natriuretic-peptide--brain and Heat-Stroke

The postmortem diagnosis of heat-related deaths presents certain difficulties. Firstly, preterminal or terminal body temperatures are often not available. Additionally, macroscopic and microscopic findings are nonspecific or inconclusive and depend on survival duration after exposure. The diagnosis of hyperthermia is therefore essentially based on scene investigation, the circumstances of death, and the reasonable exclusion of other causes of death. Immunohistochemistry and postmortem biochemical investigations have been performed by several authors in order to better circumstantiate the physiopathology of hyperthermia and provide further information to confirm or exclude a heat-related cause of death. Biochemical markers, such as electrolytes, hormones, blood proteins, enzymes, and neurotransmitters, have been analyzed in blood and other biological fluids to improve the diagnostic potential of autopsy, histology, and immunohistochemistry. The aim of this article is to present a review of the medicolegal literature pertaining to the postmortem biochemical investigations that are associated with heat-related deaths.

Topics: Adrenocorticotropic Hormone; Atrial Natriuretic Factor; Biomarkers; Blood Urea Nitrogen; C-Reactive Protein; Calcitonin; Calcium; Catecholamines; Chlorides; Chromogranin A; Creatine Kinase, MB Form; Creatinine; Electrolytes; Fever; Forensic Pathology; Growth Hormone; Heat Stroke; Humans; Magnesium; Myocardium; Myoglobin; Myoglobinuria; Natriuretic Peptide, Brain; Neopterin; Protein Precursors; Sodium; Troponin; Tryptases; Uric Acid; Vitreous Body

The aim of this study was to investigate direct effects of heat exposure on the heart molecular-biologically and pathohistologically, using rats exposed to high temperatures. The mRNA expression of natriuretic peptide type A (Nppa), natriuretic peptide type B (Nppb), actin alpha 1 skeletal muscle (Acta1), myosin heavy polypeptide 6 cardiac muscle alpha (Myh6) and myosin heavy polypeptide 7 cardiac muscle alpha (Myh7) was determined in the hearts of the rats. Whereas the expression of Nppa and Nppb rapidly increased immediately after the heat exposure, the expression of Acta1 was gradually reduced, which indicated cardiac overload. Moreover, the expression of Myh6 and Myh7 in the heart increased 4h after the heat exposure, which suggested the involvement of a compensatory mechanism. Immunohistochemical staining with anti-fibronectin antibody showed that positive cardiomyocytes could be detected sparsely 4h after the heat exposure, and they could be clearly observed 8h after the heat exposure. Our results showed that hyperthermia causes myocardial damage shortly after the exposure to heat and that the ventricle was more vulnerable to hyperthermia-induced damage than the atrium. Cardiac dysfunction may be induced not only by hypercytokinemia but also by the direct effect of heat exposure at the early period of heat stroke, which may be one of the mechanisms by which heat causes death. Elucidating the mechanism of death from heat stroke could lead to not only diagnostic improvement but also the prevention of death from heat stroke.

Topics: Animals; Atrial Natriuretic Factor; DNA, Complementary; Fever; Heart; Heart Atria; Heart Ventricles; Heat Stroke; Hot Temperature; Male; Molecular Biology; Myocardium; Natriuretic Peptide, Brain; Rats; Rats, Wistar; RNA, Messenger

The present study investigated the molecular pathology of atrial and brain natriuretic peptides (ANP and BNP) in the myocardium to evaluate terminal cardiac function in routine forensic casework with particular regard to fatal drug intoxication (n = 18; sedative-hypnotics, n = 10; methamphetamine, n = 8), hypothermia (cold exposure, n = 13), and hyperthermia (heatstroke, n = 10), compared with that in acute ischemic heart disease (AIHD, n = 35) and congestive heart disease (CHD, n = 11) as controls (total n = 87; within 48 h postmortem). Quantitative analyses of myocardial ANP and BNP messenger RNA demonstrated that their expressions in bilateral atrial and ventricular walls were high in methamphetamine intoxication and hypothermia, comparable to those in AIHD and CHD, but were low in sedative-hypnotic intoxication and hyperthermia. In pericardial fluid, both ANP and BNP levels were increased in hypothermia, while CHD cases had an elevated BNP level, and ANP level showed a tendency to increase in hyperthermia; however, immunohistochemistry showed no evident differences in myocardial ANP and BNP among the causes of death. These findings suggest terminal high cardiac strain in methamphetamine intoxication, decreased cardiac strain in sedative-hypnotic intoxication and hyperthermia (heatstroke), and persistent congestion in hypothermia (cold exposure).

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Autopsy; Cause of Death; Female; Gene Expression; Heart Atria; Heart Failure; Heart Ventricles; Heat Stroke; Humans; Hypnotics and Sedatives; Hypothermia; Illicit Drugs; Male; Methamphetamine; Middle Aged; Myocardial Ischemia; Myocardium; Natriuretic Peptide, Brain; Pathology, Molecular; Pericardial Effusion; Poisoning; Postmortem Changes; Prescription Drug Misuse; RNA-Directed DNA Polymerase; RNA, Messenger