[Experimental study of the postmortem changes in tissue structures using the lectins of the castor-oil plant].
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Postmortem changes of the dielectric properties of bovine brain tissues at low radiofrequencies.
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.
Animals↗
Postmortem changes in the levels of monoamine metabolites in human cerebrospinal fluid.
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.
3,4-Dihydroxyphenylacetic Acid↗
Postmortem changes in surface preparations of the cochlea.
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Animals↗
[Postmortem changes of fine structure in the auditory pathways (organ of Corti and nucleus cochlearis of the guinea pig (author's transl)].
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.
Animals↗
High-resolution proton magnetic resonance spectroscopy of rabbit brain: regional metabolite levels and postmortem changes.
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.
3-Hydroxybutyric Acid↗
Postmortem changes in endothelium-dependent and independent responses of porcine coronary arteries.
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.
Acetylcholine↗
Molecular species of diacylglycerols and phosphoglycerides and the postmortem changes in the molecular species of diacylglycerols in rat brains.
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.
Animals↗
[Postmortem changes after 50 years immersion (1939 reconstructed suicide)].
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.
Adult↗
Postmortem changes in the level of calcium pumping adenosine triphosphatase in rat heart sarcoplasmic reticulum.
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.
Animals↗
Postmortem changes in rat brain extracellular opioid peptides revealed by microdialysis.
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.
Anesthetics↗
Postmortem changes in hapten-specific IgE antibody responses in mice.
This Study was carried out to examine the post-mortem stability of hapten-specific immunoglobulin E (IgE) antibody in mice by the passive cutaneous anaphylaxis test in rats. In vitro IgE antibody responses in blood were stable for 3 days at room temperature. Even in cases when blood could not be obtained from the cadaver it was possible to measure the hapten-specific IgE antibody response up to 3 days after death using the supernatant of the visceral homogenates.
Animals↗
Importance of postmortem changes in measurements of thyroid function in studies of sudden infant death syndrome.
Various measurements of thyroid function were made from serum sampled at necropsy by cardiac puncture in adults and compared with the equivalent values before death. There were significant increases in serum total T3 (0.66 before death, 1.14 nmol/l after death), free T3 (0.82 to 1.52 pmol/l), and reverse T3 (1.12 to 1.75 nmol/l); and significant decreases in total T4 (73.7 to 56.6 nmol/l), free thyroxine index (FTI) (83.2 to 56.6), and free T4 (14.2 to 11.9 pmol/l). The increase in serum T3, presumably from T4 deiodination after death, observed in this study may explain the increased T3 concentration reported in serum sampled from cases of sudden infant death syndrome (SIDS).
Humans↗
[The dynamic postmortem changes of the nucleoproteins in the tissues of the liver and eye].
Postmortal changes in nucleoproteins were examined in the hepatocytes and anterior corneal and crystalline lenticular epithelial cells from 106 cadavers within 48 h after death by microfluorometry. Cryostat tissue sections were stained by acridine yellow by the method of R. Rigler (1966). The author found a natural decrease in fluorescence intensity of the examined tissue cellular nuclei at 530 nm within 4-24 h. and an increase in their fluorescence intensity at 640 nm within 4-48 h. after death. Data obtained may be used to establish the time of death.
Acridine Orange↗
Postmortem changes in uric acid and ascorbic acid in human cerebral cortex tissues excised after cardiac death.
There has been no report on the determination of uric acid (UA) in human brain and heart tissues. UA and ascorbic acid (AA) in human cerebral cortex and heart tissues excised after cardiac death have been studied by reversed-phase high-performance liquid chromatography (HPLC) with electrochemical detection (ECD). It has been found that the levels of AA and UA in the human cerebral cortex tissues tend to decrease and increase, respectively, after cardiac death as a function of time between death and forensic operation. In addition, it has been found that there is no special relationship between UA levels in human heart tissues and time after cardiac death, also that the UA levels in the heart are high as compared with those in human cerebral cortex tissues. We have emphasized that the HPLC-ECD method is useful in determining UA and AA in mammalian tissues by one-time chromatography to gain a better understanding of the relationship between disease and serum urate level.
Ascorbic Acid↗
Postmortem changes in rat brain: studies on membrane-bound enzymes and receptors.
The relationship between the stability of potential neurochemical markers and autolysis time was studied at 4 degrees C and 25 degrees C using postmortem brain samples from two rat strains. In general, qualitatively similar results were obtained with either N/Nih or Sprague-Dawley rats; however, quantitative differences were often observed, particularly in regard to benzodiazepine receptor changes. For every enzyme activity or binding property examined, no significant change was found when brains were kept at 4 degrees C for up to 72 h prior to freezing at -70 degrees C. Na,K-ATPase and low-affinity Ca-ATPase activities were also stable in brains kept at 25 degrees C for up to 72 h. Mg-ATPase activity was reduced in brains kept at 25 degrees C for 24 and 48 h. [3H]Guanidinoethylmercaptosuccinic acid [( 3H]GEMSA) binding to enkephalin convertase in the cytosol was not significantly changed in brains kept at 25 degrees C; however, a small increase was seen for [3H]GEMSA binding to the membrane fraction at 24, but not 48 and 72 h postmortem. [3H]Quinuclidinyl benzilate [( 3H]QNB) binding to muscarinic cholinergic receptors decreased in brains kept at 25 degrees C for 72 h. Opioid receptor binding also decreased in brains kept at 25 degrees C. Using [3H]2-D-alanine-5-D-leucine enkephalin to label delta opioid receptors, a statistically significant decrease in binding was observed as early as 6 h postmortem, and was completely abolished after 72 h at 25 degrees C. In contrast, [3H]naloxone binding was unchanged after 24 h at 25 degrees C, but was decreased after 48 and 72 h.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Equine vitreous humor chemical concentrations: correlation with serum concentrations, and postmortem changes with time and temperature.
Samples of equine vitreous humor were analyzed for urea nitrogen, creatinine, sodium, chloride, phosphorus, calcium, potassium, and magnesium concentrations. Fresh vitreous chemical concentrations were compared to corresponding serum concentrations and expressed as a vitreous to serum ratio. The effects of postmortem time and temperature on the stability of the chemical concentrations were determined by incubation of the samples at 4 degrees C, and 20 degrees C and 37 degrees C for 6, 12, 24, or 48 h. Chemical concentrations were generally more stable at lower temperatures and shorter incubation times.
Animals↗
Cerebral edema in developing brain. I. Normal water and cation content in developing rat brain and postmortem changes.
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