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Yohimbine was studied to examine its effectiveness in preventing central nervous system(CNS) depression and bradycardia induced by amitraz (N'-(2,4-dimethylphenyl)-N-[(2,4-dimethylphenyl-imino)-methyl]-N-methyl- methanimide). In control open-field activity experiments, the dogs showed high numbers of grid-line crossings in the first 5 min (exploratory phase), and subsequently low numbers of grid-line crossings (nonexploratory phase). An iv injection of amitraz (1 mg/kg) abolished both the exploratory and nonexploratory phases and caused bradycardia. Yohimbine alone caused a trend to increase the open-field activity in the nonexploratory phase. In addition, yohimbine prevented the bradycardia and suppression of open-field activity induced by amitraz. The results suggest that yohimbine has a potential to be used as an antidote for amitraz overdose.

Subcutaneous injection of xylazine (0.1-3.0 mg/kg) produced a dose-dependent delay of small intestinal transit without affecting gastric emptying in the conscious mice. The xylazine-induced delay of small intestinal transit was antagonized by alpha 2-adrenoceptor antagonists, e.g., yohimbine, piperoxan and tolazoline. The antagonism of xylazine activity by yohimbine was dose-dependent, and the maximal antagonistic effect was seen at 1 mg/kg. Other adrenoceptor antagonists with only alpha 1-blocking activity, e.g., thymoxamine, prazosin and phenoxybenzamine at the doses studied did not reduce the depressant effect of xylazine on small intestinal transit. A beta-adrenergic antagonist, propranolol was not effective in reducing xylazine activity. The opioid antagonist, naloxone did not reduce the effective of xylazine, nor did yohimbine antagonize the morphine-induced delay of small intestinal transit. The xylazine-induced delay of small intestinal transit was not altered by atropine, hexamethonium, haloperidol, methysergide, chlorpheniramine or cimetidine. Pretreatment of mice with reserpine and alpha-methyl-p-tyrosine or 6-hydroxydopamine failed to reduce the intestinal effect of xylazine. These results suggest that xylazine-induced delay of small intestinal transit is mediated by postjunctional alpha 2-adrenoceptors and appears not to involve activation of opioid, cholinergic, dopaminergic, histaminergic, or serotonergic receptors.

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.

Retrograde flow of spermatozoa into the urinary bladder of rams during electroejaculation (EE) was examined. In experiment 1, semen and 4 consecutive samples of the urine released during the first post-EE micturition were collected once a week from 6 rams for 5 weeks during the nonbreeding season. The overall mean concentration per milliliter and the mean total number of spermatozoa in the urine ranged from 3.06 to 4.32 X 10(6) and from 80 to 2,865 X 10(6), respectively. The spermatozoal concentration in sequential urine samples was not different between samples, indicating that these spermatozoa had mixed with the urine before micturition. The percentage of the total number of spermatozoa displaced during EE, which flowed into the urinary bladder (retrograde flow), varied among rams (range 3.9% to 80%). The overall mean percentage of retrograde flow during the nonbreeding season was 28.3%. In experiment 2, a catheter was implanted into the urinary bladder of 6 rams (4 rams were from experiment 1), and semen was collected over 4 weeks during the subsequent breeding season. A urine sample was collected from the implanted catheter before EE. Immediately after semen collection, urine was collected by evacuating the bladder. The spermatozoal concentration in the pre-EE urine ranged from 0 to 1.3 X 10(6) (mean +/- SD, 0.17 +/- 0.38 X 10(6)) and was significantly (P less than 0.0001) lower than the spermatozoal concentration in the post-EE urine, which ranged from 1.10 to 22.55 X 10(6) (mean +/- SD, 9.46 +/- 11.30 X 10(6)).(ABSTRACT TRUNCATED AT 250 WORDS)

Eighty-eight strains of Shigella sonnei isolated in northern Taiwan during the period of 1970-1974, were studied for their colicin types by a modified method of Abbott and Shannon. As a result, 67(76%) typable and 21(24%) non-typable strains were found. The prevalent colicin types of S. sonnei in northern Taiwan were types 15(52%) and 6(15%), followed by types 8(3%), 11(3%) and 12(3%). Other types were not found.

The mechanism by which xylazine raises plasma glucose but lowers insulin concentrations was examined in Holstein cows. Intravenous injection of xylazine (15-150 micrograms/kg) induced a dose-dependent hyperglycemia and hypoinsulinemia for 3-4 h. An alpha 2-adrenergic blocking agent, yohimbine, and an alpha 1- and alpha 2-adrenergic blocking agent, phentolamine, at 500 micrograms/kg each reduced or abolished xylazine-induced hyperglycemia and hypoinsulinemia. The alpha 1-adrenergic blocking agents, prazosin and phenoxybenzamine, at 500 micrograms/kg each did not exert such antagonism. Prazosin at the dose studied even prolonged xylazine-induced hypoinsulinemia. The alpha-adrenergic blocking agents alone at 500 micrograms/kg each did not change either plasma glucose or insulin concentrations. The present study suggests that xylazine-induced hyperglycemia and hypoinsulinemia are mediated by alpha 2-adrenergic receptors, possibly in beta-cells of pancreatic islets which inhibit the release of insulin. The present study further suggests the use of xylazine as a pharmacological tool in the study of adrenergic influence on in vivo insulin release.

Yearling steers were treated with ACTH to determine the effect of increased plasma cortisol concentration on bovine lymphocyte and polymorphonuclear leukocyte (PMN) function. The administration of ACTH caused a significant (P less than 0.01) increase in serum cortisol concentration and depression of lymphocyte blastogenesis in response to phytohemagglutinin and concanavalin A. The response to pokeweed mitogen was also depressed, but not significantly. Random migration by PMN was significantly enhanced by ACTH treatment, but there was no effect on ingestion of Staphylococcus aureus, nitroblue tetrazolium reduction, or antibody-dependent cell-mediated cytotoxicity by PMN. The iodination reaction, which evaluates the activity of the myeloperoxidase-hydrogen peroxide-halide antibacterial system of the PMN, was significantly impaired after ACTH treatment. These data indicate that specific parameters of lymphocyte and neutrophil function were impaired directly or indirectly by elevated in vivo concentrations of plasma cortisol.

The effect of pneumonectomy in dogs on extravascular lung water (EVLW) was studied using a double-indicator (iced indocyanine green dye) dilution technique. The EVLW was measured in five dogs before and after a left pneumonectomy while left atrial pressure was increased in 5-mm Hg increments from 10 to 25 mm Hg by serially inflating a left atrial Foley balloon. There were no significant differences in hematocrit, total protein, or plasma oncotic pressure before or after pneumonectomy. Prepneumonectomy EVLW was adjusted to reflect right lung EVLW alone. Both before and after pneumonectomy there was a significant increase in EVLW when left atrial pressure was increased to 25 mm Hg. However, EVLW values were similar before and after pneumonectomy at each level of left atrial pressure. We conclude that pneumonectomy does not acutely increase susceptibility to EVLW formation caused by a hemodynamic challenge. This implies that following pneumonectomy, if left heart filling pressures are normal, there is no clinical benefit to excessive fluid restriction.

Xylazine and ketamine are an anesthetic combination used in feline practice for routine surgical procedures. In a controlled study, we evaluated the effects of yohimbine, an antagonist of xylazine, on the anesthesia induced by this anesthetic combination in cats. Two intramuscular doses of xylazine and ketamine (2.2 mg of xylazine/kg plus 6.6 mg of ketamine/kg and 4.4 mg of xylazine/kg plus 6.6 mg of ketamine/kg) caused approximately 60 and 100 minutes of anesthesia, respectively, in control cats. When yohimbine (0.1 mg/kg) was given intravenously 45 minutes after ketamine administration, the cats regained consciousness within 3 minutes. They were ambulatory 1 to 2 minutes after regaining consciousness. Yohimbine also reversed the bradycardia and respiratory depression elicited by xylazine-ketamine. The results indicated that yohimbine may be useful for controlling the duration of xylazine-ketamine anesthesia in cats.

The effect of atropine on cardiopulmonary changes induced by xylazine-ketamine anesthesia was studied in 7 male dogs. A consecutive i.v. injection of xylazine (1.1 mg/kg) and ketamine (11 mg/kg) induced an anesthesia of approximately 20 min, and increased PaCO2 but decreased PaO2 and pHa for 20 min. The xylazine-ketamine administration increased heart rate for 5 min, which was followed by a small but significant decrease at 30 min posttreatment. The xylazine-ketamine injection decreased left ventricular and mean aortic pressure for 1 to 2 min. The low pressures returned to normal and became higher than base line levels at 5 min posttreatment. The xylazine-ketamine injection increased peripheral resistance and decreased cardiac output and cardiac index for at least 40 min. An i.v. injection of atropine sulfate (0.04 mg/kg) potentiated the effect of xylazine-ketamine on PaCO2 and PaO2, but did not change the effect of xylazine-ketamine on pHa. The atropine injection did not change the transient low left ventricular and mean aortic pressures immediate after the xylazine-ketamine administration, but did potentiate the duration of the increased heart rate, left ventricular and mean aortic pressures induced by xylazine-ketamine between 5 to 40 min. Atropine did not change the effect of xylazine-ketamine on peripheral resistance. Atropine partially antagonized the effect of xylazine-ketamine on cardiac output and cardiac index. Interpretation of the results indicates that atropine may increase cardiac work and may potentiate the pulmonary effect of i.v. administration of xylazine-ketamine.

Two doses of an alpha 2-adrenoreceptor antagonist, idazoxan, were administered to reverse the CNS depressant and bradycardia effects of xylazine in calves. Once a week for 3 weeks, each of 6 calves were administered IV one treatment of: (1) 0.2 mg of xylazine/kg of body weight followed in 10 minutes by 1 ml of 0.9% NaCl, (2) 0.2 mg of xylazine/kg followed in 10 minutes by 10 micrograms of idazoxan/kg, or (3) 0.2 mg of xylazine/kg followed in 10 minutes by 30 micrograms of idazoxan/kg. The order of the 3 treatments in each calf was selected at random. Xylazine alone caused lateral recumbency for 27.2 +/- 3.0 minutes (mean +/- SEM). Idazoxan administered at dosages of 10 and 30 micrograms/kg shortened xylazine-induced lateral recumbency to 11.5 +/- 0.8 and 10.3 +/- 0.2 minutes, respectively. Calves given xylazine alone stood at greater than 60 minutes after the onset of recumbency. Idazoxan given at dosages of 10 and 30 micrograms/kg shortened the time to standing to 16.8 +/- 1.7 and 11.3 +/- 0.2 minutes, respectively. Idazoxan given at a dosage of 30 micrograms/kg also reversed xylazine-induced bradycardia. Results indicated that idazoxan should be a useful antidote for xylazine overdose in cattle.

Once a week for 4 weeks, 5 dogs were given IM injections of xylazine (2.2 mg/kg of body weight) followed in 10 minutes by IV injections of pentobarbital (14 mg/kg). The resultant duration of anesthesia, absence of pedal reflex, and time from return of consciousness to ambulation were consistent from week to week. The mean times were 137.3, 111.8, and 56.9 minutes, respectively. A second experiment using 5 other dogs was performed to evaluate the antagonistic effect of yohimbine on the anesthesia induced by the xylazine-pentobarbital combination. When yohimbine (0.1 mg/kg, IV) was administered 10, 60, and 120 minutes after the xylazine-pentobarbital injection (given as in the 1st experiment), it abolished or markedly reduced the duration of anesthesia, absence of pedal reflex, and the time from return of consciousness to ambulation. After being given yohimbine, the dogs had a smooth recovery without postanesthetic excitement. In experiment 3, IM xylazine injections caused bradycardia without changing mean arterial blood pressure. Subsequent IV pentobarbital administration abolished xylazine-induced bradycardia for approximately 20 minutes and decreased arterial blood pressure slightly and gradually. Respiration was markedly depressed for the first 20 minutes of xylazine-pentobarbital anesthesia and gradually decreased during the rest of the 50-minute monitoring period. Yohimbine injection at postpentobarbital dosing minute 50 reversed the resumed xylazine-induced bradycardia and relieved other signs of respiratory depression associated with xylazine-pentobarbital anesthesia. The xylazine-pentobarbital combination was safe and effective for inducing and maintaining up to 2 hours of anesthesia in dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Xylazine (1.1 mg/kg of body weight, IV), an alpha 2-adrenoreceptor agonist, suppressed the increase in plasma insulin concentration induced by glucose (0.6 g/kg, IV) in dogs. Yohimbine (0.11 mg/kg, IV), an alpha 2-adrenoreceptor antagonist, given 5 minutes after xylazine, reversed effects of xylazine, whereas yohimbine alone increased plasma insulin and decreased plasma glucose concentrations. Seemingly, alpha 2-adrenoreceptors exert a negative control of insulin release.

The effect of amitraz on heart rate (HR) and mean aortic blood pressure (MAP) were studied in five conscious male dogs. An iv injection of amitraz (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia for at least 60 min. Administration of amitraz also caused an increase in MAP for 20 min. Atropine sulfate (0.045 mg/kg, iv) increased HR and prevented amitraz-induced bradycardia. In addition, atropine potentiated amitraz-induced hypertension for 45 min. Yohimbine, an alpha 2-adrenoreceptor antagonist, given iv at 0.1 mg/kg, prevented hypertension, bradycardia, and sinus arrhythmia induced by amitraz. Tolazoline, a nonselective alpha-adrenoreceptor antagonist, given iv at 5 mg/kg, reduced the bradycardia and sinus arrhythmia caused by amitraz administration but did not change amitraz-induced hypertension. Tolazoline alone also increased both HR and MAP. Prazosin, an alpha 1-adrenoreceptor antagonist, given iv at 1 mg/kg, did not affect the cardiovascular actions of amitraz. The results suggest that (1) alpha 2-adrenoreceptors mediate amitraz-induced bradycardia and hypertension, and (2) yohimbine, but not atropine, can be used to control the untoward reactions of amitraz.

Primary mediastinal seminoma is a rare neoplastic disease. Only 133 cases have been reported in the literature. Five patients with primary mediastinal seminoma had been treated at VGH from 1974 to 1986. All of them received exploratory thoracotomy but only two of them were resectable. Postoperative radiation therapy was given regardless of resection. One had additional chemotherapy due to nodal involvement. All five patients showed complete resolution and were alive and free of disease for an average follow-up period of 42.6 months (range, 5-82 months). So we conclude that mediastinal seminoma is a rare neoplastic disease and can be treated primarily by surgery. Irradiation can also induce complete remission and long term survival in those with unresectable tumors.

The effect of IV amitraz on the transit of barium sulfate through the stomach and duodenum as well as amitraz-induced bradycardia was studied in 4 dogs. Control transit time and heart rates were determined after IV injection of dimethyl sulfoxide (0.1 ml/kg), which was subsequently used as the vehicle for amitraz administration. The time for barium sulfate to move from the stomach to the duodenojejunal junction was 6.1 +/- 1.3 minutes (mean +/- SEM). An IV injection of amitraz (1 mg/kg) prolonged the transit time to 251.2 +/- 27.0 minutes, and induced marked bradycardia for at least 60 minutes. During the amitraz-induced prolongation of gastrointestinal transit, there were no vigorous gastric contractions for at least 180 minutes. Yohimbine, an alpha 2-adrenergic blocking agent, given IV 20 minutes after amitraz administration, at a dosage of 0.1 mg/kg, reversed both the gastrointestinal and bradycardic effects of amitraz. It was concluded that 1) amitraz causes decreased gastrointestinal motility and bradycardia, and 2) yohimbine may be useful in the control of the untoward reactions caused by amitraz administration.

Yohimbine was studied at various dosages to examine its effectiveness in reversing as well as preventing xylazine-induced CNS depression. Intravenous injection of xylazine (1 to 10 mg/kg) induced a dose-dependent CNS depression that was prevented by a low dosage of yohimbine (0.1 mg/kg, IV). Xylazine at a dosage of 10 mg/kg induced convulsions in 3 of 5 dogs. In addition, the CNS depressant effect of xylazine (1 to 10 mg/kg, IV) was reversed by yohimbine at dosages ranging from 0.01 to 1.0 mg/kg. Yohimbine alone at dosages of greater than or equal to 0.33 mg/kg appeared to cause apprehension for 20 to 60 minutes. The results indicated that yohimbine can be used as an antagonist to control the duration and depth of xylazine-induced CNS depression. For this purpose, it seemed that yohimbine at a dosage of 0.1 mg/kg is suitable.

Nutritional requirements for the production of isoamylase by Pseudomonas amyloderamosa mutant strain JD210 were investigated. The optimal initial pH for enzyme production in shake-flask cultivation was 5.0. Maltose and soybean protein hydrolyzate were found to be the best carbon source and nitrogen source, respectively. The enzyme production was drastically inhibited by Zn+2 and Cu+2. Other metal ions phosphates and surfactants exhibited no significant inhibitory or accelerating effect on enzyme production. According to auxanography and single omission experiments, proline and isoleucine were required for growth. The supplement of 0.1% proline increased enzyme production by around 30% compared with no addition.

Earlier work by others has shown that the catecholamines, epinephrine and isoproterenol, can raise blood calcium levels in parathyroidectomized but not intact rats, and can restrict the hypocalcemic effect of injected thyrocalcitonin (TCT). The present findings support this earlier work, further showing that such catecholamines can produce hypercalcemia in rats after removal of the thyroid gland by acute thyroparathyroidectomy (TPTX) and indicating that these drugs may raise blood calcium by mobilizing calcium from bone. Rats were fasted overnight, subjected to TPTX and concurrently injected with adrenergic agonist or antagonist drugs alone or in combination. Epinephrine, isoproterenol, and the beta-2 adrenergic agonist, salbutamol, in doses greater than or equal to 1 mg/kg raised blood calcium from low normal levels (approximately 9-10 mg/100 ml) by 1.5 to 2 mg/100 ml (p less than 0.01). Hypercalcemia was apparent by 1 hour after injection and lasted for 1-4 hours. The extent of Ca elevation was dose-related. Pretreatment of rats with the alpha-adrenergic antagonist, phenoxybenzamine, enhanced the effect of epinephrine while pretreatment with the beta-antagonist, propranolol, reduced the effect of isoproterenol. The more selective beta-2 antagonist, butoxamine, but not the beta-1 antagonist, practolol, also reduced the hypercalcemic effect of isoproterenol in TPTX rats. These results suggest that catecholamine-induced hypercalcemia in TPTX rats is mediated by beta-2 adrenergic receptors. Related studies using rats prelabeled with 45Ca further suggest that the catecholamines, like parathyroid hormone, may act to raise blood calcium by mobilizing calcium from bone. The fact that these catecholamines could induce marked hypercalcemia in acutely TPTX rats but not in intact rats indicated that endogenous TCT protects the thyroid intact rat against hypercalcemia. The present findings support this idea in showing that isoproterenol and salbutamol raised levels of immunoreactive rat TCT in both thyroid venous and peripheral blood. Catecholamines apparently can promote TCT secretion, either directly or by a small transient increase in blood calcium. This, in turem, acts to combat hypercalcemia in thhroid-intact rats.

It has been found that both adenosine deaminase (ADA) and gamma-interferon (r-IFN) are higher in tuberculous pleural effusions than in other types of pleural effusion. Both mechanisms may be related to the T-lymphocytes in effusions. We studied 39 pleural effusions: 19 tuberculous and 20 malignant [The ADA was determined according to the Giusti method and r-IFN by ELISA]. We compared the ADA and r-IFN levels in both groups of effusions and tried to determine if there was any correlation between them. The results showed: (1) The ADA enzyme level was significantly higher in tuberculous effusions than in malignant effusions as was expected (133.0 +/- 50.4 vs 32.0 +/- 17.7 U/L). (2) The r-IFN was also significantly higher in tuberculous effusions than in malignant effusions (30.4 +/- 17.4 vs 2.9 +/- 2.8 U/ml). (3) The coefficients of regression for the ADA and r-IFN levels were poor. In conclusion, both tests for measuring ADA and r-IFN levels are excellent methods for differentiating tuberculous and malignant effusions, and especially measurement of the r-IFN level could serve as a more specific test for differentiating malignant pleural effusions with high ADA levels. However, no strong correlation was found between the ADA and r-IFN levels.

Recent investigations have suggested that the alpha 2-adrenoreceptor agonist B-HT 920 is also a dopamine (DA) agonist with a selectivity for presynaptic receptors. In the present study, the emetic effect of B-HT 920 was investigated. Intravenous injections of B-HT 920 (0.32-10.0 micrograms/kg) and a DA2-agonist apomorphine (3.2-100.0 micrograms/kg) caused dose-dependent emesis. The ED50 of B-HT 920 and apomorphine were 3.2 and 12.3 micrograms/kg, respectively. When haloperidol (10.0-24.5 micrograms/kg i.v.), a DA2-antagonist, was given 5 minutes before B-HT 920 (10 micrograms/kg) or apomorphine (32 micrograms/kg), it caused a dose-dependent prevention of B-HT 920- and apomorphine-induced emesis. The ED50 of haloperidol in preventing the emetic effect of both drugs was identical (13.5 micrograms/kg). In contrast, haloperidol (32 micrograms/kg i.v.) did not prevent the emetic effect of ouabain (40 micrograms/kg i.v.). Neither did yohimbine (0.1 mg/kg i.v.), an alpha 2-adrenoreceptor antagonist, prevent the emetic effect of B-HT 920 (10 micrograms/kg). These results suggest that B-HT 920, acting like apomorphine, induces emesis by activating DA2-receptors probably in the chemoreceptor trigger zone of the area postrema.

The influence of atropine on anesthesia induced by xylazine-pentobarbital administration was studied in 5 dogs. The combination of xylazine (2.2 mg/kg of body weight, IM) and pentobarbital (14.0 mg/kg, IV) caused anesthesia with the duration of absence of the pedal reflex, duration of anesthesia, and the time from return of consciousness to ambulation to be 107.4, 123.4, and 59.2 minutes, respectively. Bradycardia and short-term respiratory depression were observed. An IM injection of atropine sulfate (0.045 mg/kg) did not significantly change the durations of absence of the pedal reflex and of anesthesia, the time from return of consciousness to ambulation, or the pattern of respiration in the anesthetized dogs. The PaO2 increased gradually in both groups; however, atropine caused a marked tachycardia and increased the PaCO2. Fifteen minutes after pentobarbital injection, administration of atropine sulfate caused a slight but significant (P less than 0.01) decrease in arterial pH. Although atropine sulfate antagonized xylazine bradycardia, the data indicated that it may have caused increased respiratory depression in dogs anesthetized with xylazine and pentobarbital.

Twenty healthy ponies were given i.v. 1.1 mg/kg of xylazine from 2 manufacturers and the pharmacokinetic parameters calculated from the disposition curves. The disposition curves for the 2 commercial preparations were not different. Yohimbine, an antagonist of the pharmacologic effects produced by xylazine, did not alter the disposition of xylazine in the plasma. A single i.v. bolus of xylazine was completely described in 17 of 20 animals by the biexponential equation: Cp = 1.30e(-0.3955t) + 0.58e(-0.033t) where Cp represents the concentration of xylazine in the plasma at time t (min). The t1/2 beta was 75 +/- 13 min and whole body clearance was 18.9 +/- 1.5 (ml/min.kg).

The effect of amitraz, a formamidine insecticide, on in vitro intestinal contractions was studied in teh transmurally-stimulated guinea-pig ileum. An electrical stimulation (with 80 V/0.5 msec/0.1 Hz shown on the dial of the stimulator) caused the ileum to contract presumably via the release of acetylcholine. Amitraz (10(-7) to 10(-6) M) produced a dose-dependent inhibition of these transmurally-stimulated contractions. This effect of amitraz was blocked and reversed by idazoxan (10(-6) M), an alpha 2-adrenoceptor antagonist, but was not prevented by prazosin (10(-6) M), an alpha 1-adrenoceptor antagonist. These results suggest that alpha 2-adrenoceptors mediate the effects of amitraz on the transmurally-stimulated guinea-pig ileum. The results also suggest that amitraz decreases intestinal contraction by activating the alpha 2-adrenoceptors in the myenteric (Auerbach's) plexus, thus inhibiting parasympathetic tone.

Pulmonary cryptococcosis, a less common fungal infection, frequently reveals nodular lesions (single or multiple) and patchy infiltrations (alveolar or interstitial) on chest X rays. A large mass-like pattern is less common. Here we report 2 cases of pulmonary cryptococcosis with negative bronchoscopic findings. One patient received a right lower lobectomy under the impression of malignancy; the other received a transthoracic needle aspiration, and numerous cryptococci were found by India ink preparation. Thus, pulmonary cryptococcosis should be included in the differential diagnosis of a mass lesion. A brief review of the literature is also included about diagnostic approach and management of pulmonary cryptococcosis.

The effects of xylazine on heart rate (HR) and mean arterial blood pressure (ABP) were studied in 5 conscious male dogs. An IV injection of xylazine (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia. Xylazine administration also caused an initial increase in ABP, which was followed by a decrease. Atropine sulfate (0.045 mg/kg, IM) increased both the ABP and HR, but prevented xylazine-induced bradycardia only in 3 of 5 dogs. The other 2 dogs had to be given a supplemental dose of atropine sulfate (0.01 mg/kg, IV) before xylazine-induced bradycardia was antagonized. In addition, atropine sulfate potentiated xylazine-induced hypertension for 60 minutes. Yohimbine, an alpha 2-adrenoreceptor blocking agent, given IV at a dosage of 0.1 mg/kg, antagonized hypertension, hypotension, and bradycardia induced by xylazine. In addition, doxapram HCl, given IV at a dosage of 5.5 mg/kg, antagonized bradycardia but potentiated xylazine-induced hypertension, and an IV injection of 4-aminopyridine at a dosage of 0.5 mg/kg did not affect the cardiovascular actions of xylazine. It was concluded that atropine sulfate at the IM dosage of 0.045 mg/kg may be insufficient to antagonize xylazine-induced bradycardia but may potentiate xylazine-induced hypertension, and yohimbine may be useful in antagonizing these untoward reactions associated with xylazine administration. Doxapram and 4-aminopyridine were not found to be beneficial.

Pupillary and cardiac responses to i.v. injections of chlordimeform (CDM, 0.3-10 mg/kg), a formamidine insecticide, and its metabolites demethylchlordimeform (DCDM, 0.03-1 mg/kg) and didemethylchlordimeform (DDCDM, 0.1-3 mg/kg) were studied in rats anesthetized with pentobarbital. Both CDM and DCDM induced a dose-dependent mydriasis and bradycardia and DCDM was 10 times more potent than CDM in causing these effects. In contrast, DDCDM did not induce a mydriasis or bradycardia. The alpha 2-adrenoreceptor antagonist, idazoxan (0.2 mg/kg, i.v.) abolished or reduced CDM- and DCDM-induced mydriasis and bradycardia, whereas the alpha 1-adrenoreceptor antagonist, prazosin (1.5 mg/kg, i.v.) did not change these effects of CDM and DCDM. SKF 525-A (50 mg/kg, i.p.), an inhibitor of enzymatic demethylation, administered 10 min before the first dose of CDM, failed to reduce the effects of CDM. The results suggested: 1) the mydriatic and bradycardic effects of CDM and DCDM are mediated by alpha 2-adrenoreceptors, 2) the monodemethylation of CDM increases its alpha 2-adrenoreceptor agonistic activities, but the didemethylation of CDM abolishes these activities, and 3) CDM can exert alpha 2-adrenoreceptor agonistic activities without undergoing a demethylation process.

The effect of xylazine on the transit of barium sulfate through the stomach and duodenum was evaluated in 4 dogs. Base-line transit time was determined while the dogs were nonsedated and undisturbed; the mean time for barium sulfate to move from the stomach to the duodenojejunal junction was 4.8 +/- 1.2 minutes. An IV injection of xylazine (1 mg/kg) prolonged the mean transit time to 157 +/- 37.8 minutes. During the xylazine-induced prolongation of gastrointestinal transit, there were no vigorous contractions for at least 90 minutes. Yohimbine, an alpha 2-adrenergic-blocking agent, given IV at a dosage of 0.1 mg/kg, did not affect gastrointestinal motility. It did, however, prevent both the gastrointestinal and sedative effects of xylazine. Atropine methylnitrate given IV at a dosage of 1 mg/kg prolonged the transit time to 13.8 +/- 2.4 minutes. After atropine methylnitrate injection, the gastrointestinal tract was more flaccid than with xylazine administration. The prolongation of transit induced by atropine methylnitrate was not prevented by yohimbine. It was concluded that gastrointestinal radiographic findings in animals under the influence of xylazine should be interpreted cautiously.

Effects of yohimbine on xylazine-pentobarbital anesthesia were evaluated in ponies. Five minutes after the IV injection of xylazine (1.1 mg/kg of body weight), pentobarbital sodium (12.7 mg/kg, IV) and additional xylazine (2.2 mg/kg, IM) were given and produced anesthesia in 12 ponies for 64.0 +/- 16.4 minutes (mean +/- SD) as well as immobilization for 89.8 +/- 34.2 minutes. Eleven ponies were given yohimbine (0.1 mg/kg, IV) 50 minutes after pentobarbital dosing. In these 11 ponies, durations of anesthesia and immobilization were shorter, 52.0 +/- 1.4 and 65.5 +/- 14.8 minutes, respectively. The xylazine-pentobarbital combination caused bradycardia that was reversed by yohimbine injection. Xylazine-pentobarbital produced a small, but steady, decrease of mean arterial blood pressure, which was compounded by yohimbine administration and was evident for approximately 2 minutes. Within a minute after yohimbine injection, the ponies' respiratory rate decreased and the length of inspiration and expiration and thoracic breathing increased. This lasted approximately 2 to 3 minutes and was followed by an increase in respiratory rate. The anesthesia also produced a decrease in PaO2 that gradually returned to base line in 12 control ponies, but was more pronounced in 11 ponies given yohimbine. The PaCO2, although remaining moderately high in control ponies, returned to base line after yohimbine injection. An increased pHa was seen 60 minutes after induction of anesthesia and was especially noticeable after yohimbine administration. Decreases in the number of WBC, hemoglobin content, PCV, plasma protein and serum aspartate transaminase resulting from xylazine-pentobarbital were reversed by yohimbine. Conversely, serum glucose values and creatine kinase activities were increased by xylazine-pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate association of Streptococcus mutans with human dental caries, 323 adolescent students of Chung Shan Medical & Dental college were examined for decayed missing filled of tooth (DMFT) and then plaques were taken from their first and second upper molar's approximal surface using sterilized dental floss for S. mutans isolation. The result showed that among the 269 caries-active individuals 246 (94.98%) had detectable S. mutans, whereas among the 64 caries-free individuals only 23 (35.93%) were found positive, which showed significant association between plaque levels of S. mutans and dental caries (p less than 0.0001). Although the value is a little higher than that found in other literatures but has no statistically significant difference.

We compared the ability of 3 alpha 2-adrenoreceptor antagonists, idazoxan (0.05 mg/kg), tolazoline (2 mg/kg), and yohimbine (0.2 mg/kg) to reverse xylazine (0.3 mg/kg)-induced respiratory changes and CNS depression in 6 ewes. Once weekly, each ewe was given a random IV treatment of xylazine, followed in 5 minutes by either an antagonist or 0.9% NaCl solution. Xylazine alone caused recumbency for 54.2 +/- 5.3 minutes (mean +/- SEM). Xylazine also increased respiratory rate and decreased PaCO2 for at least 45 minutes, but did not significantly change arterial pH or PaCO2. Idazoxan and tolazoline were equally effective in reversing the respiratory actions of xylazine; however, yohimbine was less effective in reducing the respiratory rate and was ineffective in antagonizing the decreased PaO2. Idazoxan and tolazoline decreased the duration of xylazine-induced recumbency to 6.3 +/- 0.6 and 9.5 +/- 2.3 minutes, respectively, whereas yohimbine did not significantly change this effect of xylazine. Thus, at the dosages studied, idazoxan and tolazoline appeared to be more effective than yohimbine in reversing the respiratory and CNS depressant actions of xylazine in sheep.

Xylazole (Xyl) is an analogue of xylazine (Xyn) synthesized by Lanzhou Institute of Chinese Traditional Veterinary Medicine. The effects of Xyl on heart rate and blood pressure were studied in 5 conscious dogs. Xyl 1 mg/kg iv was similar to Xyn in producing bradycardia and an initial transient hypertension followed by a lasting hypotension which was less significant than Xyn. Yohimbine (0.1 and 0.3 mg/kg), an alpha 2-adrenoreceptor blocking agent, antagonized bradycardia and hypotension induced by Xyl. Tolazoline (3.3 mg/kg), a nonselective alpha-adrenoreceptor blocking agent, reversed the bradycardia and hypotensive effect. Prazosin (1 mg/kg), an alpha 1-adrenoreceptor blocking agent, did not change Xyl-induced bradycardia and hypotension. Atropine (20 micrograms/kg) not only antagonized Xyl-induced bradycardia but also changed from bradycardia to tachycardia, and greatly potentiated Xyl-induced hypertension for more than 30 min. The results suggested that Xyl-induced cardiovascular effects are similar to Xyn that mediated by alpha 2-adrenoreceptor.

From October 1979 to December 1984, 77 patients with nonthymomatous myasthenia gravis underwent thymectomy and 74 patients were available for careful follow-up study in this review. Among these 74 patients, 18 were male and 56, female. Their ages ranged from 13 to 68 years with an average age of 30.2 years. Men tend to be affected at a later age than women (an average age of 38.0 versus 26.1 years). Duration of the disease was from one to 30 years, with an average of 4.2 years. A sternal-splitting incision was performed for all patients. Thymectomy was made by removal of all anterior mediastinal fat between the pleuropericardial reflection and phrenic nerve bilaterally. Seventy of the 74 patients benefited from thymectomy. Of these, 34 patients had remission and 36 patients had substantial improvement; three patients did not improve after thymectomy but did not increase in severity of symptoms or medication requirement. There was no postoperative death. Myasthenic crisis developed in four patients and five patients had pulmonary complications. These nine patients were among the 21 patients who did not receive either plasmapheresis preoperatively or a high dose of steroids perioperatively. Early thymectomy is recommended for patients with nonthymomatous myasthenia gravis. We also recommend that patients undergoing thymectomy should be treated either with plasmapheresis preoperatively or with high doses of steroid perioperatively.

This report reviews our experience with 96 patients with benign or malignant stricture of the esophagus who underwent interposition of the left colon with or without esophageal resection from July 1982 to June 1987. There were 67 male and 29 female patients ranging in age from 8 to 80 years. Thirty-seven patients had fibrotic stricture secondary to corrosive injury of the esophagus, 42 had cancer of the esophagus, and 17 had cancer of the gastric cardia. The incidence of postoperative complications and surgical mortality, respectively, was 16.2% and 2.7% for patients with corrosive stricture of the esophagus, 35.7% and 11.9% for patients with cancer of the esophagus, and 35.2% and 5.8% for patients with cancer of the gastric cardia. Reconstruction resulted in good function in 75.6% of the patients with corrosive stricture of the esophagus, 66.6% of the patients with cancer of the esophagus, and 70.5% of patients with cancer of the gastric cardia. The morbidity and mortality were higher in the group with malignant esophageal strictures because of advanced age, poor general condition of the patient, and extent of the surgical procedure needed. Cervical anastomotic leakage was the most frequently encountered complication (13.5%), and all the poor-function results were caused by this complication. In our experience, reconstruction of the esophagus with left colon is a satisfactory method that can be accomplished with acceptable morbidity and mortality. The left colon is a durable and functional substitute.

The LD50 from subcutaneous administration of levamisole in castrated male pigs (15 to 25 kg) was established as 39.8 mg/kg. Oral administration of dichlorvos (60 mg/kg, 3 times the anthelmintic dosage level) 1 hour before levamisole injection lowered blood cholinesterase activity to approximately 60% that of the controls, but did not change the LD50 of levamisole. In contrast, oral administration of pyrantel tartrate (25 mg/kg, an anthelmintic dosage level) did not lower blood cholinesterase activity, but rather, increased the toxicity by lowering the LD50 of levamisole from 39.8 mg/kg to 27.5 mg/kg. The data supported the hypothesis that levamisole toxicity was enhanced by nicotine-like compounds (ie, pyrantel), but was not affected by organophosphates (ie, dichlorvos).