• Journal of Korean Neurosurgical Society
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• v.57 no.1
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• pp.1-5
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• 2015

Objective : Cerebral vessels, such as intracerebral perforating arterioles isolated from rat brain, have been widely used as an ex vivo model to study the cerebrovascular function associated with cerebrovascular disorders and the therapeutic effects of various pharmacological agents. These perforating arterioles, however, have demonstrated differences in the vascular architecture and reactivity compared with a larger leptomeningeal artery which has been commonly implicated in cerebrovascular disease. In this study, therefore, we developed the method for studying cerebrovascular function utilizing the olfactory artery isolated from the mouse brain. Methods : The olfactory artery (OA) was isolated from the C57/BL6 wild-type mouse brain. After removing connective tissues, one side of the isolated vessel segment (approximately $-500{\mu}m$ in length) was cannulated and the opposite end of the vessel was completely sealed while being viewed with an inverted microscope. After verifying the absence of pressure leakage, we examined the vascular reactivity to various vasoactive agents under the fixed intravascular pressure (60 mm Hg). Results : We found that the isolated mouse OAs were able to constrict in response to vasoconstrictors, including KCl, phenylephrine, endothelin-1, and prostaglandin $PGH_2$. Moreover, this isolated vessel demonstrated vasodilation in a dose-dependent manner when vasodilatory agents, acetylcholine and bradykinin, were applied. Conclusion : Our findings suggest that the isolated olfactory artery would provide as a useful ex vivo model to study the molecular and cellular mechanisms of vascular function underlying cerebrovascular disorders and the direct effects of such disease-modifying pathways on cerebrovascular function utilizing pharmacological agents and genetically modified mouse models.

• The Journal of the Korean dental association
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• v.58 no.7
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• pp.404-411
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• 2020

This study reports the unusual complications of 22-year-old male who presented with sudden hearing loss after the right mandibular third molar extraction under local anesthesia with 3.6 ml of 2 % lidocaine. Total 8.75 mg of oral dexamethasone for 1 week immediately after extraction was prescribed in department of oral and maxillofacial surgery but hearing did not improve after 1 week. As referral to otolaryngology, total 600 mg of oral methylon and hyperbaric oxygen therapies were operated for 2 weeks. The hearing of patient was improved at 6 weeks after extraction but tinnitus was persisted even after 12 months. The reason and treatment were discussed with literature review, searching with the keywords ['hearing loss' AND ('dental' OR 'tooth extraction'OR'teeth extraction')] in PubMed and Google scholar at October 2019. Total five cases were reported after tooth extraction with local anesthesia. The sudden hearing loss could be associated with local anesthesia containing vasoconstrictors. Early steroid (extensive medication and intra-tympanic injection) and hyperbaric oxygen therapies were recommended within 2 weeks. As a proper treatment, hearing could be improved but other additional symptoms, such as tinnitus, dizziness, might be remained.

• Archives of Pharmacal Research
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• v.27 no.1
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• pp.111-117
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• 2004

Hepatic microcirculatory failure is a major component of reperfusion injury in the liver. Recent data provided some evidence that endothelium-derived vasoconstrictors and vasodilators may be functionally important to the control of the total hepatic blood flow under these conditions of circulatory failure. Since Kupffer cells provide signals that regulate the hepatic response in ischemia/reperfusion (I/R), the aim of this study was to investigate the role of Kupffer cells in the I/R-induced imbalance of vasoregulatory gene expression. Rats were subjected to 60 min hepatic ischemia, followed by 5 h of reperfusion. The Kupffer cells were inactivated by gadolinium chloride ($GdCl_3$, 7.5 mg/kg body weight, intravenously) 1 day prior to ischemia. Liver samples were obtained 5 hrs after reperfusion for RT-PCR analysis of the mRNA for genes of interest: endothelin-1 (ET-1), its receptors $ET_A and ET_B$, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1). ET-1 mRNA expression was increased by I/R. mRNA levels for $ET_A$ receptors showed no change, whereas $ET_B$ receptor transcripts increased in the I/R group. The increases in ET-1 and $ET_B$ mRNA were not prevented by the $GdCI_3$ pretreatment. The mRNA levels for iNOS and eNOS significantly increased within the I/R group with no significant difference between the I/R group and the $GdCl_3$-treated I/R group. HO-1 mRNA expression significantly increased in the I/R group and this increase was attenuated by $GdCI_3$. In conclusion, we have demonstrated that an imbalance in hepatic vasoregulatory gene expression occurs during I/R. Our findings suggest that the activation of Kupffer cells is not required for I/R-induced hepatic microvascular dysfunction.

• Journal of Dental Anesthesia and Pain Medicine
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• v.21 no.1
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• pp.49-59
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• 2021

Background: To evaluate changes in the effectiveness of phentolamine mesylate in combination with different local anesthetics (LAs) and vasoconstrictors. A prospective randomized double-blind study was conducted with 90 patients divided into three groups, with each group being administered one of three different LAs: lidocaine 2% 1/80,000, articaine 4% 1/200,000, and bupivacaine 0.5% 1/200,000. Methods: We compared treatments administered to the mandible involving a LA blockade of the inferior alveolar nerve. Results were assessed by evaluating reduction in total duration of anesthesia, self-reported patient comfort using the visual analog pain scale, incidence rates of the most common adverse effects, overall patient satisfaction, and patient feedback. Results: The differences among the three groups were highly significant (P < 0.001); time under anesthesia was especially reduced for both the lip and tongue with bupivacaine. The following adverse effects were reported: pain at the site of the anesthetic injection (11.1%), headaches (6.7%), tachycardia (1.1%), and heavy bleeding after treatment (3.3%). The patients' feedback and satisfaction ratings were 100% and 98.9%, respectively. Conclusions: Efficient reversal of LAs is useful in dentistry as it allows patients to return to normal life more readily and avoid common self-injuries sometimes caused by anesthesia. Phentolamine mesylate reduced the duration of anesthesia in the three studied groups, with the highest reduction reported in the bupivacaine group (from 460 min to 230 min for the lip and 270 min for the tongue [P < 0.001]).

• 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.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.135-144
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• 1990

The vascular responses to the vasoactive drugs were evaluated using aortic ring preparations obtained from propylthiouracil (PTU)-treated rats. The body weights and the levels of serum thyroxine $(T{_4})$ and triiodothyronine $(T{_3})$ were significantly decreased in propylthiouracil-treated rats as compared with those in age-matched control rats. The contractile responses to norepinephrine and potassium and calcium ions were significantly attenuated in aortic rings of PTU-treated rats 4 weeks after when compared with those from age-matched control animals. By the PTU treatment, however, the sensitivity to norepinephrine but not to calcium was decreased while the maximal responses to norepinephrine and calcium were reduced together. The attenuated contractile responses to the vasoconstrictors in PTU-treated rats are ascribed to the decreased ability of the muscle cells to contract. On the other hand, the relaxation responses induced by acetylcholine and histamine (endothelium-dependent relaxants) and isoproterenol and sodium nitroprusside (endothelium-independent relaxants) had tendencies to be augmented in aortic rings of PTU-treated rats when compared with those of age-matched control animals. However, the sensitivities to the endothelium-independent relaxants were different between PTU-treated and control rats whereas those to the endothelium-dependent relaxants were not. These results suggest that the altered vascular responsiveness in the PTU-treated rats seems to be due to the alteration of smooth muslce cells rather than the Influence of endothelium, and that this change is slowly progressive after hypothyroidism is evident.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.161-170
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• 1990

The effects of $H^{+}$ on the arterial contraction and their mechanisms were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the HEPES-buffered or $CO_{2}/HCO_{3}^{-}$-buffered Tyrode's solution. The contractions induced by agonists (norepinephrine, histamine, serotonin and angiotensin II) or high $K^{+}$ were observed with change of extracellular or intracellular $H^{+}$ concentration. The contractions induced by norepinephrine, histamine, serotonin, angiotensin II or high $K^{+}$ in HEPES-buffered Tyrode's solution were inhibited by increase in extracellular $H^{+}$ concentration and potentiated by decrease in extracellular $H^{+}$ concentration. The degrees of these effects were most evident in the contraction induced by serotonin and angiotensin II, moderate in those by histamine and high $K^{+}$, and least in those by norepinephrine. Maximal contraction by norepinephrine, histamine and high $K^{+}$ were not influenced by change in extracellular $H^{+}$ concentration, but influenced in those contration by serotonin and angiotensin II. The attenuated contractions by an acidic pH were not returned to the level of contraction at normal pH (7.4) by elevation of extracellular $Ca{2+}$ concentration. The agonists (norepinephrine, histamine and serotonin)-induced contractions in $Ca{2+}$-free Tyrode's solution were also attenuated by increase in extracellular $H^{+}$ concentration and potentiated by decrease in extracellular $H^{+}$ concentration. Elevation of $Pco_{2}$ in the $CO_{2}/HCO_{3}^{-}$-buffered Tyrode's solution, which increase the intracellular $H^{+}$ concentration, at constant extracellular pH (7.4), increased the contraction by 30 mM $K^{+}$. From the above results, it is suggested that the decrease in contractions by increase in extracellular $H^{+}$ concentration may be resulted from that $H^{+}$ make the receptors less sensitive to agonists and cell membrane hyperpolarize and then inhibit the $Ca{2+}$ influx as well as $Ca{2+}$ release from intracellular $Ca{2+}$ storage site.

• The Journal of Internal Korean Medicine
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• v.14 no.1
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• pp.129-138
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• 1993

This report on the $T{\acute{o}}u\;f{\bar{e}}ng$ and Migraine comes to conclude, through the study of the Oriental- Western medical references, as follow; 1. First, $T{\acute{o}}u\;f{\bar{e}}ng$ and Migraine had some concurrencies that both the two symptoms have appeared severe and recurrent headache and more often to the female. 2 Many of them e.g. Sensory disturbance, Vertigo, Nausea, Vomiting, Tinnitus etc. in the prodrome and main symptom of $T{\acute{o}}u\;f{\bar{e}}ng$ and Migraine were identical, especially the symptom of the $f{\bar{e}}ng\;t{\acute{a}}n\;t{\acute{o}}u\;t{\grave{o}}ng$ was similar to the prodrome of the Migraine. We could find out the semilarity of the symptoms through that Migraine is proximately set in unilateral, and $Pi{\bar{a}}nT{\acute{o}}u\;f{\bar{e}}ng$ is so called alias $B{\grave{a}}n\;bi{\bar{a}}n\;t{\acute{o}}u\;t{\grave{o}}ng$. 3. The pathogeny of $T{\acute{o}}u\;f{\bar{e}}ng$ include the case of ‘$f{\bar{e}}ng\;xi{\acute{e}}\;r{\grave{u}}\;n{\bar{a}}o$’, the patient feeling weak condition, $T{\acute{a}}n,\;T{\acute{a}}nshi,\;T{\acute{a}}nhu{\breve{o}},\;Y{\grave{u}}q{\grave{i}}$, etc. and, ‘$t{\acute{a}}n\;zhu{\grave{o}}\;sh{\grave{a}}ng\;y{\acute{a}}o$’, ‘$G{\bar{a}}n\;y{\acute{a}}ng\;hu{\grave{a}}\;f{\bar{e}}ng$’. There were variable that $F{\bar{e}}ng,\;Xu{\grave{e}},\;F{\bar{e}}ngr{\grave{a}},\;F{\bar{e}}ngx{\bar{u}},\;Xu{\grave{e}}x{\bar{u}},\;Hu{\check{o}}$ in the left, and $t{\acute{a}}n,\;R{\grave{e}},\;t{\acute{a}}nr{\grave{e}},\;Qir{\acute{a}}$ in the right partial pathogeny. It was referred $Sh{\grave{a}}o\;y{\acute{a}}ng\;j{\bar{i}}ng$, $Ju{\acute{e}}\;y{\bar{i}}n\;j{\bar{i}}ng$, $Y{\acute{a}}ng\;m{\acute{i}}ng\;j{\bar{i}}ng$, $T{\grave{a}}i\;y{\acute{a}}ng\;j{\bar{i}}ng$ in connection with the Meridian system. And otherwise the primary cause of Migraine is still unknown to us. Heredity is probably important, but the mode of transmission is uncertain. Recently, the important assumption is the vasomotor change caused by vasoconstrictors like that norepinephrine, epinephrine, and serotonin etc.

• Journal of Korean Neurosurgical Society
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• v.29 no.4
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• pp.451-460
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• 2000

Objective : This experiment is aimed at clarifying the characteristics of spasmodic basilar arteries in the rabbits of subarachnoid hemorrhage(SAH) with observation of vascular response to nitric oxide(NO) and endothelin-1. Material and Methods : Seventy-nine New Zealand white rabbits were divided into 4 groups : control(n=17), sham operation(n=13), postictal-2-day(n=25), and postictal-7-day group(n=24). Rabbits in the postictal-2-day group and postictal-7-day group underwent transfemoral vertebral angiography 2 days and 7 days after SAH respectively. A vascular ring of spasmodic basilar artery was harvested and suspended in organ chamber($37^{\circ}C$) to observe isometric tension changes in response to NO and endothelin-1 under both high(95% $O_2$/5% $CO_2$) and low(95% $N_2$/5% $CO_2$) $O_2$ tension. To investigate the vascular response to NO, acetylcholine from $10^{-7}M$ to $3{\times}10^{-4}M$ concentration was applied to basilar artery ring precontracted with histamine $10^{-6}-10^{-5}M$ in the organ chamber. The vascular response to endothelin-1 was observed by applying endothelin-1 from $10^{-11}M$ to $3{\times}10^{-8}M$ concentration into organ chamber. Results : Seven of 15 live rabbits which underwent angiography 2 days after SAH, were confirmed to develop vasospasm($64.3{\pm}11.2%$) whereas seven of 13 live rabbits which underwent angiography 7 days after SAH, were confirmed to develop vasospasm($64.9{\pm}10.9%$). In all groups, hypoxia significantly reduced the vascular relaxation of basilar arteries to NO. However, hypoxia made no influence on the vascular contraction of basilar arteries to endothelin-1 in all groups. In vascular relaxation of basilar arteries to NO under high $O_2$ tension between groups, the maximum relaxation of basilar arteries in the postictal-7-day group was significantly reduced compared to the postictal-2-day group. In vascular contraction of basilar arteries to endothelin-1 under high $O_2$ tension between groups, the maximum contraction of basilar arteries in the postictal-7-day group was significantly reduced compared to the postictal-2-day group. Conclusions : This experiment suggests that the characteristics of vascular response to NO and endothelin-1 in the spasmodic basilar arteries of rabbits observed 2 days after SAH is different from those observed 7 days after SAH.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.203-216
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• 1988

To delineate the mechanisms of vasoconstriction and vasodilation in cerebral arteries the effects of some vasoconstrictors and calcium antagonists on the basilar artery (BA) and arterial circle of Willis (WC) were examined and also the role of endothelium in the action of these drugs was investigated in pigs, cats and rabbits. In pig cerebral arteries, dose-dependent contractile responses were elicited by KCI, histamine, 5-hydroxytryptamine (5-HT) and angiotensin, but norepinephrine (NE), phenylephrine (PE) and epinephrine (EP) elicited dose-dependent contractions only under pretreatment with propranolol 10-6 M. The magnitudes of maximal contractile effects of these drugs were different from each other, and 5-H~ was the largest and angiotensin the smallest. Some calcium antagonists dose-dependently inhibited KCI (35 mM)-induced contraction and the order of potency in inhibiting the contraction was nifedipine > > diltiazem > flunarizine > oxybutynin > isosorbide dinitrate (ISDN) > glyceryl trinitrate. 5-HT (10-6 M)-induced contraction was dosedependently inhibited by nifedipine but slightly inhibited by diltiazem and ISDN. In rings with intact endothelium, KCI (35 mM)-induced contraction was not affected by acetylcholine (ACh) but $PGF_{2{\alpha}}$ (lO-SM)-induced contraction was dose-dependently relaxed by ACh and adenosine. This endothelium-dependent relaxation was not affected by nifedipine (l0-6M)-pretreatment but markedly inhibited by methylene blue (50,uM)-pretreatment. In the porcine arterial rings without endothelium, ACh had no effect or even contracted the $PGF_{2{\alpha}}-induced$ contraction. However, the dosedependent relaxing effect of ACh appeared when the deendothelized porcine ring and rabbit thoracic aorta with intact endotheli urn were simultaneously suspended into a bath and this relaxing effect was also inhibited by methylene blue-pretreatment. In cat cerebral arteries, 5-HT and NE elicited dose-dependent contractile responses and ACh also produced dose-dependent contraction regardless of the existence of endothelium. ACh-induced contraction was most prominent. 5-HT (IO-SM)induced contraction was not relaxed but contracted additionally by ACh even in the intact endothelial ring. In rabbit cerebral arteries, 5-HT and NE elicited dose-dependent contractile responses and 5-HT-induced contraction was more prominent. In the intact endothelial preparations, 5-HT (lO-s M)-induced contraction was markedly relaxed by the addition of ACh( IO-SM) and this endothelium-dependent relaxing effect was inhibited by atropine (l0-7M)-pretreatment but notaffected by diltiazem (l0-6M)-pretreatment. These results suggest that ACh elicits endotheliumdependent relaxing effect mediated by muscarinic receptors in cerebral arteries of pig and rabbit, and that ACh acts as vasoconstrictor in cat cerebral artery.