No abstract available.
Propranolol*

Infantile hemangioma is a common, benign tumor of infancy. Although systemic propranolol was found to be effective in the treatment of infantile hemangioma, its use is often challenging for clinicians owing to its potential side effects. Recent small studies have suggested that the topical use of timolol maleate gel, a non-selective beta-adrenergic antagonist, might be effective for the treatment of superficial infantile hemangioma. Here, we report three cases of infantile hemangioma of different sizes and depths treated with the topical timolol maleate gel-forming solution.
Hemangioma ; Propranolol ; Timolol*

Study on the influence of appropriate sustained-release excipients on the release of propranolol hydrochloride from experimental sustained-release tablet. Hydroxyl propyl methyl cellulose and Avicel PH 101 could protect the release of propranolol hydrochloride from sustained-release tablet. Establish the coating with 2 types of polymers HPMC and Eudragit L100. Test the degree of dissolution during 12 hours and compare to the reference tablet. The release of propranolol hydrochloride from sustained release tablet prepared by the formula 20th was similar to that of reference tablet, the coefficient of f2=64.54. At the same time, the quantitative method of serum propranolol was established, in order to assess the in vivo ability of products
Propranolol ; Delayed-Action Preparations

No abstract available.
Hemangioma* ; Injections, Intralesional* ; Propranolol ; Triamcinolone*

PURPOSE: To investigate the effect of beta-adrenergics on the production of nitric oxide (NO) in cultured trabecular meshwork cells. METHODS: Primarily cultured porcine trabecular meshwork cells were exposed to timolol and to propranolol at various concentrations. Cellular survival was assessed by MTT assay and the production of nitrite was assessed by Griess reaction after 24 hours and 3 days respectively. Also investigated was the effect of co-administraton of timolol and isoproterenol. RESULTS: After exposure for 24 hours, neither drug affected the cellular survival. Timolol and propranolol inhibited the production of NO significantly (p<0.05). Isoproterenol abolished timolol-induced inhibition of NO production after 24 hours. These results were similar after exposure for 3 days. CONCLUSIONS: Both timolol and propranolol inhibit the production of NO in trabecular meshwork cells and isoproterenol abolished this effect. These results suggest that beta-adrenerics involves in the production of NO in trabecular meshwork cells.
Isoproterenol ; Nitric Oxide* ; Propranolol ; Timolol ; Trabecular Meshwork*

Three groups of patients with newely diagnosed hypertension, or with hypertension not optimally controlled by previous treatment, completed a comparative study on the effects of Dihydrochlorothiazide, propranolol, and prazosin on plasma lipids after three months therapy. The drugs showed equipotent antihypertensive effects(P<0.01). Dihydrochlorothiazide administration was associated with a significant elevation of total cholesterol(42%, P<0.05), and triglyceride(8.1%, P<0.01). Changes of HDL-C(5.1%), LDL-C(3.3%), and cholesterol ratio(-4.8%) were not significant. Propranolol administration was associated with significant elevation of total cholesterol(3.8%, P<0.05), triglyceride(14.5%, P<0.005), and LDL-C(5.6%, P<0.005). Reduction of HDL-C(-7.8%, P<0.05) and cholesterol ratio(-14.7%, p<0.005) was also statistically significant. Prazosin administration was associated with significant decrease in total cholesterol(-6.6%, P<0.005), triglycride(-9.6%, P<0.005), and LDL-C(-11.7%, P<0.005), and significant elevation of HDL-C(10.6%,P<0.005) and cholesterol ratio(24.2%, P<0.005) was noted.
Cholesterol ; Humans ; Hydrochlorothiazide* ; Hypertension* ; Plasma ; Prazosin* ; Propranolol*

Profound hypothermia (15 degrees C) was induced in 36 mogrel dogs anesthetized with nitrous oxide-oxygen-d-tubocurarine. Prcpranolol (0.3 mg/kg) or MJ 1999(0.8 mg/kg) was administered intravenously 10 minutes prior to the start of cooling. Significant protection against ventricular fibrillation was provided by MJ 1999, but not by propranolol. With available evidence that hypothermia causes increased catecholamine release and that MJ 1999 is more specific in its beta-adrenergic blocking prcperties than propranolol, the authors findings suggest that ventricular fibrillation during hypothermia is due to beta-adrenergic hyperactivity.
Animals ; Dogs* ; Hypothermia* ; Propranolol* ; Sotalol* ; Ventricular Fibrillation*

1) The author investigated whether presynaptic alpha-adrenoceptors exist in the cardioaccelerator nerves of cold-blooded animals(frog, tortoise) as in ones of in mammals. 2) Each atrial preparation of a frog, tortoise and guinea-pig produced the positive chronotropic and inotropic responces to field stimulation. Each ventricular muscle preparation of frog and tortoise produced positive inotropic responces to field stimulation. 3) Both the responces of frog atrium and the inotropic response of frog ventrice to the stimulation were abolished or markedly inhibited by the presence of tetrodotoxin, guanethidine and proparanolo. Both responses of tortoise atrium to the stimulation were markedly inhibited by propranolol and the inotropic response ventricle to the stimulation was markedly inhibited by tetrodotoxin. 4) Both responses of frog and tortoise atrium, and the inotropic response of frog and tortoise ventricle to the stimulation were not affected by clonidine and yohimbine. 5) Both responses of guinea-pig atrium to the stimulation were markedly inhibited in the presence of clonidine and this clonidine-induced inhibition was not observed in the presence of yohimbine. 6) The above results suggest that presynaptic alpha-adrenoceptors do not exist in the cardioaccelerator nerves of frog and tortoise, being different from those of mammalisn animals.
Animals* ; Clonidine ; Guanethidine ; Mammals ; Propranolol ; Tetrodotoxin ; Yohimbine

Succinylcholine induces a small increase in serum K+ (0.3~0.5mEq/l) in normal patients, but it may produce fatal increases in sensitive conditions, including severe burn, massive trauma, tetanus and neuromuscular disorders. Recently, interest has been focussed on the role of the adrenergic system in extrarenal potassium hemeostasis. According to this concept, beta-adrenergic stimulation enhances and conversely a blockade imparis celluar uptake of potassium. Meanwhile propranolol, a beta-adrenergic blocker, is an incresingly, common drug among surgical patients. Therefore, the present experiment was carried out on 66 patients in order to determine whether propranolol augments or prolongs the increases in serum K+ following succinylcholine injection(2mg/kg, I.V.). Serum K+ and Na+ levels were measured just prior to induction and at 3,5,10,30,60,90 minutes following succinylcholine administration. The patients were divided into three groups: Group 1: 26 patients without propranolol treatment, Group 2: 20 patients pretreat with divided doses of propranolol (320 mg b.i.d. p.o.). and Group 3: 20 patients on chronic propranolol therapy. The results were as follows. 1) Baseline K+ valuses were significantly higher in propranolol treated patients(Groups 2 and 3) than in non-treated patients(Group 1). 2) The magnitude of maximum increases in serum K+ following succinylcholine was 0.19mEq/l, 0.16mEq/l and 0.21mEq/l in group 1,2 and 3, respectively. 3) The time to peak increases in K+ was 30min, 5min and 3 min following succinylcholine in group 1,2 and 3, respectively. 4) Serum Na+ decreased significantly following succinylcholine administration in all groups, but there was no significant difference among the groups at other times. These results indicate that propranolol neither augments nor prolongs increases in serum K+ following succinylcholin injection. Thus succinylcholine can be used safely in the presence of a beta-adrenergic blockade.
Burns ; Humans ; Potassium ; Propranolol* ; Succinylcholine* ; Tetanus

During ether anesthesia in man, succinylcholine(lmg/kg of body weight) was administered intravenously after pretreatment with 0.2% lidocaine 50-60mg or Inderal(1. 0mg). The effects were as follows: 1) Heart rates were increased during ether anestheaia. 2) Lidocaine produced no effects on heart rates rncreased by ether, but heart rates were decreased following administration of succinylcholine. 3) Inderal decreased heart rates, increased by ether anesthesia. Heart rates were increased following administration of succinylcholine.
Anesthesia ; Ether ; Heart Rate ; Lidocaine* ; Propranolol* ; Succinylcholine*