Monckeberg's medial sclerosis is a degenerative process related to age, and is particularly associated with long-standing diabetes mellitus. The media of small and medium-sized muscular arteries are usually involved. Although its pathogenesis is still unknown, its presence can predict the risk of cardiovascular events and leg amputation in diabetic patients. In our two cases, Mnckeberg's medial sclerosis was shown as a bean-sized, pulsatile mass which occurred from an inferior labial branch of the facial artery. Neither paient had a history of diabetes mellitus or calcification in any part of the body, nor an abnormality with their calcium metabolism. Herein, we report a case of a man and a woman with Mnckeberg's medial sclerosis. This condition is so rare that it has not been reported in the Korean dermatologic literature before. Moreover, Mckeberg's medial sclerosis is very rarely found without diabetes mellitus.
Amputation ; Arteries ; Calcium ; Diabetes Mellitus ; Female ; Humans ; Leg ; Metabolism ; Sclerosis*

OBJECTIVETo study the mechanism of restenosis after angioplasty and to clarify the effect of thrombin and its receptor on restenosis development.

METHODSBalloon catheter-induced injury was adopted to induce intimal hyperplasia of the carotid arteries in rats. Antisense thrombin receptor (ATR) cDNA was transfected by perfusing recombinant LXSN ATR plasmid/nanoparticle complex into the segment of the injured carotid artery.

RESULTSPCR result showed integration of the recombined gene. Dot blot showed the expression of antisense TR mediated by recombinant LXSN ATR plasmid/nanoparticle complex in the wall of common carotid arteries of the experimental group rats, which enabled to inhibit TR gene expression and intimal hyperplasia of the injured arteries.

CONCLUSIONSThrombin and its receptor play an important role in the formation of neointima after the injury, which provides a potential clue in developing a new approach for prevention and treatment of restenosis after angioplasty.

Animals ; Carotid Arteries ; Hyperplasia ; Rats ; Receptors, Thrombin ; metabolism ; Thrombin ; pharmacology ; Tunica Intima ; metabolism

OBJECTIVE: An intracranial aneurysm is an important acquired cerebrovascular disease that can cause a catastrophic subarachnoid hemorrhage. Atherosclerosis is one of possible mechanism, but its contribution to aneurysm formation is unclear. Experimentally induced cerebral aneurysm rate by high lipid diet was evaluated and compared with high salt and normal diet to elucidate the role of lipid metabolism in the process of cerebral aneurysm formation. METHODS: Thirty-seven 7-week-old male Sprague-Dawley (SD) rats received a cerebral aneurysm induction procedure. The control animals (n=11) were fed a normal diet, and the experimental animals were fed a diet containing 8% salt (n=15) and high lipid (n=11) for three months. Three months after the operation, the rats were killed, their cerebral arteries were dissected, and the regions of the bifurcation of the right anterior cerebral artery-olfactory artery (ACA-OA) bifurcations were examined histologically and aneurysm induction rates among three groups were analysed. RESULTS: Average systolic blood pressures after 3 months feeding in three groups (high salt diet group, high lipid diet group and normal diet group) were 175.9+/-3.4 mmHg, 133.7+/-5.1 mmHg and 128+/-2.9 mmHg, respectively. The difference between high lipid group and normal diet group was not significant (P=0.215). The aneurysm induction rate in three group were 87%, 63% and 36%. The difference between high lipid diet group and normal diet group was significant (Pearson k2, P=0.029). CONCLUSIONS: High lipid diet significantly increase the cerebral aneurysm induction rate in experimentally induced cerebral aneurysm model of rats. That suggests a possible adverse role for hyperlipidemia leading to aneurysm formation. Further studies are necessary to elucidate the exact role of hyperlipidemia in the pathophysiology of cerebral aneurysm.
Aneurysm ; Animals ; Arteries ; Atherosclerosis ; Cerebral Arteries ; Diet* ; Humans ; Hyperlipidemias ; Intracranial Aneurysm* ; Lipid Metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage

Cerebral metabolism can be divided into basal and active metabolism. Active electroencephalogram(EEG) represents electrophysiologic activity of the brain and become flat when such an activity is abolished. Hypothermia can protect ischemic cerebral damage by reducing cerebral metabolic rate. Profound hypothermia could induce a slow or flat EEG. It can be assumed that the cessation of brain electrical activity appear far faster in the case of cerebral ischemia combined with brain cooling than simple ischemia. To prove this assumption, we carried out this study to determine if selective brain cooling shortens time to onset of a flat electroencephalogram(EEG) after cerebral ischemia. Rabbits were anesthetized with halothane and oxygen. Brain was selectively cooled by intracarotid infusion with saline at 37degrees C (normothermic group) and 18degrees C (hypothermic group). Cerebral ischemia was induced for 2 minutes with a simultaneous clamping of contralateral carotid artery and induced hypatension. In 22 of 28(79%) episodes a flat EEG was identified, and occurred an average 10+/-1 sec in the hypothermic group, 14+/-I sec in the normothermic group. Time to onset of a flat EEG was significantly faster in the hypothermic group than normothermic group(p=0.02). These pattems may be recognized as an indication of metabolic suppression of hypothermia during cerebral ischemia.
Brain Ischemia ; Brain* ; Carotid Arteries ; Constriction ; Electroencephalography* ; Halothane ; Hypothermia ; Ischemia ; Metabolism ; Oxygen ; Rabbits

Adult ; Altitude ; Arteries ; metabolism ; Calcitonin Gene-Related Peptide ; blood ; Humans ; beta-Endorphin ; blood

Animals ; Arteries ; metabolism ; Cochlea ; blood supply ; Cystathionine gamma-Lyase ; genetics ; Rats ; Rats, Sprague-Dawley

To elucidate the Ca2+ release mechanisms in the rabbit coronary artery, arterial preparations were permeabilized with beta-escin and changes in tension were measured under varying experimental conditions. Additionally, we investigated properties and distribution of two kinds of Ca2+ release mechanisms, Ca2+-induced Ca2+ release (CICR) and IP3-induced Ca2+ release (IICR). The results obtained were summarized as follows; 1. When a rabbit coronary artery was incubated in a relaxing solution containing 30 microM beta-escin for 40 min. sensitivity to externally added Ca2+ was much higher in beta-escin permeabilized muscle than in intact preparations. The contractile effect of IP3 in beta-escin permeabilized muscle was also demonstrated; 2. Caffeine and IP3 contracted coronary arteries were permeabilized with beta-escin, but the amplitude of contraction was much larger in the presence of caffeine than of IP3. 3. Intracellular heparin completely inhibited the contractions induced by IP3, but not those by caffeine. On the other hand, procaine inhibited the responses to caffeine, but not those to IP3. Ryanodine inhibited both the caffeine- and IP3-induced contractions. 4. The amplitude of contractile responses was much larger to the maximal stimulation of CICR by applying caffeine than to the maximal stimulation of IICR by applying IP3. After the maximal CICR stimulation by caffeine, the activation of IICR by IP3 without the reloading of Ca2+ could no longer evoke contraction. On the other hand, after the maximal IICR activation, the activation of CICR could still evoke contraction although the amplitude of the contraction was smaller when compared with the case without the initial IICR stimulation. 5. Acetylcholine contracted coronary artery smooth muscles were permeabilized with beta-escin. However, in the absence of added guanosine triphosphate (GTP), the responses were very small. Acetylcholine-induced contraction was inhibited by heparin, but not by procaine. From the above results, it may be concluded that there are two kinds of mechanisms of Ca2+ release, CICR and IICR, in the rabbit coronary artery smooth muscle cell. Also, whereas the CICR mechanism distributes on the membrane of the whole smooth muscle Ca2+ store, the IICR mechanism distributes only on a part of it.
Animal ; Arteries/metabolism ; Calcium/*metabolism ; Capillary Permeability/drug effects ; Coronary Vessels/drug effects/*metabolism ; Escin/pharmacology ; In Vitro ; Intracellular Membranes/*metabolism ; Rabbits ; Support, Non-U.S. Gov't ; Tissue Distribution

OBJECTIVETo evaluate the difference of the expression level of chemokine-like factor 1 (CKLF1) mRNA and protein between human atherosclerotic plaques and normal arteries.

METHODSReal-time quantitative PCR was performed with experimental group (24 cases of atherosclerotic plaques) specimens and control group (25 cases of normal arteries) specimens. Serial microscopic sections were used for immunohistochemistry with CKLF1 antibody in 17 experimental group specimens and 10 control group specimens.

RESULTSThe endothelial cell, vascular smooth muscle cell (VSMC) and macrophage were CKLF1 positive expression cells in atherosclerotic plaques. There was a foundational expression of CKLF1 mRNA in control group (RQ(Median) = 2.4), and the expression of CKLF1 mRNA in experimental group is up-regulated significantly (RQ(Median) = 132.2, P < 0.05). The VSMC positive expression rate of CKLF1 protein was 100% in experimental group and 70% in control group, the former was up-regulated significantly.

CONCLUSIONSThe expression of CKLF1 is up-regulated in atherosclerotic plaques. It may play an important role in the process of immune and inflammatory responses of atherogenesis.

Adult ; Arteries ; metabolism ; Atherosclerosis ; metabolism ; Case-Control Studies ; Chemokines ; genetics ; metabolism ; Humans ; MARVEL Domain-Containing Proteins ; Plaque, Atherosclerotic ; metabolism ; RNA, Messenger ; genetics ; Young Adult

The external elastic lamina (EEL) serves as a barrier for cells and macromolecules between the media and adventitia in the vascular wall. We evaluated the morphological changes and quantitative assessments of the EEL architecture in the coronary circulation of pigs fed with a high cholesterol diet. Confocal microscopy analysis of the EEL from hypercholesterolemic coronary arteries revealed an altered pattern characterized by fragmentation and disorganization of the EEL associated with an increase in the thickness. Computerized digital analysis of the images obtained by confocal scanning microscopy demonstrated that compared to normal coronary arteries, the EEL of hypercholesterolemic coronary arteries decreased in the percentage of their elastin content (30.80 +/- 1.64% vs. 47.85 +/- 1.82%, p = 0.001). The percentage of elastin content was negatively correlated with the vessel wall area (r = -0.82, p = 0.001). The immunoreactivity for matrix metalloproteinase-3 (MMP-3) increased in cholesterol-fed coronary arteries, predominantly in the neointima and adventitia. This study demonstrates that experimental hypercholesterolemia induced ultrastructural changes of the EEL in coronary circulation. The EEL may also be an atherosclerosis-prone area compared with the intima. The EEL may play an important role in the development of structural changes which characterizes the early phase of coronary atherosclerosis and vascular remodeling.
Animal ; Arteries/ultrastructure ; Arteries/enzymology ; Coronary Vessels/ultrastructure* ; Coronary Vessels/enzymology ; Elastic Tissue/ultrastructure* ; Elastic Tissue/enzymology ; Female ; Hypercholesterolemia/pathology* ; Hypercholesterolemia/enzymology ; Stromelysin 1/metabolism ; Swine

It has been reported that a change in the cellular redox state may be involved in the regulation of vascular tone, but the underlying mechanism is not fully understood. The present study was designed to investigate the cellular effect of sulfhydryl modifying agents in the coronary artery of rabbit using the tension measurement and whole cell clamping method. The application of diamide, a sulfhydryl oxidizing agent, relaxed the endothelium denuded coronary arteries in a dose dependent manner. The fact that this diamide-induced relaxation was significantly attenuated by a pretreatment of 4-AP, and the coronary arteries precontracted with 100 mM K+ instead of histamine, suggests the involvement of 4-AP sensitive K+ channels in the diamide-induced relaxation of coronary arteries. Whole cell patch clamp studies revealed that the 4-AP sensitive IdK was significantly enhanced by the membrane permeant oxidizing agents, diamide and DTDP, and were reversed by subsequent exposure to the reducing agent, DTT. Neither the membrane impermeant oxidizing or reducing agents, GSSG or GSH, had any effect on the activity of IdK, indicating that intracellular sulfhydryl modification is critical for modulating IdK activity. The Diamide failed to significantly alter the voltage dependence of the activation and inactivation parameters, and did not change the inactivation process, suggesting that diamide increases the number of functional channels without altering their gating properties. Since IdK has been believed to play an important role in regulating membrane potential and arterial tone, our results about the effect of sulfhydryl modifying agents on coronary arterial tone and IdK activity should help understand the pathophysiology of the diseases, where oxidative damage has been implicated.
Animal ; Arteries/physiology ; Arteries/drug effects ; Arteries/cytology ; Coronary Vessels/physiology ; Coronary Vessels/drug effects* ; Coronary Vessels/cytology ; Female ; Male ; Oxidants/pharmacology* ; Potassium Channels/physiology ; Rabbits ; Reducing Agents/pharmacology* ; Sulfhydryl Compounds/metabolism*