The present study was intended to examine the effect of sodium vanadate on contractility of vascular smooth muscle. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various conditions. The results were summarized as follows; 1) Sodium vanadate induced contraction of vascular smooth muscle in a dose-dependent fashion. 2) The contractile effects were not blocked by treatments with adrenergic blocking agent(phentolamine) and indomethacin, indicating the direct action of the drug on vascular smooth muscle. 3) In the presence of ouabain, Na(+)-K(+)-ATPase inhibitor, sodium vanadate still increased the contractility of vascular smooth muscle. 4) Treatment with 4.4'-diisothiocyanostilbene-2.2'-disulfonic acid(DIDS) blocked completely the contractile effects of sodium vanadate. 5) In the presence of verapamil, lanthanum and ryanodine, the contractility of the vascular smooth muscle by sodium vanadate was decreased. From the above results. it was suggested that sodium vanadate acts directly on vascular smooth muscle and causes contraction. It was probably due to inhibition of Ca(++)-ATPase in plasma membrane as well as increasing the release of Ca(++) from sarcoplasmic reticulum and Ca(++) influx across the plasma membrane, but not inhibition of Na(+)-K(+)-ATPase.
Aorta, Thoracic ; Cell Membrane ; Endothelial Cells ; Indomethacin ; Lanthanum ; Muscle, Smooth, Vascular* ; Ouabain ; Ryanodine ; Sarcoplasmic Reticulum ; Sodium* ; Vanadates* ; Verapamil

Caffeine has been known to induce the contraction of rabbit aortic ring resulting from Ca2+ release from the intracellular stores. But in contrast, contraction of aortic ring induced by depolarizing agents or agonist was reported to be suppressed by caffeine. The present study was intended to examine the effect of caffeine on Ca2+ movement across the plasma membrane and actomyosin ATPase activity of vascular smooth muscle to elucidate the modes of action of caffeine on the vascular smooth muscle. Aortic ring preparation were made from the rabbit thoracic aorta and the endothelial cells were removed from the ring by gentle rubbing. The contractilty of the aortic ring was measured under varying conditions, and Ca2+ influx across the membranes of the aortic ring was measured with Ca2+ sensitive electrode with and without caffeine and the effect of caffeine on actomyosin ATPase activity were measured by modified Hartshrone's method. 45Ca wash out curves with and without caffeine were studied by Richard's method. The results were summarized as follows: 1) Caffeine inhibited the contractilty induced by norepinephrine. high K+, and histamine. but caffeine alone induced a transient contraction of vascular smooth muscle. The caffeine induced contraction was demonstrable even in the absence of external Ca2+. 2) Caffeine increased 45Ca efflux from vascular smooth muscle. 3) In the presence of propranolol, the inhibitory effect of caffeine on epinephrine induced contraction still persisted. 4) Caffeine decreased norepinephrine induced Ca2+ influx through the plasma membranes of aortic ring. 5) Caffeine decreased the actomyosin ATPase activity of vascular smooth muscle. From the above results, it is suggested that caffeine induces the contraction of vascular smooth muscle by release of Ca2+ from intracellular Ca2+ stone, but inhibits drug-induced contraction by decrease of Ca2+ influx across the plasma membranes and a decreased Ca2+ sensitivity of contractile protein in vascular smooth muscle.
Actomyosin* ; Aorta, Thoracic ; Caffeine* ; Cell Membrane ; Electrodes ; Endothelial Cells ; Epinephrine ; Histamine ; Membranes ; Muscle, Smooth, Vascular* ; Myosins* ; Norepinephrine ; Propranolol

No abstract available.
Blood Coagulation* ; Humans* ; Saliva*

Radioiodinated oxytocin prepared by the lactoperoxidase method exhibited a substantial biologic activity in uterotonic assay of the rat uterus. 125I-oxytocin was bound to the uterine membrane particulate fraction, but the unlabelled oxytocin did not inhibit the binding of 125I oxytocin to the membrane fraction of rat uterus. Cold iodinated oxytocin, however, inhibited the 125I-oxytocin binding to the membrane fraction of rat uterus in proportion to its concentration. These results suggest that 125I-oxytocin is not a suitable radioligand for oxytocin receptor binding study.
Animal ; Binding Sites ; Cell Membrane/metabolism ; Female ; Iodine Radioisotopes/metabolism* ; Oxytocin/metabolism* ; Radioligand Assay ; Rats ; Receptors, Cell Surface/analysis* ; Uterus/metabolism*

The interaction of calcium and local anesthetics was investigated with the lipid extracted human RBC membrane fragments treated with carbodiimide in order to titrate carboxyl groups. A water soluble carbodiimide [1-cyclohexyl-3-(2-morpholinoethyl) carbodiimide methotoluene-p-sulfonate], referred to as a carbodiimide reagent, and glycine methylester were used for this purpose. About 76% of carboxyl groups of the fragments were modified at a concentration of 0.05M carbodiimide reagent. The interaction of calcium and local anesthetics such as procaine and lidocaine with these fragments still showed typical competition. However, when the calcium binding was decreased to 8% at a higher concentration of carbodiimide reagent (0.08M), the local anesthetics still inhibited the calcium binding, but were not competitive in nature. In other words, if concentrations of the carbodiimide reagent were raised, the degree of inhibition by the local anesthetics was gradually decreased and was not competitive in nature. Finally, no inhibition was demonstrated when the concentration of the reagent was 0.1 to 0.4M. The above findings, seem to suggest that local anesthetics such as procaine and lidocaine interact with carboxyl groups, in addition to phosphodiester groups of phospholipids as previously reported, and inhibited competitively calcium binding to carboxyl groups of the membrane fragments.
Anesthetics, Local/pharmacology* ; Calcium/metabolism* ; Carbodiimides/pharmacology* ; Cell Membrane/metabolism ; Erythrocytes/metabolism* ; Human ; In Vitro ; Protein Binding

The interaction of calcium and local anesthetics was investigated with the lipid extracted human RBC membrane fragments treated with carbodiimide in order to titrate carboxyl groups. A water soluble carbodiimide [1-cyclohexyl-3-(2-morpholinoethyl) carbodiimide methotoluene-p-sulfonate], referred to as a carbodiimide reagent, and glycine methylester were used for this purpose. About 76% of carboxyl groups of the fragments were modified at a concentration of 0.05M carbodiimide reagent. The interaction of calcium and local anesthetics such as procaine and lidocaine with these fragments still showed typical competition. However, when the calcium binding was decreased to 8% at a higher concentration of carbodiimide reagent (0.08M), the local anesthetics still inhibited the calcium binding, but were not competitive in nature. In other words, if concentrations of the carbodiimide reagent were raised, the degree of inhibition by the local anesthetics was gradually decreased and was not competitive in nature. Finally, no inhibition was demonstrated when the concentration of the reagent was 0.1 to 0.4M. The above findings, seem to suggest that local anesthetics such as procaine and lidocaine interact with carboxyl groups, in addition to phosphodiester groups of phospholipids as previously reported, and inhibited competitively calcium binding to carboxyl groups of the membrane fragments.
Anesthetics, Local/pharmacology* ; Calcium/metabolism* ; Carbodiimides/pharmacology* ; Cell Membrane/metabolism ; Erythrocytes/metabolism* ; Human ; In Vitro ; Protein Binding

Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p<0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p<0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.
Animal ; Calcium/*metabolism ; Cytosol/metabolism ; *Heart Arrest, Induced ; Heart Ventricle/metabolism ; Hypothermia, Induced ; Myocardial Ischemia/metabolism/*prevention & control ; Myocardium/*metabolism ; Rats ; Support, Non-U.S. Gov't

The effects of the alcohol extract of Panax ginseng on the myocardial contractility particularly with respect to Bowditch and Woodworth phenomena and the norepinephrine induced contraction of the vascular smooth muscle were studied in vitro. 1) In the isolated muscle preparation of guinea pig left auricle, the administration of ginseng-alcohol extract at concentrations of 10~50mg% resulted in a significant reduction of both Bowditch and Woodworth effects. 2) In the isolated Ca++ depleted heart of rabbit ginseng-alcohol extract inhibited the Ca++ uptake and the restoration of contractile force during perfusion with a Ca++ containing solution. 3) In the isolated muscle strip of the rabbit aorta noradrenaline (5 X 10-8 g/ml) induced contraction was inhibited by the ginseng-alcohol extract at concentrations of 10~50mg%. From these results it is speculated that the hypotensive effect of ginseng is accounted for by 1) the direct inhibition of myocardial contractility which is resulted from the reduction of Ca++ influx into cardiac cell, and 2) the inhibition of the catecholamine induced contractility of vascular smooth muscles.
Animal ; Aorta/drug effects ; Cardiovascular System/drug effects* ; Ethanol/pharmacology ; Female ; Guinea Pigs ; In Vitro ; Male ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects ; Myocardial Contraction/drug effects* ; Panax* ; Plant Extracts/pharmacology* ; Plants, Medicinal* ; Rabbits

Lobular capillary hemangioma (LCH) in the nasal cavity, previously known as pyogenic granuloma, is an extremely rare benign vascular tumor in infants. LCH is a rapidly growing lesion that has a bleeding tendency due to its excessive vascularity. The authors experienced a case of LCH of the nasal cavity in a 2-month-old infant that was totally resected via the endoscopic approach after preoperative embolization. Therefore, we report this case with a brief review of the literature.
Embolization, Therapeutic ; Granuloma, Pyogenic* ; Hemangioma ; Hemorrhage ; Humans ; Infant* ; Nasal Cavity ; Nasal Surgical Procedures

In order to elucidate mechanisms of Ca++ antagonistic action of kanamycin in the biological system, the effects of kanamycin on Ca++ transport in sarcoplasmic reticulum of rabbit skeletal muscle and liver mitochondria were studied. At the same time, the effect of the agent on Bowditch and Woodworth phenomena of rabbit heart as well as the superprecipitation of actomyosin isolated from rabbit skeletal muscle were studied. Since kanamycin inhibits the Bowditch staircase phenomena in rabbit cardiac muscle, it is speculated that kanamycin inhibits Ca++ influx across the cell membrane which is required for the muscular contraction. Kanamycin also inhibits the Woodworth staircase phenomena, indicating a decrease in size of the Ca++ pool in cardiac muscle which may be brought about by an inhibition of Ca++ transport in sarcoplasmic reticulum and mitochondria. Actually, kanamycin was found to inhibit both the activities of Ca++ activated adenosine triphosphatases (ATPase) and Ca++ transport in sarcoplasmic reticulum and mitochondria. Kanamycin also inhibits both the development of superprecipitation and the activity of Ca++activated ATPase of skeletal actomyosin in rabbits. From the results obtained above, it may be concluded that kanamycin possesses a Ca++ antagonistic action in the biological system.
Animal ; Calcium/antagonists & inhibitors* ; Kanamycin/pharmacology* ; Mitochondria, Liver/metabolism ; Muscles/metabolism ; Myocardium/metabolism ; Rabbits