1. Atropine has recently been known to possess a sympathetic ganglion blocking effect. If atropine blocks the sympathetic ganglia innervating the blood vessels, the drug should cause depressor responses. The author attempted to verify this assumption in urethane-anesthetized rabbits having atropinesterase. 2. Ten and $50{\mu}g/kg$ of atropine produced little variation of the blood pressure; $250{\mu}g/kg$ slight depressor responses; $1,250{\mu}g/kg$ distinct ones. Under hexamethonium-infusion, 10 and $50{\mu}g/kg$ produced observable depressor responses; 250 and $1,250{\mu}g/kg$ produced more pronounced ones. 3. In experiments examining influence of phenoxybenzamine and bretylium on the atropine responses, the lowered blood pressure by these agents was raised by simultaneous infusion of angiotensin with hexamethonium. The depressor responses to atropine (10, 50 and $250{\mu}g/kg$) were slight after the administration of phenoxybenzamine and bretylium. 4. Propranolol did not affect the depressor responses to atropine. 5. In spinalized rabbits the lowered blood pressure was raised by the angiotensin-infusion. In these animals receiving the simultaneous hexamethonium-infusion, atropine (10, 50 and $250{\mu}g/kg$) produced little depressor responses. 6. From these results it is inferred that atropine produced the depressor responses by blocking the sympathetic ganglia innervating the blood vessels.
The passive tilt has been performed to study the orthostasis on the cardiovascular system. The orthostasis due to upright tilt was demonstrated as follows: the venous return, cardiac output and systemic arteiral blood pressure were decreased, whereas there was concomitant increase of heart rate, through the negative feedback mediated by such as the baroreceptor . Previous investigators have suggested that the tolerance to the orthostasis could he increased by blocking the cholinergic fiber with atropine which prevented vasodilation and bradycardia through the vasovagal reflex during the orthostasis. However, this hypothesis has not been clearly understood. This study was attempted to clarify the effect of atropine on the tolerance of the cardiovascular system to the upright and head-down tilt, and to investigate the change of the blood flow through head and lower leg with Electromagnetic flowmeter in both tilts before and after atropine state. Fourteen anesthetized dogs of $10{\sim}14kg$ were examined by tilting from supine position to $+77^{\circ}$ upright position (orthostasis), and then to $-90^{\circ}$ head-down position (antiorthostasis) for 10 minutes on each test. And the same course was taken 20 minutes after intravenous administration of 0.5mg atropine. The measurements were made of the blood flow(ml/min.) on the carotid artery, external jugular vein, femoral artery and femoral vein. At the same time pH, $PCO_2$, $PO_2$ and hematocrit (Hct) of the arterial and venous blood, and heart rate(HR) and respiratory rate (RR) were measured. The measurements obtained from upright and head-down tilt were compared with those from supine position. The results obtained are as follows: In upright tilt, the blood flow both on the artery and the vein through head and lower leg were decreased, however the decrement of blood flow through the head was greater than the lower leg And the atropine attenuated the decrement of the blood flow on the carotid artery, but not on the vessels of the lower leg. HR was moderately increased in upright tilt, but slightly in head-down tilt. The percent change of HR after the atropine administration was smaller than that before the atropine state in both upright and head-down tilts. Before the atropine state, RR was decreased in upright tilt, whereas increased in head-down tilt. However after the atropine state, the percent change of RR was smaller than that of before the atropine state in both upright and head-down tilts. In upright tilt, venous $PCO_2$ was increased, but arterial $PO_2$ and venous $PO_2$ were slightly decreased. Hct was increased in both upright and head-down tilts. The findings of blood $PCO_2$, $PO_2$ and Hct were not interferred by the atropine. In conclusion, 1;he administration of atropine is somewhat effective on improving the cardiovascular tolerance to postural changes. Thus, atropine attenuates the severe diminution of the blood flow to the head during orthostasis, and also reduces the changes of HR and RR in both orthostasis and antiorthostasis.
The comparative studies were made on the analgesic antipyretic effects of aminopyrine used individually and combined with parasympathetic agents (atropine sulfate). The analgesic antipyretic effects were eximined by Writhing's method to the experimental groups(mouse), and the following effects were found : 1) The active intensity of aminopyrine by it's oral administration combined with atropine sulfate is as follows. Amiinopyrine 80 mg/kg combided with Atropine sulfate 0.005 mg/kg=Aminopyrine 100 mg/kg 2) The most active range of intensity of Atropine sulfate(adjuvant) by it's oral administration is as follows. Atropine sulfate $0.004{\sim}0.005\;mg/kg$.
The purpose of this study is to evaluate the applicability of intravenous atropine sulfate therapy in infantile hypertrophic pyloric stenosis (IHPS). From 1998 to 2000 among 35 cases of IHPS, pyloromytomy was performed in 13 (Group A), and intravenous atropine was given as a primary therapy in 22 cases (Group B). In group A, all cases were cured completely. In group B, 13 (59 %) out of 22 cases were successfully treated with atropine, but 9 were failed therapy, and required operation. The recovery period to normal feeding and the hospital stay of the successful atropine group were longer than those of pyloromyotomy, 8.6 days vs. 2.9 days and 13.2 days vs. 4.1 days, respectively. In conclusion, intravenous atropine therapy did not replace pyloromyotomy, but it might be an alternative for the selected patients with contraindications for operation.
Purpose: To examine the effectiveness of various treatments; bifocal spectacles, orthokeratology, atropine, and time spent in outdoors; in slowing down the myopia progression for Asian adolescents (6-18age). Methods: The research focused on examining the most effective treatment in controlling myopia based on the literature sources that have been published. Through meta-analysis of various research papers that already has been done in this field, a lot of data was collected. For each treatment, the difference in axial length and spherical equivalent over time was measured and recorded. To quantitatively record the difference, both axial length and spherical equivalent was determined by value of control group value of treatment group. The paper compared the effectiveness of each treatment based on the data that was measured. Results: Adolescents who chose to spend time outdoors in order to slow down myopia progression had axial length difference of 0.03 mm and spherical equivalent difference of 0.17 D. Adolescents that used atropine had axial length difference of 0.36 mm and spherical equivalent difference of 0.92 D. Bifocal spectacle resulted in axial length difference of 0.21 mm and spherical equivalent difference of 0.59 D, and for orthokeratology 0.23 mm and 0.04 D, respectively. Axial length wise, myopia was most controlled by the atropine since there was a greatest difference between the group that got the treatment and the group that did not have the treatment. According to the spherical equivalent difference data, myopia was most controlled by atropine. Conclusion: Atropine showed the most effective result in controlling myopia among the four treatment. Again, compared to other three treatment, using atropine appeared to have greatest ability in slowing down myopia progression since adolescents who were treated with atropine had greatest difference from adolescents in the control group that had the same condition but didn't get the treatment. However, every treatment was only used for 2 or 3 years which is quite short time period to measure the long term effect of the four treatments. Also, since atropine is a pharmaceutical method to control myopia, it may harm adolescents' eyes compared to optical or environmental treatment.
The aim of the study was to observe the influence and related mechanism of histamine and its analogues used for hypersensitivity tests and used as an indicator of impurities in drugs on the tissue-specific intestinal contraction. Intestinal contraction includes the activation of thick or thin filament regulation. However, there are few reports addressing the question whether this regulation is involved in histamine-induced regulation. We hypothesized that histamine plays a role in tissue-dependent regulation of intestinal contractility. Denuded ileal/colonic longitudinal and circular muscles of male rats were used and isometric contractions were recorded using a data acquisition system. Interestingly, histamine alone didn't increase the contraction of the circular muscle but increased the contraction of the longitudinal muscle. Histamine together with atropine (M3 receptor antagonist) didn't inhibit the contraction of the longitudinal and circular muscle. Therefore, histamine alone and together with atropine increases the ileal longitudinal muscle contraction suggesting that additional mechanisms (decreased receptor density, postreceptor signaling or distribution of agonists) might be involved in the regulation of ileal muscle contractility. In conclusion, histamine and/or atropine has some effect on the regulation of the longitudinal contractility regardless of M3 receptor and the simpler test would be preferred as the drug impurity test compared to more complicated tests.
Lee, Hyoung Ju;Moon, Dae Sik;Jung, Young Yun;Byun, June Seob;Kim, Chong Myung
Journal of The Korean Society of Clinical Toxicology
/
v.20
no.1
/
pp.25-30
/
2022
In this study, we report the case of a 59-year-old male patient with organophosphate pesticide poisoning. He visited the local emergency medical center after ingesting 250 ml of organophosphate pesticide. The patient's symptoms improved after the initial intravenous infusion of pralidoxime 5 g and atropine 0.5 mg. However, 18 hours after admission, there was a worsening of the symptoms. A high dose of atropine was administered to improve muscarinic symptoms. A total dose of 5091.4 mg of atropine was used for 30 days, and fever and paralytic ileus appeared as side effects of atropine. Anticholinergic symptoms disappeared only after reducing the atropine dose, and the patient was discharged on the 35th day without any neurologic complications.
Although the release of lysosomal enzymes from activated PMN leukocyte can be regulated by intracellular cyclic nucleotide levels, other responses of PMN leukocyte according to the binding of neurotransmitters to either ${\beta}$-adrenergic or muscarinic receptors are still not clarified. In addition, the function of PMN leukocyte mediated by ${\alpha}$-adrenergic receptors is uncertain. Atropine, phentolamine and propranolol inhibited calcium uptake, superoxide generation, NADPH oxidase activity and phagocytic activity in activated PMN leukocyte, whereas carbachol and isoproterenol slightly further stimulated the responses of activated cells. Either carbachol or isoproterenol stimulated superoxide generation was inhibited by their antagonists, atropine and propranolol, respectively. The response of activated PMN leukocyte was inhibited by chlorpromazine, verapamil and dantrolene but slightly stimulated by lithium. On the other hand, chlorpromazine and dibucaine did not affect NADPH oxidase activity. Atropine, phentolamine and propranolol suppressed the calcium dependent phagocytic activity. Thus, the results suggest that atropine, phentolamine and propranolol may inhibit superoxide generation in activated PMN leukocyte by the inhibition of calcium influx and by their direct action on the NADPH oxidase system which is associated with autonomic receptors.
Jo, Yang-Hyeok;Rhie, Duck-Joo;Chang, Young-Soon;Hahn, Sang-June;Sim, Sang-Soo;Kim, Myung-Suk;Kim, Chung-Chin
The Korean Journal of Physiology
/
v.25
no.1
/
pp.27-35
/
1991
Generally, it has been known that cholecystokinin (CCK) release into the plasma is under cholinergic control, but secretin release is not. Thus in anesthetized dogs we studied the effect of atropine $(50\;{\mu}g/kg\;followed\;by\;50\;{\mu}g/kg/hr)$ on pancreatic secretion and plasma concentrations of bioactive CCK and immunoreactive secretin in response to intraduodenal perfusion of sodium oleate (1, 3 and 9 mmol/hr). The volume, protein output and bicarbonate output of the secretion were increased by sodium cleats and this oleate-induced secretion was decreased significantly by atropine administration. However the increased plasma CCK and secretin levels by sodium oleate were not changed by atropine. These results indicate that atropine suppressed sodium oleate-induced pancreatic secretion through inhibiting cholinergic mechanism directly rather than decreasing the release of pancreatic secretory hormones. In another set of experiments, bilateral cervical vagi were stimulated electrically to observe the changes of pancreatic secretion and the above two plasma hormone levels in the presence or absence of atropine. In the vagally stimulated dogs, the volume, protein output and bicarbonate output of the pancreatic secretion were increased significantly. Both plasma secretin and CCK were concomitantly released significantly by vagal stimulation. Atropine significantly depressed the pancreatic secretory response as well as the release of these two pancreatic secretory hormones. Therefore, we conclude that in the presence of atropine the depressed pancreatic response to vagal stimulation is at least, in part, due to decreased release of endogenous CCK and secretin. In the vagally stimulated animals, however, the involvement of direct cholinergic influence on pancreatic exocrine gland remains to be answered.
Xylazine is commonly used for anesthesia in veterinary medicine and various adverse effects are developed. To examine if the severe hypotensive response associated with xylazine-induced anesthesia might be resulted from the stimulation of presynaptic alpha-2 adrenoceptors or the increase of vagal tone, effects of yohimbine, atropine and atropine with vagotomy on xylazine-induced severe and long-lasting hypotensive responses were investigated in rabbits. The results were summarized as follows: 1) Intravenously injected xylazine(1mg/kg)-induced hypotensive responses were inhibited by yohimbine(p<0.001). 2) Intravenously injected xylazine(1mg/kg)-induced hypotensive responses were not changed by atropine. 3) Intravenously administered xylazine(1mg/kg)-induced hypotensive responses are not changed by atropine with vagotomy. These results indicate that xylazine is thought to cause severe hypotensive response during anesthesia primarily by stimulating presynaptic alpha-2 adrenoceptors and other receptors or mechanisms may participate in the hgpotensive response of xylazine.
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