• 한국의류학회지
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• 제22권7호
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• pp.826-832
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• 1998

In order to understand the influences of wearing clothings with different thermal insula-tions when men were exposed from $25^{\circ}C$ environment to 18$^{\circ}C$ environment, thermoregulatory responses were measured on 4 healthy female college students. Subjects rested wearing T-shirts, trousers, and socks called LC(total weight 541g) at 25$\pm$1$^{\circ}C$, 50$\pm$5% R.H. and then exposed to the room conditioned in 18$\pm$1$^{\circ}C$, 50$\pm$5$^{\circ}C$ R.H. with LC as it was(LC Type) or with T-shirts, trousers, socks, training wear upper garment, the training wear lower garment called HC (total weight 1368g)(HC Type) for 120 min. The results can be summarized as follows: 1) When subjects were exposed from $25^{\circ}C$ environment to 18$^{\circ}C$ environment, decrease of rectal temperature was significantly smaller in LC Type than in HC Type. 2)Increase of heat production and weight loss had no significant difference between two types of clothing. 3)Internal thermal conductance was higher in HC Type and external thermal conductance was higher in LC Type. Therefore total thermal conductance was higher in LC Type than in HC Type. 4)Decrease of skin temperature was greater in LC Type than in HC Type. 5)Subjects felt colder with LC Type than with HC Type, but did not feel differently in comfort sensation between two types of clothing. It was suggested that less decrease of rectal temperature in LC type inspite of more dry heat loss from body might be ascribed to a shift of blood from the shell area to the core area originating in the vasoconstriction and the lowered internal thermal conductance. In conclu-sion, the importance of the state of internal heat distribution in the homeostasis seemed to be reaffirmed.

• The Korean Journal of Pain
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• 제9권1호
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• pp.46-56
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• 1996

Many surgeons and anesthesiologists prefer using vasoconstrictor mixed with local anesthetic agent to reduce the incidence of side effects and prolong the duration of analgesia because most local anesthetic agents, except cocaine, were believed to possess vasodilating effect. However, some investigators recently reported vasoconstricting effect of local anesthetic agents. There is still controversy on the vasoactive effect of local anesthetic agents. So this study is aimed to clarify the vasoactive effect of local anesthetics in the animal model resembling clinical settings. Rabbits were anesthesized with ketamine and haloghane, and respirations were controlled with Harvard animal ventilator. Lidocaine (0.5%, 1.0%, 1.5%) and bupivacaine (0.125%, 0.25% and 0.5%) with or without 1:100,000 epinephrine were subdermaly injected on the femoral bupivacaine of the femoral artery were measured with Doppler flow meter in vivo. The mean arterial pressure, pulse rate, arterial blood gases, pH and level of serum electrolytes were measured at every 2 minute interval for 30 minutes. Results were as follows: 1) There was no significant vasoconstriction with 0.5% lidocaine and 0.125% bupivacaine. 2) Statistically significant (p<0.05) vasodilations were observed with lidocaine (1.0~2.0%) and bupivacaine (0.25~0.5%). 3) There were no changes on the duration of vasodilation induced by local anesthetic agents of various concentrations. 4) Onset of vasodilation induced by local anesthetic agents of high concentration were faster than that of lower concentrations. 5) In the mixed injection group of epinephrine and local anesthetic agent, the vasoconstriction induced by epinephrine was completely reversed by local anesthetics, approximately 5 minutes later. In conclusion, local anesthetic agents at dose exceeding 1.0% lidocaine and 0.25% bupivacaine increase local blood flow significantly in animal study in vivo which is applicable in human clinical settings. The increase blood flow may be due to dilatation of blood vessel. Further study on the analysis of association between amount of absorbed local anesthetics in blood vessels and dilatation of blood vessels is needed.

• 한국응급구조학회지
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• 제23권3호
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• pp.165-173
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• 2019

Purpose: Norepinephrine (NE) is a neurotransmitter of the sympathetic nervous system. It is used for treating hypotension on distributive shock, central nervous system injury, or sepsis. There are several reports that state that alcohol suppresses vasoconstriction by NE. Thus, our hypothesis is that the effect of NE is reduced in alcohol-drinking patients with distributive shock. We investigated whether alcohol suppresses NE-induced contraction and aimed at finding a solution to this problem. Methods: For this study, we used the aorta from male Sprague-Dawley rats (9-11 weeks) and an isometric contraction system. Results: Our results showed that alcohol suppresses NE contraction and does not affect epinephrine induced a contraction. Moreover, in the presence of alcohol, a 7:3 mixture of NE and epinephrine induced a contractile force similar to that induced by NE under normal conditions. Conclusion: We found that the vasoconstrictive force of NE decreased in the blood vessels in which alcohol was present, which was not because endothelial cells. The reduced contractile force was most similar to that induced by a 7:3 mixture of NE and epinephrine.

• Experimental and Molecular Medicine
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• 제50권12호
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• pp.11.1-11.9
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• 2018

Estrogen has diverse effects on cardiovascular function, including regulation of the contractile response to vasoactive substances such as serotonin. The serotonin system recently emerged as an important player in the regulation of vascular tone in humans. However, hyperreactivity to serotonin appears to be a critical factor for the pathophysiology of hypertension. In this study, we examined the modulatory mechanisms of estrogen in serotonin-induced vasoconstriction by using a combinatory approach of isometric tension measurements, molecular biology, and patch-clamp techniques. $17{\beta}$-Estradiol (E2) elicited a significant and concentration-dependent relaxation of serotonin-induced contraction in deendothelialized aortic strips isolated from male rats. E2 triggered a relaxation of serotonin-induced contraction even in the presence of tamoxifen, an estrogen receptor antagonist, suggesting that E2-induced changes are not mediated by estrogen receptor. Patch-clamp studies in rat arterial myocytes showed that E2 prevented Kv channel inhibition induced by serotonin. Serotonin increased Src activation in arterial smooth muscle required for contraction, which was significantly inhibited by E2. The estrogen receptor-independent inhibition of Src by E2 was confirmed in HEK293T cells that do not express estrogen receptor. Taken together, these results suggest that estrogen exerts vasodilatory effects on serotonin-precontracted arteries via Src, implying a critical role for estrogen in the prevention of vascular hyperreactivity to serotonin.

• 융합정보논문지
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• 제12권4호
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• pp.119-125
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• 2022

심혈관계 활성이 예측되는 phenylephrine, isoprenaline, prazosin의 단독 및 병용 투여에서 혈관수축 억제능을 관찰하였고 아직 보고가 빈약한 수축성 조절 기전에 대해 조직 선택적 조절 가설을 세워서 조사하였다. 내피가 손상된 혈관을 수조내에 현수시켰고 혈관에 의한 기계적 신호가 등장력 변환기에서 전기적 신호로 변환되어 생리측정기에 표시되었다. 내피가 손상된 혈관에서 phenylephrine은 조직에 비선택적으로 지속적인 수축을 유지하였고 phenylephrine과 병용된 isoprenaline은 등척성 수축 실험에서 흉부, 복부 대동맥 등 조직에 비선택적으로 평활근에 대한 직접 작용으로 수축성을 일시적으로 감소시켰고 phenylephrine과 병용된 prazosin은 조직에 비선택적으로 평활근에 대한 직접 작용으로 수축성을 지속적으로 감소시켰다. 따라서 일부 조직에서 adrenergic beta receptor 밀도가 감소되거나 수용체 결합력이 감소되거나 수용체 결합 후 신호전달이 감소되거나 약물의 분포가 감소되어 isoprenaline이 phenylephrine의 지속적 작용에 대해 일시적으로 억제하고 prazosin이 지속적으로 억제하는 것으로 생각된다.

• Tuberculosis and Respiratory Diseases
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• 제41권3호
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• pp.231-238
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• 1994

연구배경: 저산소증에 의한 폐동맥수축의 기전은 저산소증 자체가 폐혈관 평활근에 직접 작용하여 수축을 유발한다는 것과, 저산소증에 의해 조직으로 부터 여러 매개물질이 유리되어 혈관평활근을 수축시킨다는 설이 제시되고 있지만 정확히 밝혀져있지 않다. 최근에는 저산소증이 EDRF의 생성을 억제하여 혈관수축을 유발시킨다고하여 관심이 되고 있다. 본 연구에서는 흰쥐 폐동맥에서 내피세포 의존형 혈관이완을 조사하고, 저산소증에 의한 폐동맥수축에 EDRF의 작용을 조사하였다. 방법 : 300~350g의 수컷 흰쥐(Sprague Dawley)의 폐동맥을 박리하여 길이가 2mm되는 폐동맥고리를 Krebs용액으로 채워져 있으며, 95% $O_2$/5% $CO_2$(산소상태)와 95% $N_2$/5% $CO_2$(저산소상태)가 각각 공급되는 magnus관에서 가는 stainless 갈고리로 고정한 다음 Gilson사의 polygraph에 부착된 isometric transducer(FT.03 Grass, Quincy, USA)에 의해 등장성 수축곡선을 그리도록 장치하였다. 결과: 1) 내피세포가 있는 폐동맥에서 PE($10^{-6}M$)에 의한 혈관수축은 Ach($10^{-9}-10^{-5}M$) 및 SN($10^{-9}-10^{-5}M$)의 농도에 비례해서 이완되어 거의 기초장력까지 이완되었으나, 내피세포를 제거한 폐동맥에서는 Ach($10^{-9}-10^{-5}M$)에 의한 혈관이완은 거의 상실되었다. 2) L-NMMA($10^{-4}M$)으로 전처치한 경우 Ach($10^{-9}-10^{-5}M$)에 의한 혈관이완은 전처치하지 않은 경우보다 의미있게 감소하였다. 3) L-arginine($10^{-4}M$)과 L-NMMA($10^{-4}M$)을 전처치 하였을 경우 Ach($10^{-9}-10^{-5}M$)에 의한 혈관이완은 L-NMMA에 의해 거의 영향을 받지 않았다. 4) PE($10^{-6}M$)에 의한 폐동맥 수축은 산소상태보다 저산소 상태에서 훨씬 강했으며, Ach($10^{-9}-10^{-5}M$)에 의한 혈관이완은 산소상태보다 저산소상태에서 의미있게 감소하였다. 5) L-arginine($10^{-4}M$)을 전처치 하였을 경우 저산소상태에서의 Ach($10^{-9}-10^{-5}M$)에 의한 혈관이완은 산소상태에서의 Ach 에 의한 혈관이완 정도로 회복되었다. 결론: 흰쥐 폐동맥에서 내피세포의존성 혈관이완은 NO가 관여하며, 저산소증에 의한 폐동맥 수축은 내피세포내의 EDRF 생성의 저하와 관련이 있을 것으로 사료된다.

• 약학회지
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• 제58권4호
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• pp.223-228
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• 2014

The present study was undertaken to investigate the influence of sulforaphane on vascular smooth muscle contractility and to determine the mechanism involved. We hypothesized that sulforaphane, the primary ingredient of broccoli of cruciferous vegetables, plays a role in vascular relaxation through inhibition of Rho-kinase in rat aortae. Intact of denuded arterial rings from male Sprague-Dawley rats were used and isometric tensions were recorded using a computerized data acquisition system. Interestingly, sulforaphane significantly inhibited fluoride, phorbol ester or thromboxane $A_2$ mimetic-induced contraction in denuded muscles suggesting that additional pathways different from endothelial nitric oxide synthesis such as inhibition of Rho-kinase or MEK might be involved in the vasorelaxation. Furthermore, sulforaphane inhibited thromboxane $A_2$-induced increases in pERK1/2 levels suggesting the mechanism including inhibition of thromboxane $A_2$-induced increases in ERK1/2 phosphorylation. This study provides evidence that sulforaphane induces vascular relaxation through inhibition of Rho-kinase or MEK in rat aortae.

• 약학회지
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• 제57권5호
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• pp.376-381
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• 2013

The present study was undertaken to investigate the influence of curcumin on vascular smooth muscle contractility and to determine the mechanism involved. We hypothesized that curcumin, the primary ingredient of Curcuma longa, plays a role in vascular relaxation through inhibition of Rho-kinase in rat aortae. Denuded arterial rings from male Sprague-Dawley rats were used and isometric tensions were recorded using a computerized data acquisition system. Interestingly, curcumin inhibited fluoride-induced contraction but didn't inhibit phorbol ester-induced contraction suggesting that additional pathways different from endothelial nitric oxide synthesis might be involved in the vasorelaxation. Furthermore, curcumin significantly inhibited fluoride-induced increases in pMYPT1 levels. On the other hand, it didn't significantly inhibit phorbol ester-induced increases in pERK1/2 levels suggesting the mechanism involving inhibition of fluoride-induced MYPT1 phosphorylation. This study provides evidence that curcumin induces vascular relaxation through inhibition of Rho-kinase in rat aortae.

• Annals of Clinical Neurophysiology
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• 제1권1호
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• pp.55-59
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• 1999

Vasoconstriction of intracerebral arteries is the leading cause of delayed cerebral infarction and mortality following aneurysmal subarachnoid hemorrhage. Transcranial Doppler studies show and increase in the flow velocities of basal cerebral arteries, which usually start around day 4 following a subarachnoid hemorrhage, and peaking by days 7 to 14. Angiographic studies confirm the presence of at least some degree of MCA vasospasm when the flow velocities are higher than 100 cm/sec. Mean velocities in the 120 to 200 cm/sec range correspond to 25 to 50% luminal narrowing. MCA and ACA vsospasm is detected with around 90% specificity. Sensitivity is 80% and 50% respectively. A 200cm/sec threshold and rapid flow velocity increase exceeding 50 cm/sec on consecutive days, has been associated with subsequent infarction. Transcranial Doppler is also used to monitor the effects of endovascular treatment of vasospasm. Flow velocities decrease following successful angioplasty or papaverine infusion. Overall, transcranial Doppler studies are considered to have acceptable accuracy for the evaluation of vasospasm in aneurysmal subarachnoid hemorrhage, with limitations that have to be taken into consideration in the clinical setting.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1996년도 춘계학술대회
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• pp.193-193
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• 1996

Endothelin-1, which is a peptide originally isolated from cultured porcine aortic cell, has been found to play a crucial role in potentiating the vasoconstriction mitogenesis, and chemotaxis. In the present study, we examined the level of endothelin-1 in the brain, spinal cord and blood from rat with experimental allergic encephalomyelitis(EAE). At the peak stage of EAE(grade 3), endothelin-1 level in the spinal cord of rat with EAE increased two folds as compared with that of sham-treated rats, and subsequently decreased to the level of control at the recovery stage. In the endothelin-1 immunocytochemistry, endothelin-1 immunopositive cells and ED-1, macrophage marker immunopositive cells observed in the spinal cord of peak stage(grade 3). These Findings suggest that endothelin-1 play the important role in progression of EAE.