Facial Baroparesis Caused by Scuba Diving

Middle ear barotrauma is one of the common complications of SCUBA diving representing acute otalgia, hearing loss, and bleeding. But occurrence of facial palsy is rare. Here we report a case of a 30-year-old navy diver suffered middle ear barotrauma with transient facial palsy after SCUBA diving. He felt difficulty in equalizing the pressure in middle ear with Valsalva maneuver during diving, and suffered right facial palsy and aural fullness after diving. Clinical examination showed remarkable bulging of the right tympanic membrane and right facial palsy without other neurological findings. But facial palsy was disappeared immediately after myringotomy. We considered that the etiology of this case was neuropraxia of facial nerve in middle ear caused by over pressure of middle ear

Case Report Facial Baroparesis Caused by Scuba Diving

Middle ear barotrauma is one of the common complications of SCUBA diving representing acute otalgia, hearing loss, and bleeding. But occurrence of facial palsy is rare. Here we report a case of a 30-year-old navy diver suffered middle ear barotrauma with transient facial palsy after SCUBA diving. He felt difficulty in equalizing the pressure in middle ear with Valsalva maneuver during diving, and suffered right facial palsy and aural fullness after diving. Clinical examination showed remarkable bulging of the right tympanic membrane and right facial palsy without other neurological findings. But facial palsy was disappeared immediately after myringotomy. We considered that the etiology of this case was neuropraxia of facial nerve in middle ear caused by over pressure of middle ear

TRIC-A Channels in Vascular Smooth Muscle Contribute to Blood Pressure Maintenance.

小胞体カウンターイオンチャネルTRICチャネルによる血圧調節機構とTRICチャネル遺伝子多型による本態性高血圧リスク. 京都大学プレスリリース. 2011-08-02.TRIC channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation channels postulated to mediate counter-ion movements facilitating physiological Ca(2+) release from internal stores. Tric-a-knockout mice developed hypertension during the daytime due to enhanced myogenic tone in resistance arteries. There are two Ca(2+) release mechanisms in vascular smooth muscle cells (VSMCs); incidental opening of ryanodine receptors (RyRs) generates local Ca(2+) sparks to induce hyperpolarization, while agonist-induced activation of inositol trisphosphate receptors (IP(3)Rs) evokes global Ca(2+) transients causing contraction. Tric-a gene ablation inhibited RyR-mediated hyperpolarization signaling to stimulate voltage-dependent Ca(2+) influx, and adversely enhanced IP(3)R-mediated Ca(2+) transients by overloading Ca(2+) stores in VSMCs. Moreover, association analysis identified single-nucleotide polymorphisms (SNPs) around the human TRIC-A gene that increase hypertension risk and restrict the efficiency of antihypertensive drugs. Therefore, TRIC-A channels contribute to maintaining blood pressure, while TRIC-A SNPs could provide biomarkers for constitutional diagnosis and personalized medical treatment of essential hypertension