Forensic Review of Hot Bath-Related Death in the Elderly: Focused on Japanese Studies / 대한법의학회지

Hot bath-related deaths occur occasionally in Korea, particularly in the winter season among elderly people. The postmortem determination of the cause and manner of death is often difficult because the investigation depends predominantly on postmortem external examination. Moreover, the pathogenesis of sudden death during immersion in a hot bath tub is not easily explained. Confusion regarding the manner of death, whether accidental or natural, causes some conflicts in the compensation of life insurance. This study reviewed the literature, particularly Japanese studies about epidemiology, pathophysiology, and the disputes regarding determination of the manner of death. We concluded that the cause and manner of death are not as simple as only natural disease or drowning; there are complicated cases mixed with accidental and natural causes. Extensive epidemiological studies and thorough investigation, including full autopsy and toxicologic studies, are essential for comprehensive understanding of hot bath-related deaths in Korea.

Forensic Review of Hot Bath-Related Death in the Elderly: Focused on Japanese Studies / 대한법의학회지

Hot bath-related deaths occur occasionally in Korea, particularly in the winter season among elderly people. The postmortem determination of the cause and manner of death is often difficult because the investigation depends predominantly on postmortem external examination. Moreover, the pathogenesis of sudden death during immersion in a hot bath tub is not easily explained. Confusion regarding the manner of death, whether accidental or natural, causes some conflicts in the compensation of life insurance. This study reviewed the literature, particularly Japanese studies about epidemiology, pathophysiology, and the disputes regarding determination of the manner of death. We concluded that the cause and manner of death are not as simple as only natural disease or drowning; there are complicated cases mixed with accidental and natural causes. Extensive epidemiological studies and thorough investigation, including full autopsy and toxicologic studies, are essential for comprehensive understanding of hot bath-related deaths in Korea.

Expression of Connexin 43 in the Myocardium in Sudden Unexplained Nocturnal Death Syndrome / 대한법의학회지

Sudden unexplained nocturnal death syndrome (SUNDS) occurs predominantly in Southeast Asian people including Koreans. SUNDS is problematic for forensic pathologists because the diagnosis depends on the "exclusion of diagnosis." Moreover, the pathogenesis of SUNDS is still unclear although some cases are known to be intimately related to the Brugada syndrome. Connexin 43 (Cx43) is a principal protein of gap junction in adult cardiac myocytes, being distributed to the intercalated discs and phosphorylated in normal condition. Ischemia and hypoxia alter the expression of total Cx43 (tCx43) resulting in redistribution of non-phosphorylated Cx43 (npCx43) to the sarcoplasm or lateral cell borders of cardiac myocytes by continuing dephosphorylation. This study aimed to compare the immunoexpression pattern of Cx43 in the cardiac myocytes of SUNDS and ischemic heart disease (IHD). The study group was 26 cases of SUNDS and the control group of 24 cases of IHD with severe coronary atherosclerosis, showing no myocardial ischemic change. There was a significantly different expression of both tCx43 and npCX43 between the SUNDS and IHD group. A greater reduction in both tCx43 and npCx43 and a more delayed redistribution pattern was seen in the myocardium of SUNDS when compared with IHD. In conclusion, these results suggest that the reduced Cx43 expression in SUNDS may be inherent and indicate a risk of arrhythmia.

The alteration of Ca2+-activated K+ channels in coronary arterial smooth muscle cells isolated from isoproterenol-induced cardiac hypertrophy in rabbit

It has been proposed that Ca2+-activated K+ (KCa) channels play an essential role in vascular tone. The alterations of the properties of coronary KCa channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present studies were carried out to determine the properties of coronary KCa channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the present study are as follows: (1) the unitary current amplitudes and the slope conductance of coronary KCa channels were decreased without changes of the channel kinetics in isoproterenol-induced cardiac hypertrophy; (2) the sensitivity of coronary KCa channels to the changes of intracellular concentration of Ca2+ was reduced in isoproterenol-induced cardiac hypertrophy. From above results, we suggest for the first time that the alteration of KCa channels are involved in impaired coronary reserve in isoproterenol-induced cardiac hypertrophy.

Activation of ATP-sensitive potassium channels by the predominant metabolite of isoflurane in rabbit ventricular myocytes

Background: Recent in vivo experimental evidence suggests that isoflurane-induced cardioprotection may involve KATP channel activation. However, it was demonstrated that isofluran inhibited KATP channel activities in the inside-out patch mode. To explain this discrepancy, the present investigation tested the hypothesis that a metabolite of isoflurane, trifluoroacetic acid (TFA), contributes to isoflurnae-induced cardioprotection via KATP channel activation during myocardial ischemia and reperfusion. Methods: Single ventricular myocytes were isolated from rabbit hearts by an enzymatic dissociation procedure. Patch-clamp techniques were used to record single-channel currents. KATP channel activities were assessed before and after the application of TFA with the inside-out patch mode. Results: TFA enhanced channel activity in a concentration-dependent fashion. The concentration of TFA for half-maximal activation and the Hill coefficient were 0.03 mM and 1.2, respectively. TFA did not affect the single channel conductance of KATP channels. Analysis of open and closed time distributions showed that TFA increased burst duration and decreased the interburst interval without changes in open and closed time distributions shorter than 5 ms. TFA diminished ATP sensitivity of KATP channels in a concentration-response relationship for ATP. Conclusions: TFA, a metabolite of isoflurane, enhanced KATP channel activity in a concentration-dependent fashion. These results imply that TFA could mediate isoflurane-induced cardioprotection via KATP channel activation during myocardial ischemia and reperfusion.

cAMP-dependent signalling is involved in adenosine-stimulated Cl- secretion in rabbit colon mucosa

An important property of the intestine is the ability to secrete fluid. The intestinal secretion is regulated by a number of substances including vasoactive intestinal peptide (VIP), ATP and different inflammatory mediators. One of the most important secretagogues is adenosine during inflammation. However, the controversy concerning the underlying mechanism of adenosine-stimulated Cl- secretion in intestinal epithelial cells still continues. To investigate the effect of adenosine on Cl- secretion and its underlying mechanism in the rabbit colon mucosa, we measured short circuit current (ISC) under automatic voltage clamp with DVC-1000 in a modified Ussing chamber. Adenosine, when added to the basolateral side of the mucosa, increased ISC in a dose-dependent manner. The adenosine-stimulated ISC response was abolished when Cl- in the bath solution was replaced completely with gluconate. In addition, the ISC response was inhibited by a basolateral Na-K-Cl cotransporter blocker, bumetanide, and by apical Clchannel blockers, dephenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), glibenclamide. Amiloride, an epithelial Na+ channel blocker, and 4,4-diisothiocyanato-stilbene-2,2-disulphonate (DIDS), a Ca2+-activated Cl- channel blocker, had no effect. In the mucosa pre-stimulated with forskolin, adenosine did not show any additive effect, whereas carbachol resulted in a synergistic potentiation of the ISC response. The adenosine response was inhibited by 10 micrometer H-89, an inhibitor of protein kinase A. These results suggest that the adenosine-stimulated ISC response is mediated by basolateral to apical Cl- secretion through a cAMP-dependent Cl- channel. The rank order of potencies of adenosine receptor agonists was 5'-(N-ethylcarboxamino)adenosine(NECA) > N6-(R-phenylisopropyl)adenosine(R-PIA)>2-(p-(2-carbonylethyl)-phenyl-et hylamino)-5'-N-ethylcarboxaminoadenosine(CGS21680). From the above results, it can be concluded that adenosine interacts with the A2b adenosine receptor in the rabbit colon mucosa and a cAMP-dependent signalling mechanism underlies the stimulation of Cl- secretion.