity increased an average of 13-fold in the 30-min sample following anesthetic overdose. Perfusion of a calcium-free, 10 mM EGTA-containing medium through the dialysis probe significantly attenuated the amplitude of this response, with the average increase being only threefold. Shorter sampling intervals (5 min) indicated that release of opioid peptide material into the extracellular environment occurs within the first 5 min of ischemia resulting from severance of the blood supply to the brain. HPLC analysis identified the majority of the postmortem-induced immunoreactive material as Met- and Leu-enkephalin.