• 건강소식
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• v.31 no.10 s.347
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• pp.30-31
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• 2007

임신중독증에 대한 원인은 아직 확실히 밝혀지지 않았다. 유전적∙인종적인 요인이 많이 작용한다는 설도 있고 칼슘이 부족하여 일어난다는 설도 있다. 또는 태반 조직에 대한 면역 작용 때문이라는 설도 있다. 근본적인 원인이 무엇이든 결과적으로 임신중독증이 생기는 의학적 이유는 혈관 수축으로 인한 것으로 말초혈관 수축에 의해 고혈압이 발생하고 신장혈관 수축에 의한 신장 손상으로 단백뇨가 생기고 이차적으로 그것이 원인이 되어 부종이 생기는 것이다. 임신중독증에 대한 원인은 아직 확실히 밝혀지지 않았다. 유전적∙인종적인 요인이 많이 작용한다는 설도 있고 칼슘이 부족하여 일어난다는 설도 있다. 또는 태반 조직에 대한 면역 작용 때문이라는 설도 있다. 근본적인 원인이 무엇이든 결과적으로 임신중독증이 생기는 의학적 이유는 혈관 수축으로 인한 것으로 말초혈관 수축에 의해 고혈압이 발생하고 신장혈관 수축에 의한 신장 손상으로 단백뇨가 생기고 이차적으로 그것이 원인이 되어 부종이 생기는 것이다.

• Journal of Chest Surgery
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• v.41 no.5
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• pp.541-549
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• 2008

Background: Vasoconstrictor-induced reduction in arterial graft diameter can cause significant flow deprivation. The aim of this study was to evaluate the effect of vasodilator pretreatment on vasoconstrictor-induced blood vessel spasm in vitro. Material and Method: Rabbit brachial arteries (BA) and celiac arteries (CA) were cut into rings $(3{\sim}4mm)$ and suspended with a force displacement transducer (TSD $125C^{(R)}$, Biopac Inc. USA) in a tissue bath filled with 5 mL modified Krebs solution bubbled with 5% $CO_2$ and 95% $O_2\;at\;38^{\circ}C$. The rings were contracted with vasoconstrictors, and the developed tension changes were considered control values. The rings were then pre- treated with $30{\mu}M$ nitroglycerin, nicardipine, verapamil, and papaverine, respectively, for 40 minutes and rinsed with the physiologic buffered salt solution three times every 15 min. The vasoconstrictor-induced tension changes after the previous procedure were considered experimental values. Data are expressed as the percentage tension induced by vasoconstrictors before and after pretreatment with vasodilators. Result: Nicardipine depressed vasoconstriction induced by norepinephrine, angiotensin II (All), and U46619 in both the BA and the CA more significantly than did nitroglycerin (p<0.01) and verapamil (p<0.05). Verapamil depressed vasoconstriction induced by 5-hydroxytryptamine (5HT), All, and U46619 in the BA and by 5HT in the CA more significantly than did nitroglycerin (p<0.01). Conclusion: These findings suggest that both nicardipine and verapamil effectively depressed vasoconstrictor action. Nicardipine is thought to be more effective than verapamil for the prevention of vasoconstrictor action.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.345-355
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• 2010

Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.

• Journal of Industrial Convergence
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• v.20 no.7
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• pp.131-137
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• 2022

In the study, we endeavored to assess the convergence effect of Silybum marianum-derived silymarin and epidemiologically-correlated alcohol intake on vascular contractility and to determine the mechanism involved. There were few reports addressing the question whether thin or thick filament modulation is included in ethanol and silymarin-induced regulation. We hypothesized that ethanol at a low concentration and silymarin play a role in agonist-dependent regulation of vascular contractility. Denuded arterial muscles of Sprague-Dawley male rats were suspended in organ baths and isometric tensions were transduced and recorded using isometric transducers and an automatic data acquisition system. Interestingly, both silymarin and ethanol didn't encourage silymarin alone-induced inhibition in agonists-induced contraction suggesting that endothelial nitric oxide synthesis might be involved in ethanol or silymarin-induced modulation of vascular contractility and additional pathways besides endothelial nitric oxide synthesis such as ROCK inactivation might be involved in the silymarin-induced modulation of vascular contractility.

• Journal of Convergence for Information Technology
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• v.12 no.4
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• pp.119-125
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• 2022

In the study, we endeavored to investigate the effect of phenylephrine, isoprenaline and prazosin on the tissue-specific vascular contractility and to determine the mechanism involved. There were few reports addressing the question whether thin or thick filament modulation is included in phenylephrine, isoprenaline and prazosin-induced regulation. We hypothesized that isoprenaline and prazosin play a role in tissue-dependent regulation of vascular contractility. Denuded arterial muscles of Sprague-Dawley male rats were suspended in organ baths and isometric tensions were transduced and recorded using isometric transducers and an automatic data acquisition system. Interestingly, sustained continuous contraction of thoracic and abdominal aorta. Furthermore, isoprenaline and prazosin together with phenylephrine inhibited transiently and persistently vasoconstriction of thoracic and abdominal aorta suggesting that additional mechanisms (e.g. decreased receptor density, chemical interaction, postreceptor signaling or distribution of agonists) might be included in the modulation of vascular contractility.

• Korean Journal of Ichthyology
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• v.12 no.1
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• pp.38-45
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• 2000

Depending on the fish species the vascular tone is distinctively regulated by numerous vasoactive substances. In most fish species the regulatory role of autonomic neurotransmitters and other vasoactive substances are not well defined. This research was designed to delineate the regulatory role of various endogenous autonomic neurotransmitters known to be important in mammalian vascular systems on isolated Israeli carp ventral aorta. Acetylcholine(ACh) contracted the aorta regardless of the pre-existing level of vascular tone, and the contraction was almost completely abolished by a cholinergic-muscarinic antagonist atropine. Endogenous, multiple receptor ($\alpha$ and $\beta$)-acting adrenergic agonist epinephrine (Epi) relaxed the vessel in the presence and absence of the pre-existing tones. Another endogenous multiple receptoracting agonist norepinephrine (NE) weakly contracted the aorta in non-preconstrcted state, but the response was reversed to relaxation when preconstricted. Isoproterenol, ${\alpha}\;{\beta}$ adrenergic receptor agonist, was a potent vasodilator whereas an ${\alpha}_1$ agonist phenyephrine was a contractor. The ${\alpha}_2$ adrenergic receptor agonist clonidine has not any significant effect in altering the vascular tone. The vasorelaxing action of Epi, NE and isoproterenol was significantly attenuated by $\beta$ receptor antagonist propranolol. These results imply that ACh may primarily play a contractor role via muscarinic receptor activation while adrenergic agonists, Epi and NE, are relaxants through activation of $\beta$ adrenergic receptors in vivo.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.04a
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• pp.86-86
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• 1993

혈관근의 수축 또는 이완 반응에서 $Na^{＋}$/Ca$^{2＋}$ exchange계의 역할을 알아보고자 먼저 가토와 흰쥐 흉부 대동맥에서 수축과 이완 반응을 검색하고 이때의 혈관 이완 반응을 증개하는 cAMP와 cGMP농도를 측정하였다. 내피세포가 존재한 표본에서 acetylcholine은 norepinephrine 수축 반응을 이완시켰고 이완 반응은 methylene blue로 소실되었으며 isoproterenol과 nitroprusside는 내피 존재와 제거 양표본에서 이완 반응을 일으켰으며 이때 isoproterenol은 CAMP농도를, nitroprusside는 cGMP농도를 증가시켰다.

• Journal of fish pathology
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• v.9 no.1
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• pp.41-51
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• 1996

The present study was undertaken to investigate the physiological characteristics of the adrenergic responses in the tilapia dorsal aorta. Epinephrine, norepinephrine, clonidine and methoxamine in the presence of propranolol($3{\times}10^{-6}$M), induced only endothelium-independent and concentration-dependent vasocontractions in tilapia dorsal aorta. The rank order of potency of adrenergic agonists inducing vasocontraction was epinephrine>norepinephrine>phenylephrine>clonidine>ethoxamine, Yohimbine produced a parallel shift of the concentration-vascontraction curves of epinephrine, norepinephrine, phenylephrine and clonidine to the right, while prazosin depressed the maximum responses of epinephrine and norepinephrine. Calcium-free physiological solution and verapamil markedly reduced epinephrine or norepinephrine-induced vasocontractions. These results suggest that a-adrenergic agonists produce only on endothelium-inedpenent casoconstrictions in tilapia dorsal aorta and these effect of a-adrenergic agonists, which might be associated with both calcium release from intracellular stores and calcium influx through voltage-dependent calcium channel.

• The Korean Journal of Nuclear Medicine
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• v.35 no.4
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• pp.241-250
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• 2001

Purpose: Vasospasm is a complication of aneurysmal subarachnoid hemorrhage (aSAH). We assessed the role of acetazolamide-enhanced brain perfusion SPECT (ACZ-SPECT) with Tc-99m ECD for predicting the prognosis of patients with aSAH. Materials and methods: Two SPECT studios (baseline with 740 MBq and ACZ-SPECT with 1480 MBq) with image subtraction were performed in 21 patients with aSAH. All patients had brain CT and angiogram. Vasoreactivity on ACZ-SPECT, perfusion defect on baseline SPECT, and vasospasm on angiogram were correlated with Hunt-Hess grading, extent of SAH (unilateral or bilateral) on CT, and clinical outcome. Vasoreactivity was considered decreased when cerebral/cerebellar uptake ratio difference from baseline SPECT to ACZ-SPECT was greater than 2SD of normal control values. Results: Decreased vasoreactivity was observed in 38% (8/21), perfusion defect in 81% (17/21), and vasospasm in 38% (8/21). The preserved vasoreactivity group showed better outcome scale (92%, 12/13) and the decreased vasoreactivity group showed poorer outcome scale (62.5%, 5/8) (p=0.014). Extensive SAH was more frequently seen in the decreased vasoreactlvlty group (87.5%, 7/8) than in the preserved vasoreactivity group (30.7%, 4/13)(p=0.017). The perfusion defect and vasospasm did not show good correlation with outcome scale, extent of SAH, and Hunt-Hess grading (p=ns). Vasoreactivity represented the patient's outcome better than the vasospasm in all of the vasoreactivity/vasospasm-mismatched cases (6 cases). Conclusions: Our data show that decreased vasoreactivity on ACZ-SPECT does not always represent vasospastic condition. But patients with decreased vasoreactivity reveal poorer outcome than patients with angiographic vasospasm do. Therefore ACZ-SPECT is a valuable, noninvasive test for predicting the prognosis of patients with aSAH.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.289-289
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• 1994

흰쥐 적출 대동맥을 이용하여 혈관근의 $Na^{+}$/$Ca^{2+}$ 교환계의 기능과 성질을 구명코자 $Na^{+}$/$Ca^{2+}$ 교환계를 통한 수축 반응을 관찰하고 이때의 조직내 $Ca^{2+}$ 농도, cGMP 농도 및 이 수축에 대한 차단제와 저산소 처리의 영향을 조사하였다. 흰쥐 적출 대동맥은 $Na^{+}$ free 영양액하에서 수축반응을 일으켰고 이 수축 반응 ($Na^{+}$ free 수축반응)은 KCl 농도 증가에 비례하여 증가하였다. KCI 21.6mM 하의 $Na^{+}$ free유발 수축반응은 amiloride전처리하에서 용량-의존성으로 억제되었고 특히 tonic 수축반응이 예민하게 소실되었으며, benzamil과 verapamil 전처리하에서도 유의하게 억제되었다.