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Reduced Vascular Smooth Muscle (VSM) Sensitivity to Contraction in ex vivo Hemorrhaged Rabbit Epigastric Artery (EA)
Author(s) -
Ratz Paul H.,
Barbee Robert Wayne,
Miner Amy S.,
Reynolds Penny S.,
Contaifer Daniel
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1080.1
Subject(s) - contraction (grammar) , phenylephrine , vascular smooth muscle , medicine , anesthesia , femoral artery , chemistry , endocrinology , cardiology , blood pressure , smooth muscle
Compensation to hemorrhage includes vasoconstrictor‐induced VSM contraction. Severe hemorrhage can lead to reduced VSM reactivity to vasoconstrictors and decompensation. Vasoconstrictors not only cause VSM contraction, but also can activate a cellular negative feedback mechanism that causes prolonged VSM desensitization, termed VSM memory. To explore the hypothesis that VSM memory plays a role in decompensation, we studied EA reactivity ex vivo 45 min after severe hemorrhage. Compared to control rabbit EA removed before hemorrhage, EA after hemorrhage displayed depressed contractions to phenylephrine (PE) and histamine (HA). These data suggest that VSM memory participates in vascular decompensation during hemorrhagic shock. We more fully characterized VSM memory in rabbit and mouse arteries in vitro . Strong receptor stimulation (10–30 μM PE) for 30 min followed by PE washout to cause complete relaxation reduced the ability of G protein‐coupled receptor (GPCR) agonists (PE, HA, U‐46619 and vasopressin) and a non‐GPCR agonist (KCl) to subsequently contract renal, femoral, epigastric and mesenteric arteries for at least 1 hr after PE washout. These data indicate that high catecholamine concentrations can induce a generalized VSM desensitization in rabbit and mouse arteries (VSM memory) that may be responsible, in part, for vascular decompensation during hemorrhage. Funding: R01HL061320