Priapism is a well recognized complication of some oral medications. Those most commonly cited are: antipsychotic drugs, especially the phenolhiazine: trazodone and chlorpromazine :and the antihyperlensive drugs hydralazine, guanethidine and prazocin. We report a case or priapism associated with the use of chlorpromazine who experienced 2 episodes or priapism and never experience priapism after cessation of the drug.
Antipsychotic Agents ; Chlorpromazine* ; Guanethidine ; Hydralazine ; Priapism* ; Trazodone

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

We produced the cauaalgiform pain by unilateral 1/3-1/2 ligation of sciatic nerve in rats.. Withdrawal thresholds to non-noxious stimulation were reduced(mechanical allodynia), and withdrawal thresholds to heat stimulation were reduced(heat hyperalgesia) too. After that, we injected 50 mg/kg guanethidine intraperitoneally for the study of the effects of chemical sympathectomy in postopertive 7th day, 37th day respectively. The results were as follows 1) Mechanical allodynia was alleviated partially in 12 hours, first day after sympathectomy. 2) Heat hypera1gesia was alleviated completely in first day to 4th day after sympathectomy, and reappeared after 5th day.
Animals ; Causalgia ; Guanethidine ; Hot Temperature ; Hyperalgesia ; Ligation* ; Rats* ; Sciatic Nerve* ; Sympathectomy ; Sympathectomy, Chemical*

5% Ismelin solution was used for the treatment of lid retraction in thyrotoxic patients. All but one diminiabed in size of palpebral fissures and in consequence they required less effort in closing their eyes. However, all of them developed congestion of the eyes which foroce them to stop their eye drops. One patient developed a filamentary keratitis and one other patient developed an ulcer in the bulbar conjunctiva. In spite of the significant ptosis following eye drops the punctate stainings of the conjunctiva and cornea persisted.
Conjunctiva ; Cornea ; Estrogens, Conjugated (USP) ; Guanethidine* ; Humans ; Keratitis ; Ophthalmic Solutions ; Ulcer

5% Ismelin solution was used for the treatment of lid retraction in thyrotoxic patients. All but one diminiabed in size of palpebral fissures and in consequence they required less effort in closing their eyes. However, all of them developed congestion of the eyes which foroce them to stop their eye drops. One patient developed a filamentary keratitis and one other patient developed an ulcer in the bulbar conjunctiva. In spite of the significant ptosis following eye drops the punctate stainings of the conjunctiva and cornea persisted.
Conjunctiva ; Cornea ; Estrogens, Conjugated (USP) ; Guanethidine* ; Humans ; Keratitis ; Ophthalmic Solutions ; Ulcer

Although the conclusion is controversial, there has long been an appealing notion that catecholamines may be involved in some way in the pathogenesis of primary hypertension and almost invariably most of hypotensive drugs involve at various sites of the neuron and produce their effect by depletion of norepinephrine in the sympathetic nerve ending. The authors undertook the comparative study on catecholamine depleting action of 3 most effective drugs available for the treatment of hypertension, reserpine, guanethidine and alpha-methyldopa, measuring the plasma catecholamine levels and urinary exceretion of caecholamine by the modified fluorometric method of Weil-Malherbe and Bone during the treatment of hypertension. The results are as follows: 1) Before the administration of hypotensive drugs, mean blood pressure was 180/110mmH, mean psalma epinephrine level was 0.36+/-0.23gamma%, mean plasma norepinephrine level was 0.48+/-0.35gamma%, 24 hours urinary excretion of epinephrine was 3.6+/-0.12gamma/day and 24 hours urinary excretion of norepinephrine was 68.9+/-0.34gamma/day. 2) In group 1 (reserpin administered group), the mean blood pressure was 190/110mmHg before the treatment and which was declined to 155/89mmHg on the last day of 4th week, in group 2 (guanethidine administered group), the mean blood pressure measured before the treatment was 185/110mmHg and which was declined to 150/85mmHg on the last day of 4th week, and in group 3 (alpha-methylodpa administered group), the mean blood measured pressure measured before the treatment was 182/110mmHg and which was declined to 153/88mmHg on the last day of 4th week. 3) After the treatment for 4 weeks with reserpin guanethidine and alpha-methyldopa, the mean plasma epinephrine levels were declined from 0.37+/-0.12gamma% to 0.11+/-0.08gamma% in group 1, from 0.38+/-0.16gamma% to 0.14+/-0.10gamma% in group 2 and from 0.33+/-0.23gamma% to 0.10+/-0.09gamma% in group 3. 4) The mean plasma norepinephrine levels were declined from 0.05+/-0.21gamma% to 0.22+/-0.12gamma% in group 1, from 0.51+/-0.25gamma% to 0.20+/-0.10gamma% in group 2 and from 0.51+/-0.21gamma% to 0.20+/-0.11gamma% in group 3 after the treatment of 4 weeks respectively. 5) Urinary exceretion of epinephine was declined from 32.3+/-0.16gamma/day to 10.4+/-0.10gamma/day in group 1, from 34.5+/-0.34gamma/day to 17.2+/-0.16gamma/day in group 2, and from 28.2+/-0.14gamma/day to 10.3+/-0.11gamma/day in group in group 3 after the treatment of 4weeks duration. 6) The mean value of 24 hours urinary excretion of norepinephrine was declined to from 72.2+/-0.35gamma/day to 28.5+/-0.14gamma/day in group1, from 69.2+/-0.34gamma/day to 22.6+/-0.21gamma/day in group 2 and from 68.6+/-0.34gamma/day to 18.2+/-0.10gamma/day in group 3 after the treatment of 4 weeks duration. 7) From the above result we can summarized as follows: Antihypertensive effect of each drugs was; guanethidine>alpha-methylodopa>reserpin in order but depressing action plasma norepinephrine levels was; alpha-methyldopa>guanethidine>reserpin and depressing effect of urinary norepinephrine excretion was; alpha-methyldopa>guanethidine>reserpin, in order.
Antihypertensive Agents* ; Blood Pressure ; Catecholamines ; Epinephrine ; Guanethidine ; Humans ; Hypertension ; Methyldopa ; Nerve Endings ; Neurons ; Norepinephrine ; Plasma* ; Reserpine

The bradycardiac and presor to intravenous and intraventricular methoxamine were examined in urethane-anesthetized rabbits 1) Intravenous methoxamine produced bradycardiac pressor responses. Atropine (2 mg/kg, i,v.) weakened but not abloished the bradycardiac effect. 2) The bradycardiac effect elicited by intravenous methoxamine was not affected by int-ravenous prazosin, rehimbiine, guanethidine and propranolol, butt was attenuated by intra venous chlorisondamine reserpine. 3) The pressor effect elioited by intravenous methoxamine was weakened by prazosin, but was scarcely affected, rather potentiated, by intraTenous yohimblne, guanethidine, chlorisondamine, propranolol and resperpine. 4) Intraventricular methoxamine produced pressor and bradycardiac responses. 5) The bradycardiac effect elicited by intraventricular methoxamine was net affected by intravenous atropine, prasosin and yohimbine. This was attenuated by intravenous guane- thidine, chlorisondamine, propranolol and reserpine, and by intraventricular atropine prazosin and propranolol, respectively. 6) The pressor effect elicited by intraventricular methoxamine was attenuated by intra- ventricular and intravenous prazosin. This was not affected by intravenous atropine, gua-nethidine, chlorisondamine, propranolol, reserpine and yohimbine, and by intraventricular atropine, prasosin and Propranolol, respectivelr. 7) From these results it was inferred that bradycardiac effect elicited by methoxamine was not an action through the mediation of aleph 1-adrenoceptors but was a result from non-specific actions on some brain receptors.
Atropine ; Brain ; Chlorisondamine ; Guanethidine ; Methoxamine* ; Negotiating ; Prazosin ; Propranolol ; Rabbits* ; Reserpine ; Yohimbine

The present study was aimed to investigate whether and to what extent hypertension affects the relaxation of the corpus cavernosum. The corpus cavernosum was isolated from 12-week 2- kidney, 1-clip hypertensive rats. The corporal strips were isolated and suspended longitudinally in an organ bath. They were precontracted with phenylephrine, and their responses to electrical field stimulation (EFS) were examined. EFS caused a frequency-dependent contraction (60%) or relaxation (40%) of the corpus cavernosum precontracted with phenylephrine. The contraction response was inhibited or abolished and only frequency-dependent relaxation appeared in the presence of atropine (0.00001mol/L) and guanethidine (0.00001mol/L). The relaxation response to EFS of the corporal preparation precontracted with phenylephrine was attenuated or abolished in the presence of L-NAME (0.0001mol/L). The corporal preparation from the hypertensive rats also showed a frequency-dependent relaxation, however, the degree of which was lower at a low frequency of stimulation than that from the normotensive control. These results suggest that endothelium-derived nitric oxide released upon neural stimulation partly mediate the relaxation of the corpus cavernosum. It is also suggested that hypertension is associated with a partly attenuated relaxation response to EFS.
Animals ; Atropine ; Baths ; Guanethidine ; Hypertension ; Kidney ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Phenylephrine ; Rats* ; Relaxation

Reflex sympathetic dystrophy is a common posttraumatic pain syndrome for which no relia- bly effective method of therapy has been found. Oral therapy has been attempted with steroid, tricyclic antidepressant, beta-blocker, and antiseizure medications, none of which are predictably helpful. Multiple invasive treatment, including sympathetic blockade and intravenous regional local anesthetic, reserpine, or guanethidine blocks, have been employed, but again with inconsistent success. Transcutaneous nerve stimulation is effective in some patients but aggravates symptoms in others. Following a report of the use of subarachnoid block in the treatment of reflex sympathetic dystrophy, a symptom that is characterized by vasospasm and cold intolerance, we experienced the ability of subarachnoid block to relieve the symptoms of reflex sympthetic dystrophy.
Guanethidine ; Humans ; Reflex Sympathetic Dystrophy* ; Reflex* ; Reserpine ; Transcutaneous Electric Nerve Stimulation

To see the inhibitory mechanism of gentamicin in response to electrical field stimulation (EFS) using the rat bladder smooth muscle, atropine or guanethidine was treated but had no effect. Methylsergide, a non-selective 5-HT1, 5-HT2 receptor antagonist was also treated but had on effect. Kinase inhibitors, such as chelerythrine (PKC inhibitor), ML-9 (MLCK inhibitor), or Y27632 (rho kinase inhibitor) were pretreated before gentamicin treatment, but did not have effect. For U73122, a phospholipase C (PLC) inhibitor however, the inhibitory effect to gentamicin was significantly attenuated in all frequencies given by the EFS. Therefore gentamicin induced inhibitory effect on EFS response in rat bladder smooth muscle was not mediated by the activation of adrenergic, cholinergic, or serotonergic receptor. The inhibition of gentamicin might be mediated through the PLC dependent pathway, but not through the PKC, MLCK or rho kinase dependent pathway.
Animals ; Atropine ; Gentamicins* ; Guanethidine ; Muscle, Smooth* ; Phosphotransferases ; Rats* ; rho-Associated Kinases ; Type C Phospholipases ; Urinary Bladder*