Intravenous Injection Of Atropine Research Articles

Effects of oral quinidine on left ventricular performance in normal subjects and patients with congestive cardiomyopathy

To evaluate the effects of oral quinidine therapy on left ventricular performance, 10 normal subjects and 8 patients with Cardiomyopathy were studied with echocardiography at rest, after intravenous injection of atropine and during infusion with phenylephrine. The echocardiographic studies were performed during oral quinidine therapy and during placebo administration. In the normal subjects heart rate was significantly faster with quinidine than with placebo (74 ± 8 (standard deviation) versus 68 ± 9 beats/min, P < 0.01), but there was no significant change in blood pressure or left ventricular size and performance. After administration of atropine, heart rate was identical with and without quinidine but the mean normalized velocity of left ventricular dimension shortening was significantly less with quinidine than with placebo (1.28 ± 0.19 versus 1.44 ± 0.21, P < 0.01). During acute pressure loading with phenylephrine there was no difference in left ventricular size or performance during quinidine therapy. In the patients with Cardiomyopathy, no significant differences in left ventricular function were detected with this protocol during quinidine therapy. It is concluded that oral quinidine therapy appears to have little adverse effect on left ventricular performance at rest or during acute pressure loading.

Preliminary studies on cholinergic control of pituitary gonadotrophin secretion in the ewe

Administration of neostigmine, a cholinomimetic, to anoestrous ewes diminished the increase in jugular plasma luteinising hormone and follicle-stimulating hormone induced by oestradiol. Intravenous injection of atropine had no effect on the gonadotrophin surge.

Comparison in guinea-pigs and in rats of the effects of vagotomy and of atropine on respiratory resistance modifications induced by an acute carbon monoxide or nitrogen hypoxia

1. 1.Pulmonary resistance was estimated using a continuous record of tracheal pressure in groups of 15 male guinea-pigs and in groups of 15 male rats of same ages, urethane anesthetized, artificially ventilated and inhaling during 4 min 21.50 torr pCO (F 1 = 2.84% carbon monoxide) or 6.73 torr pO 2 (F 1 = 0.89% oxygen). 2. 2. Pulmonary resistance changes were induced in both species by inhalation of both gaseous mixtures, but rats appeared to be more sensitive than guinea-pigs to the carbon monoxide mixture and to the hypoxic mixture. 3. 3. Bilateral cervical vagotomy attenuated and suppressed the pulmonary resistance changes provoked by these two types of hypoxia in rats, but had no effects in guinea-pigs. 4. 4. Intravenous injections of atropine, at an acetylcholine-blocking dose, was inactive in both species and in both types of hypoxia.

The effect of pelvic nerve stimulation and some drugs on the urethra and bladder of the dog.

Pelvic nerve stimulation caused an increase in pressure in both the urethra and bladder of anaesthetised dogs. The increases were only partially blocked by intravenous injection of atropine and were not significantly reduced by phentolamine, propranolol or methysergide. Quinidine produced some reduction in the bladder but not the urethral response. Hexamethonium reduced but did not abolish the responses to pelvic nerve stimulation. Close arterial injection of acetylcholine and 5-hydroxytryptamine increased the bladder and urethral pressures; noradrenaline produced a biphasic increase in urethral pressure but had no effect on the bladder; ATP increased bladder pressure but the response of the urethra was variable. The results indicate that some fibres in the pelvic nerve to the urethra as well as to the bladder are atropine resistant and suggest that transmission does not involve 5-hydroxytryptamine or noradrenaline and probably not ATP. The significance for treatment of detrusor dysfunction is discussed.

Effect of anticholinergic drugs on the electrical activity of the antrum and duodeno‐jejunum in sheep

The changes induced in the electrical activity of the small intestine by atropine sulphate, diphemanil methylsulphate, hyoscine butylbromide and prifinium bromide were studied in conscious sheep fitted with chronically implanted electrodes. Increased spike potential activity was induced by carbachol. The mean slow‐wave frequency of the antrum was 7.35 ± 0.18/min with burst of spike potentials randomly superimposed on about 63% of the slow waves. The occurrence of the spike bursts was inhibited for 18—30 min after an intravenous injection of atropine (0.75 mg/kg) and during its infusion at the rate of 0.05 mg/kg/min. The activity of the proximal part of the small intestine, which is characterized by migrating myoelectric complexes moving down slowly at hourly intervals, was replaced by irregular series consisting of spike bursts of about 3 min duration, at intervals of about 12 min for a total of 110 min. Such an effect, in which the level of spike activity was reduced, was also observed with hyoscine, diphemanil and prifinium during 80, 120 and 180 min periods respectively. The injection of carbachol was followed by continuous spike activity in which the mean spike level was nearly doubled, as occurs at the onset of diarrhoea. An inhibitory effect was observed at both antral and duodeno‐jejunal levels with the four drugs used, that of hyoscine being least marked. The effect of prifinium was more pronounced than that of atropine or diphemanil, especially on the jejunum. The results suggest that the ability of these drugs to reduce the level of spike activity accompanying disruption of migrating myoelectric complexes and to inhibit the carbachol‐induced increased level of spiking may account for the antispasmodic effects observed after the use of anticholinergic drugs in gastrointestinal disorders. Prifinium had the longest lasting effect at both antral and duodeno‐jejunal levels and seemed to be a good atropine substitute to alleviate gastro‐intestinal hypermotility.

Relationship Between Gastric Secretion and Serum Gastrin Levels in Dogs Anesthetized with Morphine and Urethane

The serum levels of immunoreactive gastrin (IRG) and secretion of gastric juice were simultaneously determined in dogs anesthetized with morphine and urethane. There was a significant positive linear correlation between secretion and serum IRG level in these dogs. Serum IRG level and gastric secretion were reduced by bilateral vagotomy at the neck. The amount of gastric juice was reduced dose-dependently by an intravenous injection of atropine (0.001–0.016 mg/kg), hexamethoniurn (0.064–1 mg/kg) and secretin (2–8 U/kg). The reduction of gastric secretion paralleled that of the serum IRG level. However, the reduction of gastric secretion did not parallel that of serum IRG level under the influence of prostaglandin E1 (0.002–0.008 mg/kg i.v.) and duodenal acidification. Prostaglandin E1 and duodenal acidification reduced gastric secretion without the reducing serum IRG level. These findings were discussed in relation to the mechanism of gastric juice stimulation by morphine, and it is suggested that endogenous gastrin release through the vagal and non-vagal pathways participates in morphine-induced gastric secretion. The difference in inhibitory effect between duodenal acidification and secretin suggests the possibility that substances other than secretin may participate in the regulation of gastric secretion in dogs.

Effects of atropine and beta-blockade on temperature regulation and performance during prolonged exercise.

The effects of intravenous injections of Atropine (1.8 mg) and practolol (15 mg) on the thermoregulatory responses to 1 h of exercise on a motordriven treadmill have been investigated on six healthy subjects. The results show that Β-blockade had little effect on thermal responses to work except for a small but significant (p<0.05) decrease in mean skin temperature (¯T sk ) and peripheral tissue heat conductance (K). Metabolic (M) and total heat (H) production, and evaporative sweat loss (E) and rectal temperature (T re ) were similar to control values. In contrast, atropine, particularly at work loads beyond 60% maximal aerobic power output (VO2 max), raised T re (p<0.001), ¯T sk (p<0.001) and reduced E by approximately 50%. At the highest work loads T re increased as a linear function of time during the latter part of exercise, and at the 60th min was almost independent of relative stress (expressed as % VO2 max) imposed on the subjects. At the lower work loads the majority of subjects reached thermal equilibrium before the end of exercise by maintaining their convective heat transfer from core to periphery by increasing peripheral blood flow (as indicated by K), and raising their heat losses to environment by convection and radiation. The latter pathways for heat dissipation were enhanced by the subjects ability to sustain a ¯T sk ∼4‡ C above control values independently of M. Atropine had no effect on M or H but greatly affected work performance, no subject was able to exercise at loads >70% VO2 max for 1 h. These results demonstrate the ability of the thermoregulatory system to adapt to Β-adrenergic and to parasympathetic blockade during light exercise, and underline the effects of a reduction in the capacity of the sweating mechanism on physiological performance at higher rates of work.

Sinus node function and conduction system after complete repair of tetralogy of Fallot.

Twenty-three children underwent electrophysiological studies during routine postoperative catheterization two months to five years after complete correction of tetralogy of Fallot. The aim of the study was to investigate the whole conduction system, including sinus node function, suing His bundle recordings and atrial pacing. H-V intervals were normal at rest and with pacing in twenty-two patients, including four patients with evidence of bifascicular block on the surface ECG. One patient with cardiomegaly and evidence of diffuse myocardial damage had a prolonged H-V interval but did not develop a block at this level during pacing A-H interval was slightly prolonged in four patients and normal in all others. The threshold of pacing-induced atrioventricular block ranged from 75 to 240/min and was somewhat age dependent (r = -0.55). Two patients fell below the 95% confidence limit of this regression and are considered abnormal. One returned to normal after intravenous injectionof atropine. Corrected sinus node recovery time ranged from 60 to 2000 msec. Three patients had values above 500 msec which are considered abnormal. These patients had other minor signs of sinus node dysfunction, i.e., episodes of sino-atrial block at rest or intermittent sinus bradycardia. Thus, while the His Purkinje system performed satisfactorily in all patients, sinus node dysfunctional and A-V node dysfunction were demonstrated in a few patients after correction of tetralogy of Fallot.

The influence of the splanchnic nerves on the external secretion, blood flow and electrical conductance of the cat pancreas

1. Electrical stimulation of the cut peripheral end of the splanchnic nerves results in a biphasic change in electrical conductance measured across the tail of the pancreas. A phase of decreased conductance is followed by a more prolonged phase of increased conductance.2. Simultaneous measurements of pancreatic blood flow indicate that the phase of decreased conductance occurs as a result of vasoconstriction, whilst the phase of increased conductance is due to vasodilatation.3. The initial phase of decreased conductance and vasoconstriction is abolished by alpha-receptor blocking agents such as phenoxybenzamine and the phase of increased conductance blocked by beta-receptor blocking agents such as pronethalol.4. Short periods of electrical stimulation applied to the splanchnic nerves result in a secretion of amylase and a reduction in the volume rate of secretion.5. When the vasoconstrictor response was abolished by phenoxybenzamine, nerve stimulation still reduced the rate of secretion, suggesting that the inhibitory effect is in part due to a direct action of the secretory cells.6. After bretylium tosylate, splanchnic nerve stimulation no longer produced vasomotor changes in the pancreas and the inhibitory effect on the volume response was converted to one of augmentation, but the secretion of enzymes was unaffected.7. The secretion of amylase on splanchnic stimulation was abolished by intravenous injection of atropine, suggesting that a cholinergic mechanism is involved.8. Noradrenaline did not mobilize pancreatic enzymes.

Effect of ganglionic blockade on the responses of coronary blood flow to cardiac sympathetic stimulation in the dog.

The effects of ganglionic blockade were studied on the changes in coronary blood flow and myocardial contraction produced by electrical stimulation of the left cardiac sympathetic nerves in anesthetized open-chest dogs. Stimulation of the left ventral ansa subclavia (AS) and the ventrolateral cervical cardiac nerve (VLCCN) produced 2 peaks of increase in coronary blood flow, in myocardial contractile force (MCF) and in left ventricular pressure (LVP). The first peak was, in some experiments, preceded by an initial transient decrease in coronary blood flow. Bilateral cervical vagotomy or intravenous injection of atropine did not affect the initial changes in coronary blood flow. In dogs pretreated with intravenous propranolol or practolol, the stimulation of either AS or VLCCN evoked a prolonged decrease in coronary blood flow without appreciable changes in systemic blood pressure and myocardial contractility. The decrease in coronary flow resulting from AS stimulation was blocked not only by intravenous injection of phentolamine but also by hexamethonium (C6) given into the pericardial cavity or in the coronary artery. On the other hand, the decrease elicited by stimulation of VLCCN was abolished by phentolamine but not influenced by intracoronary and intrapericardial C6, while hypotension and brady-cardia produced by cervical vagosympathetic stimulation were completely blocked by C6. From the present data, it may be concluded that in coronary vessels there exist adrenergic alpha receptors corresponding to the sympathetic vasoconstrictor nerve of which preganglionic fibers terminate in the stellate and inferior cervical ganglia, and that the intracardiac ganglion cells play little role in the coronary vasoconstrictor response after beta adrenergic receptor blockade.

Effects of atropine and eserine on the electroencephalogram, on behaviour and on light-induced epilepsy in the adolescent baboon ( Papio papio)

1. 1. Conscious adolescent baboons ( Papio papio) have been given intravenous injections of atropine or eserine and the effects on the EEG, on behaviour, and on myoclonic responses to intermittent light stimulation (ILS) have been observed. 2. 2. The classical alerting effects produced by eserine (0.2 mg/kg) were maximal 5–10 min after injection and were accompanied by a sustained, high voltage fronto-Rolandic rhythm at 9–11 c/sec, resembling human mu rhythm in morphology and reactivity. 3. 3. After atropine (2 or 5 mg/kg), periods of agitation and of sedation were seen. The sedation was most marked 20–60 min after injection. During this period an enhancement of EEG paroxysmal features was seen. Spikes and polyspikes and waves occurred predominantly in the fronto-Rolandic cortex, but also more diffusely. 4. 4. Beginning within 1–3 min of the injection of atropine and continuing for several hours, there was marked enhancement of the amplitude and frequency of lambda waves, which appeared in sustained bursts during the phases of agitation. Such sustained bursts of lambda waves were not seen after intravenous methylatropine (4–6 mg/kg) or intraocular homatropine. 5. 5. After atropine (0.25–5.0 mg/kg) and after eserine (0.05–0.3 mg/kg), baboons with high, low or variable photosensitivity continued to display their characteristic responses to ILS when tested at the times of the maximal EEG drug effects. Neither drug made insensitive animals sensitive or led to ILS-induced seizures in photosensitive animals. 6. 6. It is concluded that the paroxysmal motor responses of baboons to ILS are not determined by the degree of activity in cholinergic non-specific cortical afferent or cortico-cortical cholinergic systems.

SAFE REVERSAL (1): ATROPINE FOLLOWED BY NEOSTIGMINE: An Electrocardiographic Study

SUMMARY An electrocardiographic investigation was carried out in ten healthy adult patients anaesthetized using thiopentone, nitrous oxide and oxygen with tubocurarine. The arterial carbon dioxide tension was raised by adding 2.5 per cent carbon dioxide to the fresh gas flow whilst intermittent positive pressure ventilation was maintained throughout the whole period of anaesthesia and reversal. The Pco2 varied between 45 and 90 mm Hg and the pH values varied between 7.12 and 7.30. The intravenous injection of atropine 1.2 mg followed after 2 minutes by neostigmine 2.5 mg did not produce any serious cardiac arrhythmia provided adequate oxygenation was ensured throughout the whole period of reversal.

Nonparallel gastric and salivary gland inhibition produced by anticholinergic drugs in sham-fed dogs.

After esophagostomy and gastrostomy dogs were sham fed at timed intervals after a single intravenous injection of atropine, heteronium bromide, or saline. For each interval the doses necessary to reduce gastric juice volume and saliva weight by 50% were determined (50% doses). At 20- and 40-min. intervals gastric secretion was more sensitive than salivary secretion to anticholinergic inhibition, whereas at 100 and 160 min. the sensitivity was approximately equal. The change in the ratio of salivary 50% dose to gastric 50% dose demonstrates that gastric inhibition and salivary inhibition with either drug are not parallel.

Digital computer analysis of fetal heart-rate data

A review is presented of the techniques and instrumentation developed for isolating and detecting the fetal heart sound and for extracting and recording the fetal heart rate in a form suitable for subsequent analysis by means of a digital computer. In typical experiments some form of stress is applied to the mother and the latency and magnitude of the relative changes in rate dynamics as they appear, first in the mother, and then in the fetus are recorded for future analysis. Two forms of stress have been tested: one is produced by cigarette smoking; the other by the intravenous injection of atropine. The forms of analysis thus far used have included calculation of running arithmetic means and the normalized auto-correlation and cross-correlation functions. Sample results are presented.

An analysis of coronary flow and related factors following vagotomy, atropine, and sympathectomy.

Coronary blood flow in the dog has been measured by the nitrous oxide desaturation method before and after acute bilateral cervical vagotomy, intravenous injection of atropine, and chronie sympathectomy. Vagotomy and atropine markedly increased coronary flow, myocardial oxygen consumption, and heart rate, but decreased left ventricular efficiency. Chronic sympathectomy resulted in the following smaller but statistically significant changes: a decrease in coronary flow, myocardial oxygen consumption, and heart rate, but an increase in left ventricular efficiency. Increasing the oxygen content of the arterial blood decreased the coronary flow. A comparison of diallylbarbiturate acid and urethane with morphine and chloralose anesthesia gave similar flow values, but cardiac efficiency was increased in the latter case. An analysis of the relationships between coronary flow, left ventricular oxygen consumption, and the arteriovenous oxygen difference is presented.

Action of atropine on rabbit blood cholinesterase.

There have been some investigations as to the influence of atropine on the activity of cholinesterase (ChE). Roepke (1) demonstrated that atropine inhibited horse serum ChE competitively with an affinity for the enzyme much higher than that of acetylcholine, and Schaller (2) also pointed out that atropine inhibited human blood ChE. On the other hand, Scoz and Michole (3) found that very small quantity of atropine increased blood ChE in vitro, and Yoshida et al. (4) reported that atropine intensified the destruction of acetylcholine by rabbit serum in vivo and in vitro. I have also undertaken this work using rabbit blood to investigate this problem.The activity of abbit blood ChE was determined by the Warburg's manometer. Into the main compartment of each flask were placed definite quantities of enzyme material diluted twenty times with bicarbonate-Ringer solution saturated with C02. One cc of substrate (acetylcholine, to make a 0.0025 molar solution) saturated with CO2 was added to a side arm of each series of flasks. Atropine sulfate was added in varying concentrations to the enzyme solution. The total fluid content of each flask was 5.0 cc. After equilibrating at 37.5°C, the content of the side arm was tipped into the reaction chamber. Controls and blanks were run simultaneously. Gas evolution resulting from the liberation of acetic acid and its action on bicarbonate was measured in the conventional manner. The results of the experiment are presented in the accompanying tables. Activity of enzyme was indicated in the vo'ume (cmm) of CO2 gas liberated by 0.1 cc blood or serum in one hour.In vivo: The activity of rabbit serum ChE after intravenous injection of atropine was compared with that before injection. There was no change between them (Table 1).In vitro: Firstly, when atropine was added to rabbit serum directly, the activity of its ChE was inhibited (Table 2). Secondly, after defibrinated rabbit blood was incubated with atropine at 37.5°C for ten minutes, the activity of ChE in serum from the blood was determined. In that case the activity was higher than control in high concentration of atropine. But when whole blood under the same treatment was used, the activity of its ChE was inhibited in high concentration of atropine (Table 3). It was probably because atropine liberated the ChE contained in blood cell into serum that the activity of ChE in serum from the blood with atropine was higher than that without atropine.There is an interpretation that the influence of atropine on the parasympathomimetic effect or acetylcholine action can be attributed to the activating action.of atropine on the ChE (4). However, this interpretation has been found inappropriate from my observation, because atropine did not activate rabbit blood ChE both in vivo and in vitro.Acknowledgement: The author wishes to express his gratitude to Professor Z. Kanda for suggesting this investigation and for his continued. guidance and help throughout the course of this work.

A study of viscerocardiac reflexes: II. The experimental production of cardiac irregularities in icteric dogs with an analysis of the rôle played by nausea and vomiting

The results of this study seem to indicate clearly that nausea, retching and vomiting (induced by the subcutaneous injection of apomorphine) may cause in normal unanesthetized dogs cardiac irregularities, such as heart-blocks, cardiac arrests, ventricular and auricular ectopic beats. These are most likely to occur during retching. There were also changes in rate, nausea causing usually a tachycardia and retching a bradycardia. The intravenous injection of atropine almost completely inhibited the cardiac irregularities associated with nausea, retching and vomiting following the injection of apomorphine. The results indicate that during marked excitation of the vomiting center the cardio-inhibitory mechanism is affected, the degree to which it is affected depending upon its sensitivity. Icterus per se caused both the appearance and the disappearance of electrocardiographic abnormalities in a few instances. The changes in rate were variable, but the tendency was towards an increase. Slowing of the heart rate, however, may occur. Preexisting icterus increased the occurrence of the cardiac irregularities which are associated with the elicitation of nausea, retching, vomiting and pain by distention of the biliary passages. The irregularities following the injections of apomorphine could not be said to parallel closely the degree of icterus; but the changes due to distention of the biliary system did parallel the degree of icterus. This may have been due to the probable fact that apomorphine is a stronger stimulus. The results of the experiments on the icteric animals, we believe, indicate that icterus sensitizes the cardiovagal mechanism. Electrocardiographic abnormalities, such as extrasystoles, arrests, ectopic, ventricular, A-V blocks, etc., occurred in 10 per cent of the students while nauseated or retching during the swallowing of a stomach tube. No change in the rate was observed in one student. In the others there was an increase in rate which was dependent upon the ease with which the tube was swallowed. It is interesting to note that a bradycardia did not occur, whereas in dogs during retching bradycardia occurred very uniformly. In all experimental procedures, changes in the P-wave, the QRS complex and the T-wave occurred, none of the changes being characteristic.