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At least 163 records · Page 9Linked to original sources
PubMed1999

How and why does the platelet count in postmortem blood change during the early postmortem interval?

We examined the changes in the early postmortem platelet count in postmortem blood and the reasons for these changes by counting the platelets, by performing in vitro hypostatic tests, by estimating the percentage of erythrocytes by volume in postmortem blood samples, by immunohistochemistry (anti-CD61, anti-fibrinogen), and by immunoelectron microscopy (anti-CD62, anti-CD63, anti-thrombospondin). The apparent initial increase in the platelet count in postmortem blood was found to be caused by hypostatic phenomena. The subsequent discontinuous decrease in the platelet count despite continuing hypostasis in the corpse can be explained in part by postmortem thrombolysis and the development of reversible platelet-platelet aggregates. The main point is, that changes in the postmortem blood environment cause potentially reversible adhesion of platelets to pre-adsorbed fibrinogen on erythrocytes. Thus the decrease in the number of platelets in postmortem blood is not attributable to postmortem clotting but to a decrease in the number of countable platelets in postmortem blood.

Adult↗
PubMed1992

[What histology is normal and abnormal in the liver?].

Normal and abnormal morphologies of the liver were histopathologically reviewed. Characteristic structure and specialized functions of the liver, and the age and life style of the patients should be taken into consideration of the evaluation of abnormal liver morphologies. The latter were generally classified into pathologic changes, nonspecific and non-significant findings, agonal changes and postmortem changes. Pathologic changes were subdivided into several categories according to their pathogenesis and etiologies. While postmortem changes lack of vital reaction, apoptosis, a programmed cell death, is also lacking inflammatory reaction. These findings should be comprehensively analyzed in the pathologic evaluation.

Age Factors↗
PubMed1993

Investigation of postmortem functional changes in human cerebral arteries.

This study demonstrated the time-dependent changes in postmortem responses of isolated human middle cerebral artery strips to vasodilators. The relaxation induced by prostaglandin (PG) I2 or nitroglycerin remained stable for 24 h postmortem. In arterial strips precontracted with PGF2 alpha, substance P and bradykinin both elicited relaxation that was almost completely abolished by removal of the endothelium. The endothelium-dependent response to both peptides was significantly degraded in strips obtained > 12 h postmortem. These results indicate a selective functional or anatomical vulnerability of the vascular endothelium compared with that of the vasodilator mechanisms of the smooth muscle in the postmortem period. However, cerebral arteries isolated from human cadavers within 12 h postmortem should be adequate for studies of both smooth muscle and endothelial reactivity to vasodilators.

Adult↗
PubMed1995

Postmortem acetaminophen pharmacokinetics: an experimental study of site and time-dependent concentration changes.

Postmortem blood drug concentrations are obtained routinely for assessment of the cause of mortality. However, the relationship of postmortem drug concentration to blood concentrations at the time of death remains poorly characterized. Using Ketamine sedation, 10 New Zealand white rabbits were sacrificed 20 minutes after oral gavage with liquid acetaminophen 160 mg/kg as a model drug. Blood samples were obtained from peripheral (femoral vein) and central sites (heart & inferior cava) over time and compared with heart blood concentrations obtained at the time of sacrifice. The mean +/- SE antemortem acetaminophen concentration was 63.1 +/- 14.6 mcg/ml. Postmortem central blood concentrations were as follows: T = 3 h: 200.8 +/- 129.2 micrograms/mL, T = 6 h: 100.8 +/- 39.6 micrograms/mL and T = 12 h: 480.8 +/- 128.8 micrograms/mL. Postmortem peripheral site results were: T = 3 h: 50.2 +/- 21.4 micrograms/mL, T = 6 h: 100.8 +/- 18.1 and T = 12 h: 117.7 +/- 37.2 micrograms/mL. Overall, blood acetaminophen concentrations increased significantly over time for central sampling sites. Drug concentration increases seen in the central sampling sites were several times higher than that seen in peripheral blood. Blood samples taken from peripheral sites did not alter significantly. The results of this controlled study were consistent with previous autopsy case series and case reports suggesting that postmortem drug concentrations do not reflect premortem values. Variables affecting postmortem drug concentrations include both postmortem sampling time and anatomic blood collection site.

Acetaminophen↗
PubMed1980

Postmortem biochemical changes in canine blood.

Antemortem and postmortem blood samples from 60 dogs were evaluated for sodium, chloride, potassium, urea nitrogen, glucose, creatinine, calcium, phosphorus, total protein, albumin, and carbon dioxide levels. Temperatures were 4, 20 and 37 degrees C. Postmortem intervals were 3, 6, 12, and 48 h. Blood urea nitrogen, calcium, and protein values remained stable after death, indicating diagnostic significance. Potassium, creatinine, and phosphorus levels increased with time and sodium, chloride, and total carbon dioxide levels decreased with time; therefore, determining these chemical values could be beneficial in estimating time of death. Glucose values were of limited value.

Animals↗
PubMed1990

1H-NMR studies of postmortem biochemical changes in rat skeletal muscle.

1H-nuclear magnetic resonance (NMR) has been applied to the study of postmortem biochemical changes in perchloric acid extracts of rat skeletal muscle. Several metabolites have been detected and the dependence upon the postmortem time has been considered. The simultaneous quantitative determination of metabolites showing up at very low and very high fields has been suggested to yield a satisfactory delineation of the thanatochronology.

Animals↗
PubMed1980

Postmortem biochemical changes in canine cerebrospinal fluid.

Time and temperature effects on postmortem cerebrospinal fluid samples from 60 adult mongrel dogs were studied. After death the dogs were held at 4, 20, or 37 degrees C for intervals of 3, 6, 12, 24, or 48 h. Antemortem and postmortem cerebrospinal fluid was evaluated for sodium, chloride, potassium, urea nitrogen, glucose, creatinine, calcium, phosphorus, and carbon dioxide. Sodium and urea nitrogen values remained stable. Chloride may be of forensic science value. Low levels of postmortem calcium might indicate antemortem hypocalcemia; high levels of postmortem glucose may indicate antemortem hyperglycemia. Calcium and creatinine levels increased slightly but continually after death; carbon dioxide values dropped.

Animals↗
PubMed1980

Postmortem biochemical changes in canine vitreous humor.

Time and temperature effects on postmortem vitreous humor from 60 adult mongrel dogs were studied. After death the dogs were held at 4, 20, or 37 degrees C for intervals of 3, 6, 12, 24, or 48 h. Antemortem and postmortem vitreous was analyzed for sodium, chloride, potassium, urea nitrogen, glucose, and creatinine. Potassium levels rose with increases in temperature and time. Sodium, chloride, and urea nitrogen values were stable at 4 degrees C for 48 h; they were less stable at higher temperatures. Glucose dropped to less than half within 3 h at all temperatures. Creatinine values were inconsistent. In that postmortem glucose and sodium levels remained below antemortem levels, diagnosis of hyperglycemia and hypernatremia should be possible. Consequently, a diagnosis of hypoglycemia could not be supported; the diagnosis of hyponatremia could be made in the early postmortem period.

Animals↗
PubMed2001

Postmortem microscopic changes observed at the human head hair proximal end.

Only two types of human hair roots (proximal ends) derived from decomposing scalps are reported in the literature. The most common representation of the putrid root includes a postmortem dark root band in published photomicrographs. In this study, 22 cases were reviewed in which there was reliable time of death documentation from medical investigator reports. A review of these cases finds that the most common putrid hair proximal end change does not contain the postmortem root band. Four primary types of hair proximal end postmortem change were identified. This study finds no correlation of time of death with scalp hair proximal end decomposition. In addition two examples are presented that suggest that hair roots do not decompose after fresh removal from the scalp and exposure to the outside elements.

Adult↗
PubMedDate not supplied

Neurochemical changes following postmortem ischemia in the rat retina.

Glutamate and gamma-aminobutyric acid (GABA) are the dominant amino acids in the retina and brain. The manufacturing and degradation pathways of both of these amino acids are intricately linked with the tricarboxylic acid cycle leading to rapid redistribution of these amino acids after metabolic insult. Postmortem ischemia in mammalian retina predominantly results in a loss of glutamate and GABA from neurons and accumulation of these amino acids within Müller cells. This accumulation of glutamate and GABA in Müller cells may occur as a result of increased release of these neurotransmitters from neurons, and decreased degradation. Quantification of the semisaturation value (half-maximal response) for glutamate and GABA Müller cell loading during postmortem ischemia indicated a shorter semisaturation value for GABA than glutamate. Such changes are consistent with a single aerobically dependent GABA-degradation pathway, and the existence of multiple glutamate-degradation pathways. Comparison with the in vitro ischemic model showed similar qualitative characteristics, but a markedly increased semisaturation time for glutamate and GABA Müller cell loading (a factor of 5-10) in the postmortem ischemia model. We interpret these differences to indicate that the in vitro condition provides a more immediate and/or severe ischemic insult. In the postmortem ischemia model, the delayed glial cell loading implies the availability of internal stores of both glucose and/or oxygen. Increased glial and neuronal immunoreactivity for the amino acids involved in transamination reactions, aspartate, alanine, leucine, and ornithine was observed, indicating a potential shift in the equilibrium of transamination reactions associated with glutamate production. These findings provide evidence that, in the rat retina, there are multiple pathways subserving glutamate production/degradation that include a multitude of transamination reactions. Further evidence is therefore provided to support a role for all four amino acids in glutamate metabolism within a variety of retinal neurons and glia.

Alanine↗