Changes of blood pressure, heart rate, ECG, respiration rate and pupil size by intracerebroventricular(ICV) infusion of hypertonic NaCl with 0.04 ml/min for 5 min(total 0.2ml) were observed in urethane-anesthetized rabbits. ICV infusion of 0.75M NaCl produced slight pressor effect (11mmHg) and did not affect other parameters. ICV infusion of 1.5M NaCl began to increase blood pressure from 2~3 min after the infusion and produced maximal increase(24mmHg) at 5~10 min. Then the pressor effect was recovered to the original level at 30~60 min. Change of heart rate by the infusion was not clear, but ST-segment of ECG was markedly depressed. Respiration rate increased about 1.5 times than the control in accordance with the pressor effect and the state was continued even after the recover of the pressor effect. Both pupils dilated markedly and light-reflex was lost. Changes of parameters by ICV infusion of 3.0M NaCl were similar to those by 1.5M NaCl and some rabbits caused severe arrhythmias and died. The purpose of present study is to investigate the mechansim(s) of the pressor effect induced by the ICV infusion of 1.5M NaCl. The pressor effect of 1.5M NaCl was attenuated by the continuous infusion of vasopressin antagonist(20microm/kg/min) but not affected by intravenous treatment with 2mg/kg phentolamine, 2mg/kg propranolol and 1mg/kg chlorisondamine. The pressor effect was not altered with ICV 0.12mg/kg phenoxybenzamine, 0.4mg diltiazem, 0.1mg/kg mecamylamine and 0.2mg/kg atropine. After ICV infusion of 25microg/kg/min of diazepam, however, the pressor effect was completely abolished and restored 3~4 hours after stopping diazepam infusion. The pressor effect was rather potentiated than inhibited in bilateral adrenalectomized or nephrectomized rabbits. Infusion of 2microg/kg/min of saralasin for 10 min in the bliateral adrenalectomized rabbit did not affect the pressor effect at all. These results suggest that hypertensive effect induced by ICV infusion of hypertonic NaCl is mediated by the increase of vasopressin secretion.
Arrhythmias, Cardiac ; Atropine ; Blood Pressure ; Chlorisondamine ; Diazepam ; Diltiazem ; Electrocardiography ; Heart Rate ; Infusions, Intraventricular* ; Mecamylamine ; Phenoxybenzamine ; Phentolamine ; Propranolol ; Pupil ; Rabbits* ; Respiratory Rate ; Saralasin ; Vasopressins

This study was undertaken to observe the effects of organic or inorganic calcium antagonists and to investigate the involvement of cyclic nucleotides in regulating the vascular tone in the chorionic artery from normal or preeclamptic placenta. KCI and prostaglandin (PG) F2 alpha produced marked and constant contractions in chorionic arterial preparations of both normal and preeclamptic placentas. Nifedipine (NIF), verapamil (VER) and diltiazem (DIL) reduced the tension that had been produced by KCI and PGF2 alpha in a concentration-dependent fashion in both preparations, and the potency order of the three agents was NIF> VER > DIL. In preeclamptic arteries, however, the magnitudes of vasodilatation induced by NIF and DIL were much smaller than those in normal chorionic arteries. Mg2+ and Cd2+ also relaxed the tension induced by KCI and PGF2 alpha. In preeclamptic chorionic artery, the vasodilatation induced by Mg2+ was significantly potentiated, while that by Cd2+ was not. Removing endothelium did not alter cyclic GMP content in both preparations. In both preparations contracted by PGF2 alpha, nitroprusside markedly increased cyclic GMP content, but neither cyclic GMP nor cyclic AMP content was affected by acetylcholine, NIF, isopro-terenol, or Mg2+. The above results suggest that neither cyclic AMP nor cyclic GMP is involved in regulating the vascular tone of chorionic artery and that sensitivity of the artery in preeclampsia to the inhibitory action of calcium antagonist might be different from that in normal placenta.
Arteries/physiopathology ; Calcium Channel Blockers/*pharmacology ; Cyclic AMP/analysis ; Cyclic GMP/analysis ; Dinoprost/pharmacology ; Female ; Human ; Placenta/*blood supply ; Potassium Chloride/pharmacology ; Pre-Eclampsia/*physiopathology ; Pregnancy ; Vasoconstriction/*drug effects

BACKGROUND: This study was aimed at defining the varying responses of porcine coronary artery(PCA) to various wavelengths of ultraviolet irradiation, and at relating them to the changes in cyclic GMP contents. METHODS: The ring preparations of PCA with intact or removed endothelium were irradiated with the ultraviolet or visible light of wavelengths(240-520mm) from xenon lamp of a spectrofluorometer, and the changes in vascular tension were recorder on polygraph. For cyclic GMP assay, rat thoracic aorta was frozen after irradiation and homogenated. The supernatant was extracted with water-saturated ether and the cyclic GMP contents were measured with radioimmunoassay. RESULTS: Ultraviolet irradiation relaxed the preparations(UVR-relaxation) in resting state and those precontracted by prostaglandin F2alpha, the maximal relaxation occurring at 410nm, and the magnitude depending on the duration of irradiation. The UVR-relaxation was not affected by removing the endothelium, while it was markedly potentiated by pretreatment with Bay K 8644. The Bay K 8644-induced potentiation of UVR-relaxation was abolished by hemoglobin and slightly reduced by wrapping the rings with aluminum foil. Cyclic GMP contents in the increase was markedly potentiated by pretreatment with Bay K 8644. CONCLUSION: The observations suggest that UVR-relaxation in procine coronary artery is caused by activating the nitric oxide-cyclic GMP system, which is most sensitively activated by UVR of 410nm and that its potentiation induced by Bay K 8644 may be related nitrous substance released from the agent upon UVR.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester* ; Aluminum ; Animals ; Aorta, Thoracic ; Bays* ; Coronary Vessels* ; Cyclic GMP ; Dinoprost ; Endothelium ; Ether ; Light* ; Passive Cutaneous Anaphylaxis ; Radioimmunoassay ; Rats ; Relaxation* ; Ultraviolet Rays ; Vasodilation ; Xenon

Effects of Ultratiolet (UV) light was studied in isolated thoracic aortae of rabbits and porcine coronary arteries. The following results were obtained. 1) Radiation of UV light did not affect both arterial rings in resting tension. 2) Both arterial preparations contracted with various vasoconstrictors (KCI,NE,PE,BayK 8644 and (+S202 etc.) were relaxed by UV light radiation in a radiation time-dependent fashion. 3) The magnitudes of the relaxation were not significantly different in both the rings with or without intact endothelium. 4) MB and LY markedldy reduced the UV light-induced relaxation in both the rings. 5) PP significantly attenuated the UV light-induced relaxation of rabbit thoracic aorta, but did not affect that of porcine coronary artery. 6) The UV Light-induced relaxation of porcine coronary artery was significantly attenuated by DT or NF, while that of rabbit thoracic aorta was not. 7) (+)S202 significantly potentiated the UV light-induced relaxation of porcine coronary artery contracted with KCI or Hist. Above results suggest that the UV light-induced relaxation of vascular smooth muscles is independent on the endothelium, and the relaxation results from primarily activation of guanylyl cyclase and is in part related to adenylyl cyclase and calcium metabolism. In adddition, a dihydropyridine calcium agonist, (+)S202, may sensitize vascular smooth muscle to the relaxing effect of UV light through some unknown mechanism.
Adenylyl Cyclases ; Aorta, Thoracic ; Calcium* ; Coronary Vessels ; Endothelium ; Guanylate Cyclase ; Metabolism ; Muscle, Smooth* ; Muscle, Smooth, Vascular ; Rabbits ; Relaxation* ; Ultraviolet Rays ; Vasoconstrictor Agents

It is well known that bloody cerebrospinal fluid(BCSF) obtained from patient with subarachnoid hemorrhage will contracts isolated brain arteries, but the effects of non-bloody CSF(non-BCSF), which does not contain blood components, has not been reported yet. In this study, CSFs were obtained from 12 patients hospitalized at the Department of Neurosurgery, Chonnam University Hospital from February to September 1994. Among the CSFs from these 12 patients, 3 cases were bloody and 9 cases were not. It was found that all BCSFs produced marked contractions in ring preparations of porcine isolated basilar and circle of Willis arteries. The non-BCSFs fell into two groups:one which contracted the preparations in a volume-dependent fashion(30-1000 microliter) and the other did not. The purpose of this study was to investigate the mechanism(s) of contractile response to the first group on-BCSF in the porcine isolated brain artery. Concentration-dependent contractions induced by KCl were not affected by the pretreatment with 500 microliter non-BCSF, while contraction induced by 5-hydroxytryptamine(5-HT) and phenylephrine(PE) were significantly potentiated by the same pretreatment of non-BCSF. Although volume-dependent contractions induced by the non-BCSF were not affected by the pretreatment with 10(-6) M phentolamine and 10(-4) M L-NAME, the contractions was significantly attenuated by the presence of 10(-6) M indomethacin and nimodipine. It was also found that the contraction induced by prostaglandin F2alpha(PGF2alpha) was relaxed by nitroprusside and atriopeptin(ANP) in a concentration-dependent manner and such relaxations were not affected by nitroprusside and ANP were not affected in the presence of 500 microliter non-BCSF. Above observations suggest that components, of non-BCSF from patients with brain lesion contains an unknown substance(s) that induces contraction of porcine isolated brain arteries and the above contractile effect involves the extracellular calcium influx and/or cyclooxygenaseprostaglandin system but not the NO-guanylate cyclase system.
Arteries* ; Atrial Natriuretic Factor ; Brain* ; Calcium ; Cerebrospinal Fluid* ; Circle of Willis ; Humans ; Indomethacin ; Jeollanam-do ; Neurosurgery ; NG-Nitroarginine Methyl Ester ; Nimodipine ; Nitroprusside ; Phentolamine ; Relaxation ; Subarachnoid Hemorrhage

PURPOSE: For medical students to have a meaningful learning experience, the curriculum must integrate what students are learning in class with the skills and knowledge required in the clinicalsetting. To satisfy these needs, an integrated curriculum (IC) has been operating at Chonnam National University Medical School since 1999. The purpose of this study was to evaluate the changes in IC students during two implementation periods, the first in 2001 and the second in 2004. This study focused on the student viewpointin order to create an authentic IC program. METHODS: Questionnaires were used to evaluate the differences in the student perception of IC. The content of the questionnaire dealt with the appropriateness of time management, coherence of the content, teachinglearning method, and IC evaluation. RESULTS: There were positive responses from the second implementation period than from the first, for almost all sub-items. However, the results showed that IC has to be reinforced by instructors teaching a coherentcontent, by using a variety of teaching-learning methods, by having the students participate actively, and by offering holistic and integrated assessments. CONCLUSION: The following three steps are recommended for the improvement of IC: facilitate an IC committee, develop teaching-learning methods, and guide student participation.
Curriculum* ; Humans ; Jeollanam-do ; Learning ; Schools, Medical ; Students, Medical ; Time Management ; Surveys and Questionnaires

A K+-channel blocker, 4-aminopyridine(4-AP) increases neurotransmitter release from motor nerve terminals and has been shown to restore neuromuscular transmission in the myasthenic syndrome. It has been reported that the intravenous injection of 4-AP in the myasthenic patients caused many central adverse effects including anxiety and restlessness, but did not affect the blood pressure. The aim of this study was to observe the effect of intracerebroventricularly administered 4-AP on the blood pressure and to elucidate the mechanism of the action in urethane-anesthetized rabbits. Intracerebroventricular(icv) 4-AP produced pressor effects in a dose-dependent fashion, but intravenous(iv) 4-AP of the same dose did not altered the blood pressure. Tetraethylammonium, a K+-channel blocker which differs from 4-AP structurally, had little effect on the blood pressure, but 3,4-diaminopyridine, another derivative of the aminopyridine, produced pressor effect similar to 4-AP. The pressor effect of icv 4-AP was not affected by the treatment with iv phenoxybenzamine and chlorisondamine, and in bilateral adrenalectomized rabbits. These results suggest that the 4-AP pressor effect is not related to the periphral sympathetic nerve nor adrenal gland. The pretreatment with icv phentolamine and prazosin did not altered the 4-AP pressor. However, the icv 4-AP pressor effect was significantly attenuated by the treatment with icv yohimbine, and significantly potentiated by the treatment with icv clonidine. The treatment with icv diltiazem markedly inhibited the icv 4-AP pressor effect. It is concluded that 4-AP-sensitive K+-channels in rabbit brain might play a role in the regulation of blood pressure and that the 4-AP pressor effect is closely related to the central alpha2-adrenoceptors and L-type calcium channels.
4-Aminopyridine* ; Adrenal Glands ; Anxiety ; Arterial Pressure* ; Blood Pressure ; Brain ; Calcium Channels, L-Type ; Chlorisondamine ; Clonidine ; Diltiazem ; Humans ; Injections, Intravenous ; Neurotransmitter Agents ; Phenoxybenzamine ; Phentolamine ; Prazosin ; Psychomotor Agitation ; Rabbits ; Tetraethylammonium ; Yohimbine

This study was designed to observe anoxia-induced responses and to clarify their possible mechanisms in porcine basilar and circle of Willis arteries. Anoxia produced a transient vasoconstriction, which then recovered to the basal tension of a 3-5 min. later, and the reoxygenation that follows produced the biphasic(relaxation-contraction) response in the intact endothelial rings under resting tension. The anoxia-induced contraction was potentiated by pretreatment with KC1 and PGF2alpha. Reoxygenation produced only sustained relaxation. Removal of the endothelium and pretreatment with nimodipine or indomethacine markedly attenuated the anoxia-induced contractions. Anoxia transiently and significantly increased cyclic GMP contents in the endothelium-intact preparations, but did not affect them in the endothelium-removed ones. The above results suggest that anoxia-induced contraction is endothelium-dependent and is resultant to the release of a Prostaglandin-like substance(s) .
Anoxia* ; Arteries ; Cerebral Arteries* ; Circle of Willis ; Cyclic GMP ; Dinoprost ; Endothelium ; Indomethacin ; Nimodipine ; Relaxation ; Vasoconstriction

Proliferating trichilemmal cyst(proliferating trchilemmal tumor, PTC) most commonly occurs in the scalp and is generally benign. Malignant transformation of PTC is rare, and the appearance of a spindle cell(sarcomatoid) carcinoma is extremely rare. The authors experienced a case of malignant proliferating trchilemmal tumor with spindle cell carcinoma on the scalp in a 41-year-old male. The tumor was widely resected and covered with split thickness skin graft after Terudermis(R) graft. Imaging studies and fine needle aspiration cytology showed no regional lymph node involvement or distant matastasis.
Adult ; Biopsy, Fine-Needle ; Humans ; Lymph Nodes ; Male ; Scalp ; Skin ; Transplants

BACKGROUND: To evaluate the role of free fatty acids on the ischemic myocardium, influences of various free fatty acids upon transmembrane action potential and ATP-sensitive K+(KATP) channel activity were examined in the ventricular myocardium and single cardiac myocytes. METHODS: KATP channel activities were measured in the enzymatically (collagenase) isolated single rat ventricular cardiac myocytes by the method of the excised inside-out and the cell-attached patch clamp, and transmembrane action potentials were recorded using the conventional 3M-KCl microelectode techniques in the rat ventricular myocardium. RESULTS: Free fatty acids [FFAs; arachidonic acid (AA), linoleic acid (LA) and lysophosphatidylcholine (LPC)] reduced the KATP channel activity in a dose-dependent manner in the inside-out patch, and 50%-inhibition concentrations (IC50) were 88 +/- 11.2, 49 +/- 12.5, and 188 +/- 17.4 M respectively. Both frequency of channel opening and the mean open-burst duration were markedly decreased, but the amplitude of single channel currents were not changed by the FFAs. AA (50 micrometer) and LPC (50 micrometer) did not affect the dinitrophenol (DNP, 50 micrometer)-induced KATP channel activity, whereas LA (50 micrometer) had a tendency to reduce the activity. The channel inhibition effects by 10 micrometer AA in the inside-out patch were significantly augmented by diclofenac (10 micrometer), but was not changed by nordihydroguaiaretic acid. FFAs never stimulated KATP channel activity, even in the inside-out patch where KATP channel activity reduced in the presence of internal ATP (100 micrometer). Time for 90% repolarization (APD90) significantly increased during superfusion of the FFAs, to 22 (50 micrometer AA), 24 (50 micrometer LA), and 18 (50 micrometer LPC) % from those of the contol at the time of 10 min superfusion, but the other action potential characteristics were not changed by the FFAs. AA (10 micrometer) attenuated cromakalim (10 micrometer)-induced APD90 shortening effects. CONCLUSION: It was inferred that FFAs inhibit the KATP channel activity directly by themselves and/or indirectly by their metabolites in the rat ventricular cardiomyocytes, and therefore, duration of action potential lengthens to be a burden over the ischemic myocardium accounting for the injury of myocardium at the late stage of ischemia.
Action Potentials* ; Adenosine Triphosphate ; Animals ; Arachidonic Acid ; Cromakalim ; Diclofenac ; Fatty Acids, Nonesterified* ; Ischemia ; Linoleic Acid ; Lysophosphatidylcholines ; Masoprocol ; Myocardium* ; Myocytes, Cardiac ; Potassium Channels* ; Potassium* ; Rats*