• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.37-37
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• 2003

We have shown the $Ca^{2+}$-activated chloride current is present in cardiac myocyte in rabbit pulmonary vein (Kim et al., 2002). This current amplitude was increased as [N $a^{+}$]$_{i}$ was increased and we suggested this chloride current may be involve in the spontaneous action potential frequency change. Since this current is activated by the increase of intracellular $Ca^{2+}$, we would like to test what is the inducer of the increase of [C $a^{2+}$]$_{i}$ between a L-type $Ca^{2+}$-current or a reverse mode of N $a^{+}$-C $a^{2+}$ exchange current. White rabbit (1.5 kg) was used and anesthetized with Ketamin (100 mg/kg). Pulmonary vein (PV) was isolated and sleeve area between left atrium and PV was dissected. Using collagenase (Worthington 0.7 mg/cc), single cardiac myocytes were isolated. In the presence of 15 mM of N $a^{＋}$, three steps of voltage pulses were applied (holding potential : -40 ㎷, -80 ㎷ for 50 msec, 30 ㎷ for 5 msec, 10 ㎷ steps from -70 ㎷ to 60 ㎷). The inward and outward tail current was activated after brief 5 msec prepulse. The outward tail current was blocked by the removal of extracellular chloride substituted by glucuronic acid or by a chloride channel blocker, 5 mM 9-AC. But the inward tail current was still remained even though the amplitude was decreased. The reversal potentials were changed to the direction of the change of chloride equilibrium potential ( $E_{Cl}$ ) but the shift of equilibrium potential was not enough to match to the theoretical equilibrium potential shift. In the presence of L-type $Ca^{2+}$ channel blocker, nifedipine 1 uM, inward tail currents were greatly reduced but the outward current tail currents were still remained. In the presence of N $a^{+}$-C $a^{2+}$ exchange current blocker, 10 uM KB-R7943, the inward and outward tail currents were blocked almost completely. We tried to test the $Ca^{2+}$sensitivity of the chloride current with various [C $a^{2+}$]$_{i}$ in pipette solution from 100 nM to 1 uM but we failed to activate $Ca^{2＋}$-activated chloride currents even though the cell became contracted in the presence of 1 uM $Ca^{2+}$. From these results, we could conclude that the increase of [C $a^{2+}$]$_{i}$ to activate the outward $Ca^{2+}$-activated chloride current was mainly induced by the activation of the reverse mode of N $a^{+}$-C $a^{2+}$ exchanger, But for the increase of [C $a^{2+}$]$_{i}$ to activate the inward tail current, L-type $Ca^{2+}$ current may be the major provoking current. Since the cytosolic increase of [C $a^{2+}$]$_{i}$ through pipette solution have failed to activate $Ca^{2+}$-activated chloride current, this chloride current may have very low $Ca^{2+}$ sensitivity or a comparmental increase $Ca^{2+}$ such as in subsarcolemmal space may activate the chloride current. Since there are several reports and models that the increase of $Ca^{2+}$ in subsarcolemmal space would be over several to tens of uM, both possibility may be valid together.uM, both possibility may be valid together.

• 핵의학기술
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• 제23권2호
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• pp.38-42
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• 2019

관상동맥 석회화 검사에 컴퓨터단층촬영(Comtuted tomography, CT)을 사용하지만 고위험군인 미세석회화 감별에는 어려움이 있다. $^{18}F$-sodium fluoride ($^{18}F-NaF$)가 미세석회화를 진단하는데 매우 유용하다는 연구가 해외에서 보고되고 있다. 본 논문에서는 $^{18}F-NaF$ PET 영상으로 석회화를 정량평가 하고 그 유용성을 알아보고자 한다. 환자는 총 45명($67.1{\pm}6.9$세)으로 $^{18}F-NaF$을 250 MBq 주입하고 1시간 뒤 30분간 영상을 획득하였다. 장비는 Discovery 710 (GE Healthcare, MI, USA)을 사용하였으며 모든 환자는 PET 검사 전 혈관조영CT (CTAngiography, CTA)를 촬영 하였다. 석회화의 SUVmax를 측정하고 좌심방의 배후방사능을 측정하여 Target to Background (TBR) 구한 뒤 정량 분석하였다. ROC 곡선(Receiver Operating Characteristic Curve)을 통하여 고위험군을 분류하였다. 융합영상에서 관상동맥 석회화는 226개로 나왔으며 SUVmax는 $1.15{\pm}0.39$으로 나왔다. 28명(62%)에서 58개가 고위험군으로(TBR>1.25)분류 되었다. 나머지 168개는 $TBR{\leq}1.25$로 나왔다. $^{18}F-NaF$ PET 영상으로 미세석회화의 정량평가가 가능하였고 고위험군을 분류할 수 있었다. 혈관조영CT와 $^{18}F-NaF$ PET을 병행한다면 위험도가 높은 미세석회화를 조기 진단하는 새로운 영상 진단법이 될 수 있을 것으로 사료된다.