• Journal of Digestive Cancer Research
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• v.5 no.1
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• pp.58-61
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• 2017

5-Fluorouracil (5-FU) has been widely used in the treatment of various solid tumors. However, 5-FU cardiotoxicity is being reported with increasing frequency. The main symptom of cardiotoxicity is chest pain at rest with ischemic electrocardiographic changes. Up until now, the underlying mechanism has been suspected to be coronary artery spasm. However, this chest pain associated with 5-FU has several characteristics that are incompatible with coronary artery spasm; eg, inefficacy of calcium-channel blocker and a slow increase in cardiac enzyme levels. We experienced a case of 5-FU-induced cardiotoxicity which showed clinical findings consistent with acute myocardial infarction. Based on the clinical findings, coronary angiography, and no stenosis was noted. However, we concluded that the cardiotoxicity in this case was due to ischemia caused by coronary artery spasm. Because vasodilatator was effective and secondary attack was followed.

• The Korean Journal of Physiology
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• v.26 no.2
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• pp.123-128
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• 1992

The present study was undertaken to examine if endogenous nitric oxide is partly responsible for the high calcium induced vasorelaxation in vitro. Isolated porcine coronary arterial rings were suspended in the tissue chamber and their changes in isometric tension were recorded. KCI little affected the vascular tension in the calcium free media, but subsequent addition of cumulative doses of $CaCl_3$ from 1 to 40 mM caused a contraction followed by complete relaxation. The maximum tension was noted at the calcium concentration in the media of 5 mM, and then the tension progressively declined at 10-40 mM. The relaxation was slightly attenuated in the endothelium-denuded preparation. The relaxation was converted into a contraction by the addition of methylene blue. The relaxation response was not affected in the presence of indomethacin, but was significantly attenuated by $N^w-nitro-L-arginine$ methyl ester pretreatment. These results suggest that the calcium induced vasorelaxation is in part attributable to the release of endogenous nitric oxide.

• Korean Journal of Veterinary Research
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• v.39 no.4
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• pp.702-709
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• 1999

The present study was performed to elucidate the effects of extracellular $Ca^{2+}$ on contractile responses in isolated porcine coronary artery ring using by perivascular nerve stimulation (PNS). Especially, the study was focused on the source of $Ca^{2+}$ on $P_{2X}$-purinoceptor mediated muscle contraction which one of $P_2$-purinoceptor subtypes. The following results can be drawn from these studies : 1. The phasic contractions induced by PNS were inhibited with muscarinic receptor antagonist, atropine ($10^{-6}M$). 2. The phasic contractions induced by PNS were significantly inhibited by sequential treatment with atropine and adrenergic neural blocker, guanethidine ($10^{-6}M$). 3. The phasic contractions induced by PNS were inhibited with $P_{2X}$-purinoceptor desensitization by repetitive application of $\alpha$,$\beta$-Me ATP ($10^{-4}M$). 4. The phasic contractions induced by PNS were so weakened in calcium-free medium. 5. The phasic contractions induced by PNS were inhibited with calcium channel blocker, verapamil ($10^{-6}{\sim}5{\times}10^{-6}M$). 6. The phasic contractions induced by PNS on pretreated with verapamil ($10^{-6}{\sim}5{\times}10^{-6}M$) were not changed by $\alpha$,$\beta$-Me ATP ($10^{-4}M$). These results demonstrate that the neurogenic phasic contractions induced by PNS are due to adrenergic-, cholinergic- and $P_{2X}$-purinergic receptors and the origin of $Ca^{2+}$ on $P_{2X}$-purinoceptor mediated muscle contraction is extracellular $Ca^{2+}$ through plasmalemmal $Ca^{2+}$ channels.

• The Korean Journal of Physiology
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• v.26 no.1
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• pp.45-54
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• 1992

Effects of pH, $PCO_2$, and adenosine on the vascular contractility were investigated in the pig coronary arteries. The helical strips of isolated coronary arteries were immersed in the HEPES or $HCO_3^-/CO_2$-buffered Tyrode's solution equilibrated with 100% $O_2\;or\;95%\;O_2-5%\;CO_2\;at\;35^{\circ}C$. The contraction was recorded isometrically using a force transducer. The amplitudes of contraction induced by ACh, high $K^+$, and electrical Held stimulation (EFS) were decreased by elevating extracellular pH (pHo) and were increased by lowering pHo. A shift from $0%\;CO_2\;to\;5%\;CO_2$ at constant pHo (pH 7.4) reduced the contractions induced by ACh, high $K^+$, EFS. However the contraction induced by 100mM $K^+$ was less influenced by the change of pHo or $CO_2$. The contraction induced by ACh in $Ca^{2+}$free Tyrode's solution as well as the contraction developed by the addition of extracellular of $Ca^{2+}$ were decreased by lowering pHo and were increased by elevating pHo. High $K^+$ (25mM) induced contraction at pH 6.8 was not returned to the level of the contraction at pH 7.4 by the elevation of extracellular. calcium $[Ca^{2+}]_o$. Adenosine-induced relaxation was more significant with 5% $CO_2$ than 0% $CO_2$ in the high $K^+$-induced contraction and was more significant with low pHo than high pHo in the contraction induced by EFS. From the above results, it is suggested that $H^+$ and $CO_2$ inhibit $Ca^{2+}$ influx as well as $Ca^{2+}$ release from intracellular $Ca^{2+}$ storage sites and enhance the relaxing effect of adenosine in the pig coronary artery.

• Journal of the Korean Society of Radiology
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• v.10 no.4
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• pp.285-290
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• 2016

The purpose of our study was to retrospectively evaluate the cause of a decreased calcium score of follow-up studies on coronary artery calcium scores (CACs) computed tomography (CT). The subjects were healthy 100 people(85 males $60.6{\pm}6.9$ years, 15 females $67.2{\pm}7.3$ years). The subjects decreased CACs were divided into 4 subgroups depending on Agatston classification, minimal (1-10), mild (11-100), moderate (101-400), severe (400<). As a result of decreased CACs were scan location disagreement 51%, motion artifact 26%, equipment changes 14%, operator mistakes 5%, input miss 2%, image loss 1%, arrhythmia 1%. In the mild group, the most common decreased CACs were 49 people. In the minimal group, the most significant variation reduction has occurred to 6 people. Scan location disagreement was considered a partial volume effects due to the scan starting position. It showed less than 100 CACs a high variation (19.7%) in more than 100 CACs, a lower variation (2.2%), these could be seen that the variation range is different that can be tolerated according to the calcification score. Motion artifact factor was found in 26%, which is so closely related to the preceding tests that affect the higher heart rate like this pulmonary function test, exercise stress test.

• Journal of the Korean Society of Radiology
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• v.83 no.1
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• pp.54-69
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• 2022

Early detection of potential asymptomatic coronary artery disease is very important, as patients with sudden cardiac death often do not show symptoms such as chest pain or motor dyspnea. Coronary CT angiography (CCTA) has long been unjustified as a screening tool for asymptomatic patients because of the risks posed by radiation exposure. However, there are still various opinions regarding the usefulness of CCTA for screening for coronary artery disease (CAD) in asymptomatic healthy individuals or patients. This review investigated the usefulness of coronary artery calcium score and CCTA as screening tests for CAD in asymptomatic healthy individuals or patients through various literature reviews. With the development of CT technology, recent studies have been conducted in asymptomatic CAD patients with a reduced radiation dose of less than 1 mSv. A total of 2.6% of asymptomatic subjects on CCTA found significant CAD over 70%, and it was concluded that screening CCTA for CAD showed prognostic power in predicting the future occurrence of CAD in asymptomatic people. However, after the completion of the current NIH SCOT-HEART 2 study, it may be possible to determine whether CCTA is appropriate as a screening tool for CAD in asymptomatic healthy individuals.

• Biomolecules & Therapeutics
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• v.5 no.3
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• pp.239-245
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• 1997

Trimetoquinol (TMQ) and its analogs are known to have thromboxane $A_2$ antagonistic action. We also reported that GS389, chemically similar to TMQ, has competitive antagonistic action in rat aorta and human platelets. In the present study, we investigated the pharmacological characteristics of GS283 and GS 386, analogs of GS389, using vascular smooth muscle, human platelets and rat brain homogenates. In isolated pig coronary artery (PCA), both of GS283 and GS386 relaxed U46619-contracted rings in concentration dependent manner. Pretreatment with several concentrations of GS283 and GS386 shifted the dose-response curves to the right, and reduced of maximum contration dose-dependently. Furthermore, GS283 and GS386 strongly inhibited $Ca^{2+}$ -induced contraction in the PCA. In human platelets, U46619- and A23187-induced platelet aggregation was inhibited by GS283 and GS386, concentration-dependently. Anti-platelet aggregation was related to the compound\`s ability to inhibit ATP release at each stimulation. In rat brain homogenates, receptor-binding assay resulted that both GS283 and GS386 have a relative affinity to $\alpha$-adrenergic receptor. Taken together. we concluded that the mechamism of action of GS283 and GS86 is not related with in TXA$_2$ receptor but concerned with calcium antagonistic action and a-blocking action.n.

• Korean Journal of Radiology
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• v.24 no.4
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• pp.284-293
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• 2023

Objective: To validate a simplified ordinal scoring method, referred to as modified length-based grading, for assessing coronary artery calcium (CAC) severity on non-electrocardiogram (ECG)-gated chest computed tomography (CT). Materials and Methods: This retrospective study enrolled 120 patients (mean age ± standard deviation [SD], 63.1 ± 14.5 years; male, 64) who underwent both non-ECG-gated chest CT and ECG-gated cardiac CT between January 2011 and December 2021. Six radiologists independently assessed CAC severity on chest CT using two scoring methods (visual assessment and modified length-based grading) and categorized the results as none, mild, moderate, or severe. The CAC category on cardiac CT assessed using the Agatston score was used as the reference standard. Agreement among the six observers for CAC category classification was assessed using Fleiss kappa statistics. Agreement between CAC categories on chest CT obtained using either method and the Agatston score categories on cardiac CT was assessed using Cohen's kappa. The time taken to evaluate CAC grading was compared between the observers and two grading methods. Results: For differentiation of the four CAC categories, interobserver agreement was moderate for visual assessment (Fleiss kappa, 0.553 [95% confidence interval {CI}: 0.496-0.610]) and good for modified length-based grading (Fleiss kappa, 0.695 [95% CI: 0.636-0.754]). The modified length-based grading demonstrated better agreement with the reference standard categorization with cardiac CT than visual assessment (Cohen's kappa, 0.565 [95% CI: 0.511-0.619 for visual assessment vs. 0.695 [95% CI: 0.638-0.752] for modified length-based grading). The overall time for evaluating CAC grading was slightly shorter in visual assessment (mean ± SD, 41.8 ± 38.9 s) than in modified length-based grading (43.5 ± 33.2 s) (P < 0.001). Conclusion: The modified length-based grading worked well for evaluating CAC on non-ECG-gated chest CT with better interobserver agreement and agreement with cardiac CT than visual assessment.

• YAKHAK HOEJI
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• v.33 no.3
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• pp.167-174
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• 1989

KR-1008 and KR-30006 are 1,4-dihydropyridine derivatives, new vasodilatory calcium antagonists from KRICT. Calcium antagonistic properties of the compounds were studied in the isolated heart (Langendorff preparation), pulmonary artery (vasodilation), and in the papillary muscle (negative inotropic effect) of the guinea pig. Antihypertensive effect were also investigated after i.v. or oral administration in the SHR (spontaneously hypertensive rat). They produced a sigificant inhibition of Ca-induced contraction in the guinea pig pulmonary artery at the concentrations of above $10^{-8}M$. The negative inotropic effect of the electrically stimulated papillary muscle appeared from the concentration of $10^{-6}M$, which is about hundred times higer than the concentration of vasodilation effect. Left ventricular pressure also decreased from the concentration of $3\;{\times}\;10^{-6}M$ in KR-1008 and KR-3006 in the Langendorff heart preparations. Coronary flow rate increased from $10^{-6}M$ in KR-1008 and nicardipine and appeared no change in KR-30006. The antihypertensive effect of KR-1008 (EC 20: $2.9\;{\mu}g/kg$) was potent more than nicardipine (EC 20: $3.4\;{\mu}g/kg$) and than Kr-30006 (EC 20: $6.8\;{\mu}g/kg$) was, after i.v. bolus injection in the anesthetized SHR. The antihypertensive effect in the conscious SHR appeared 30 minutes after oral administration of 10 mg/kg and persisted 4 hrs in KR-1008 and 12 hrs in KR-30006. Heart rate tended to increase for 0.5-1 hr after oral administration of the test compounds.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.93-101
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• 1988

Pharmacological actions of an antispasmodic agent, oxybutynin were investigated in the isolated procine coronary arteries. The coronary rings were contracted by acetylcholine (ACh) and KCl in a dose-dependent fashion. The ACh-induced contractions were signifcantly potentiated by removal of endothelium and $EC_{50}=0.52\;{\mu}M$ of intact endothelial rings was about 2 times greater than $EC_{50}=0.28\;{\mu}M$ of rings without the endothelium. These results suggest that the endothelium plays an inhibitory role in ACh-induced contraction. Oxybutynin and atropine inhibited dose-dependently $1.0\;{\mu}M$ ACh-induced contraction and atropine inhibited dose-dependently $1.0\;{\mu}M$ ACh-induced contraction and the $IC_{50s}$ were 11.0 nM and 0.47 nM, respectively. Atropine did not affect 35 mM KCl-induced contraction but oxybutynin inhibited the contraction to the basal tension in a dose-dependent manner. The $IC_{50}$ of oxybutynin on the KCl-induced contraction was $49.7\;{\mu}M$. The dose-response curve to ACh was parallelly shifted to the right by pretreating coronary rings with $IC_{50}$ of atropine (0.47 nM) or oxybutynin (11.0 nM) but the curve to KC1 was rightward shifted in a noncompetitive manner under pretreatment with $IC_{50}$ of oxybutynin $(49.7\;{\mu}M$). Oxybutynin inhibited $0.1\;{\mu}M$ Bay K 8644-induced contraction to the basal tension in a dose dependent manner, but $35\;{\mu}M$ histamine-induced contraction was inhibited to only 50e/e of the original level even in maximal concentration $(5{\times}10^{-4}M)$ of oxybutynin. These results suggest that oxybutynin causes antispasmodic action through sensitive blocking action on muscarinic receptors and inhibitory action on calcium influx in the procine coronary artery.