Key result
An increase in post-mortem interval from 2 to 8 hours significantly decreased the phenylephrine-induced elevation of perfusion pressure in rat tail arteries from 49 mmHg to 8 mmHg.
Why the study?
Does post-mortem interval affect vascular responses to ionotropic and metabotropic receptor activation in rat tail arteries?
Does post-mortem interval affect vascular responses to ionotropic and metabotropic receptor activation in rat tail arteries?
Post-mortem interval significantly decreases vascular responses to metabotropic receptor activation but not ionotropic receptor activation, suggesting potential markers for estimating PMI.
Requires strict PMI control in ex vivo vascular studies; leaves open forensic marker utility pending human data.
The contractibility of blood vessels depends on their normal structure and the availability of calcium ions; it changes under the influence of numerous contracting and relaxing factors, which control the activities of various pathways of intracellular and intercellular signaling. The main aim of the study was to investigate, by means of perfusion pressure in rat tail arteries, the role of Ca2+ in vascular response to α‑1 adrenoceptor activation by phenylephrine (PHE) and Bay K8644 agonist of the L‑type calcium channel and caffeine before and after a post‑mortem interval (PMI) of 2, 4, 6 and 8 h. A phasic increase of perfusion pressure in rat tail arteries, as induced by PHE or caffeine, in Ca2+‑free solutions was used as an indicator of intracellular Ca2+ release through the inositol 1,4,5‑triphosphate and ryanodine receptor pathways, respectively. In Ca2+‑free‑ethylene glycol tetraacetic acid (EGTA)‑poly(sodium styrenesulfonate) (PSS) and in Ca2+‑EGTA‑PSS, the PHE induced elevation of perfusion pressure significantly decreased. Vascular responses to caffeine (20 mmol/l) in Ca2+‑free‑EGTA‑PSS, with an increase of PMI from 2‑8 h, did not change significantly. A similar effect was observed with vascular responses to KCl 40 mmol/l in Ca2+‑EGTA‑PSS. To confirm whether the inhibitory effect of 2, 4, 6 and 8 h PMI was mediated through the formation of NO, nitro‑L‑arginine (L‑NNA), a potent NO synthase inhibitor, was used. Exposure to L‑NNA (10‑5 M) blocked the inhibition induced by an increase of PMI. The blocked effects of L‑NNA were reversed by L‑arginine (10‑4 M). In conclusion, these patterns of change in artery responses provide insight into the post‑mortem change in the receptor‑mediated signaling components in epithelial and smooth muscle cells, and support the further study of post‑mortem vascular responses triggered by G protein‑coupled receptors (metabotropic) and channel‑linked receptors (ionotropic) as potential markers for estimating short and long‑term PMIs, respectively.
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Bloch-Bogusławska et al. (2014) studied Post-mortem interval estimation (n=15). Post-mortem interval (PMI) vs. Shorter PMI (2 hours) or control was evaluated on Maximal perfusion pressure induced by phenylephrine in Ca2+-free-EGTA-PSS (p=<0.05). An increase in post-mortem interval from 2 to 8 hours significantly decreased the phenylephrine-induced elevation of perfusion pressure in rat tail arteries from 49 mmHg to 8 mmHg.
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