Injection Of Atropine Research Articles

Scleral changes induced by atropine in chicks as an experimental model of myopia

To determine the effects of intravitreal atropine on scleral growth in the form-deprived chick as an experimental model of myopia. Five groups of five chicks were studied from day 0-12 post-hatching. One group remained untreated (C), and four were form-deprived by monocular light diffusers to induce myopia. Two groups (RL and A) wore diffusers for 9days, and the other two groups (D and D+A) wore diffusers throughout the study. Group D received no further treatment (myopia positive control). Groups A and D+A received intravitreal injections of atropine for days 9-12. Measurements of refractive error and axial length were performed on days 0, 9, and 12. Sclera changes were assessed in cartilaginous and fibrous layers by histological analysis. All form-deprived eyes had a myopic refractive error on day 9. All atropine-treated groups were hyperopic on day 12. The effect of atropine was most evident in Group D+A in which diffusers were maintained throughout treatment and changes in refractive error were statistically significant. The observed changes in axial length were in line with the changes in refractive error. The scleral fibrous layer thickness increased, and the sceral cartilaginous layer underwent a slight thinning compared to Group D, the myopia positive control. If the signals that induce growth remain during atropine treatment, morphological changes in sclera are produced: the scleral fibrous layer thickened, and the sceral cartilaginous layer thinned. These changes resulted in refractive error recovery, and the ocular growth was stopped. The data suggested the atropine was acting throughout the scleral fibrous layer.

Abstract 608: Unilateral Renal Denervation Enhances Baroreflex Function in Conscious Rabbits

Renal nerve denervation (DNx) is currently being assessed as a therapy for drug-resistant hypertension and other disorders characterized by sympatho-excitation, such as chronic heart failure (CHF). We hypothesized that renal DNx enhances arterial baroreflex (BR) control of heart rate (HR) in normal and CHF rabbits. All animals were instrumented with ventricular pacing leads and an arterial pressure (AP) radiotelemetry transducer. After recovery the left kidney was denervated by stripping the renal artery of all visible fibers. Intact animals were subjected to a sham operation. Two weeks later, CHF animals were subjected to rapid ventricular pacing. BR changes in HR and AP were induced by iv sodium nitroprusside and phenylephrine (PE) infusions alone and after injection of atropine or metoprolol. BR function was determined by fitting mean AP and HR data to a 4 parameter logistic equation. Renal DNx increased HR range from 156 ± 34 bpm in intact rabbits compared to 298 ± 39 bpm in DNx rabbits (p = 0.022). This was primarily due to a decrease in the minimum HR following PE infusion. During blockage with metoprolol HR range was increased from 140 ± 39.35 bpm in Sham to 262.75 ± 9.97 bpm in DNx rabbits (p = 0.016) suggesting an improvement in the vagal components of BR function. In intact rabbits with CHF, HR range was 110 ± 16 bpm compared to 294 ± 15 bpm in CHF renal DNx animals (p = .002). These data suggest renal DNx enhances the autonomic components of BR control of HR in the normal and CHF states.

Abstract 79: Knockdown of ACE2 in the Paraventricular Nucleus Partially Reverses the Protective Effects of Brain ACE2 in DOCA-salt Hypertension

To identify which brain regions are critical for ACE2 regulation of blood pressure (BP), we generated transgenic mice harboring a loxP-flanked human ACE2 transgene specifically in the brain (hACE2 flox ) and tested the impact on DOCA-salt hypertension. hACE2 flox and non-transgenic (NT) mice were implanted with telemetry probes for conscious BP monitoring. DOCA (1 mg/g, sc) was implanted following baseline BP recording and drinking water was replaced by 1% NaCl solution. Two weeks later, hACE2 flox mice were divided into 2 groups (n=7/group) and injected bilaterally with an adenovirus encoding Cre recombinase (Ad-Cre) or a control virus (LacZ) to the paraventricular nucleus (PVN; 10 7 particles/200 nl; ±0.3 mm lateral, 0.6 mm caudal, 5.0 mm ventral). NT mice were also injected with LacZ. BP was continuously recorded for 1 more week. Autonomic function was analyzed using a pharmacological method involving ip injection of propranolol (4 mg/kg) and atropine (1 mg/kg). Changes in heart rate (ΔHR, bpm) were used as index of sympathetic and parasympathetic tones. Baseline mean BP was not different among NT+LacZ (105 ±3 mmHg), hACE2 flox +LacZ (107 ±2 mmHg) and hACE2 flox +Ad-Cre (106 ±2 mmHg) groups, nor was sympathetic (-91 ±4, -101 ±8, -101 ±14 bpm) or vagal tones (+169 ±7, +152 ±10, +168 ±9 bpm). Three weeks after DOCA-salt treatment, mean BP was dramatically increased in NT+LacZ mice (141 ±3 mmHg, P <0.01 vs. baseline) but only modestly increased in hACE2 flox +LacZ mice (127 ±4 mmHg, P <0.05 vs. NT). In addition, cardiac sympathetic drive was significantly increased (-193 ±27 bpm, P <0.01 vs. baseline) while vagal tone was impaired (+113 ±11 bpm) in NT+LacZ mice. However, DOCA-salt-mediated autonomic dysfunction was prevented in hACE2 flox +LacZ mice (sympathetic drive: -119 ±7 bpm, vagal tone: +146 ±9 bpm, P <0.05 vs. NT+LacZ). Selective knockdown of ACE2 in the PVN by Ad-Cre tended to increase BP (133 ±3 mmHg) and sympathetic activity (-168 ±35 bpm) as well as decrease vagal tone (+138 ±34 bpm) in hACE2 flox , compared to LacZ transfected hACE2 flox mice. These data suggest that ACE2 overexpression in the brain blunts the development of hypertension by preventing autonomic dysfunction, and PVN might not be essential for the ACE2-mediated blunting of neurogenic hypertension.

A case of coronary artery spasm caused by manipulation of the neck: heart rate variability analysis

A 66-year-old man with no history of ischemic heart disease underwent cervical lymph node dissection. General anesthesia was induced and maintained with remifentanil, along with propofol. With manipulation of the neck and a subcutaneous injection of lidocaine supplemented with adrenaline before the operation, a sudden decrease in blood pressure (BP) and elevation of the ST-T segment appeared on the monitoring electrocardiogram (ECG). Ephedrine, phenylephrine, adrenaline, and nitroglycerin were administered; however, the hypotension was sustained and the ECG abnormalities progressed, along with further elevation of the ST-T segment and a complete atrioventricular block. Following an injection of atropine, the changes in ECG and BP were attenuated. Heart rate variability (HRV) was analyzed using fully recorded monitor variables, and revealed an increase in the high-frequency domain at the time of the cervical manipulation, suggesting simultaneous vagal stimulation and coronary artery spasm. We concluded that the cervical manipulation had increased the vagal tone and we note that HRV analysis was useful to interpret this coronary event.

Acute exercise adjustments of cardiovascular autonomic control in diabetic rats

We evaluated the role of cardiovascular autonomic changes in hemodynamics at rest and in response to exercise in streptozotocin-induced diabetic rats. Male Wistar rats were divided into nondiabetic (ND, n = 8) and diabetic (D, n = 8) groups. Arterial pressure signals were recorded in the basal state and after atropine or propranolol injections at rest, during exercise and during recovery. At rest, vagal tonus was reduced in D (37 ± 3 bpm) in comparison with the ND group (61 ± 9 bpm). Heart rate during exercise was lower in D in relation to ND rats associated with reduced vagal withdrawal in the D group. The D rats had an increase in vagal tonus in the recovery period (49 ± 6 bpm). Exercise-induced hemodynamic adjustment impairment in diabetic rats was associated with reduced cardiac vagal control. The vagal dysfunction was attenuated after aerobic exercise, reinforcing the positive role of this approach in the management of cardiovascular risk in diabetics.

μ1- and 5-HT1-dependent mechanisms in the anterior pretectal nucleus mediate the antinociceptive effects of retrosplenial cortex stimulation in rats

AimThis study examines if injection of cobalt chloride (CoCl2) or antagonists of muscarinic cholinergic (atropine), μ1-opioid (naloxonazine) or 5-HT1 serotonergic (methiothepin) receptors into the dorsal or ventral portions of the anterior pretectal nucleus (APtN) alters the antinociceptive effects of stimulating the retrosplenial cortex (RSC) in rats. Main methodChanges in the nociceptive threshold were evaluated using the tail flick or incision pain tests in rats that were electrically stimulated at the RSC after the injection of saline, CoCl2 (1mM, 0.10μL) or antagonists into the dorsal or ventral APtN. Key findingsThe injection of CoCl2, naloxonazine (5μg/0.10μL) or methiothepin (3μg/0.10μL) into the dorsal APtN reduced the stimulation-produced antinociception from the RSC in the rat tail flick test. Reduction of incision pain was observed following stimulation of the RSC after the injection of the same substances into the ventral APtN. The injection of atropine (10ng/0.10μL) or ketanserine (5μg/0.10μL) into the dorsal or ventral APtN was ineffective against the antinociception resulting from RSC stimulation. Significanceμ1-opioid- and 5-HT1-expressing neurons and cell processes in dorsal and ventral APtN are both implicated in the mediation of stimulation-produced antinociception from the RSC in the rat tail flick and incision pain tests, respectively.

A new method for induction of atrioventricular nodal reentrant tachycardia: do we really need it?

We have read with interest the article by Sharif et al .1 The authors tested the new method for induction of atrioventricular nodal reentrant tachycardia (AVNRT). The study group consisted of 10 patients with recurrent episodes of paroxysmal supraventricular tachycardia documented by electrocardiography, in whom tachycardia was not inducible during electrophysiological testing even after isoproterenol infusion and atropine injection. However, dual atrioventricular (AV) node physiology was observed in all cases. The authors attempted to …

Safety and efficacy of exercise testing with atropine in patients with recent uncomplicated ST elevation acute myocardial infarction

Abstract

Gastric mucosal damage in water immersion stress: Mechanism and prevention with GHRP-6

To investigate the mechanism of gastric mucosal demage induced by water immersion restraint stress (WRS) and its prevention by growth hormone releasing peptide-6 (GHRP-6). Male Wistar rats were subjected to conscious or unconscious (anesthetized) WRS, simple restraint (SR), free swimming (FS), non-water fluid immersion, immersion without water contact, or rats were placed in a cage surrounded by sand. To explore the sensitivity structures that influence the stress reaction besides skin stimuli, a group the rats had their eyes occluded. Cervical bilateral trunk vagotomy or atropine injection was performed in some rats to assess the parasympathetic role in mucosal damage. Gastric mucosal lesions, acid output and heart rate variability were measured. Plasma renin, endothelin-1 and thromboxane B2 and gastric heat shock protein 70 were also assayed. GHRP-6 was injected [intraperitoneal (IP) or intracerebroventricular (ICV)] 2 h before the onset of stress to observe its potential prevention of the mucosal lesion. WRS for 6 h induced serious gastric mucosal lesion [lesion area, WRS 81.8 ± 6.4 mm² vs normal control 0.0 ± 0.0 mm², P < 0.01], decreased the heart rate, and increased the heart rate variability and gastric acid secretion, suggesting an increase in vagal nerve-carrying stimuli. The mucosal injury was inversely correlated with water temperature (lesion area, WRS at 35 °C 56.4 ± 5.2 mm² vs WRS at 23 °C 81.8 ± 6.4 mm², P < 0.01) and was consciousness-dependent. The injury could not be prevented by eye occlusion, but could be prevented by avoiding contact of the rat body with the water by dressing it in an impermeable plastic suit. When water was replaced by vegetable oil or liquid paraffin, there were gastric lesions in the same grade of water immersion. When rat were placed in a cage surrounded by sand, there were no gastric lesions. All these data point to a remarkable importance of cutenuous information transmitted to the high neural center that by vagal nerves reaching the gastric mucosa. FS alone also induced serious gastric injury, but SR could not induce gastric injury. Bilateral vagotomy or atropine prevented the WRS-induced mucosal lesion, indicating that increased outflow from the vagal center is a decisive factor in WRS-induced gastric injury. The mucosal lesions were prevented by prior injection of GHRP-6 via IP did, but not via ICV, suggesting that the protection is peripheral, although a sudden injection is not equivalent to a physiological release and uptake, which eventually may affect the vagal center. From the central nervous system, vagal nerves carry the cutaneous stimuli brought about by the immersion restraint, an experimental model for inducing acute gastric erosions. GHRP-6 prevents the occurrence of these lesions.

Management of Anesthesia for Rubinstein-Taybi syndrome

Management of Anesthesia for Rubinstein-Taybi syndrome

A Case of Successful Recovery from High Dose Intravenous Nicorandil Infusion in Refractory Coronary Vasospasm with Hemodynamic Collapse

A 70-year-old male came to the emergency room of the authors’ hospital because of sudden cardiac arrest due to inferior wall ST elevation myocardial infarction. His coronary angiography revealed multiple severe coronary spasms in his very long left anterior descending artery. After an injection of intracoronary nitroglycerine, his stenosis improved. The cardiac arrest relapsed, however, accompanied by ST elevation of the inferior leads, while the patient was on diltiazem and nitrate medication to prevent coronary spasm. Recovery was not achieved even with cardiac massage, intravenous injection of epinephrine and atropine, and intravenous infusion of nitroglycerine. The patient eventually recovered through high-dose nicorandil intravenous infusion without ST elevation of his inferior leads. Therefore, intravenous infusion of a high dose of nicorandil must be considered a treatment option for cardiac arrest caused by refractory coronary vasospasm.

Comparison between accelerated and conventional dobutamine stress protocols for myocardial perfusion scintigraphy

The conventional dobutamine (Dob) stress protocol for myocardial perfusion scintigraphy (MPS) is long, with frequent adverse effects, and generally requires atropine injection to reach target heart rate. Atropine is usually administered at the end of the protocol, when adverse effects are more frequent. Earlier atropine injection may be useful to shorten the stress protocol and reduce adverse effects. We sought to compare a Dob stress protocol with early atropine injection to a conventional Dob stress protocol in the same patients undergoing MPS. 30 patients underwent Dob-MPS with a conventional protocol (steps of 10, 20, 30 and 40 mcg/kg/min at 3 min intervals, adding atropine to the maximal Dob dose if necessary to achieve 85% of the age-corrected maximal predicted heart rate) and with an accelerated protocol with early atropine injection (at the end of the first stage). We compared stress duration, maximal heart rate (HR), percentage of maximal predicted HR, rate-pressure product, ST changes, MPS scores and the incidence of adverse effects between the 2 protocols. The accelerated protocol was shorter than the conventional protocol (7.1 ± 3.4 min vs. 11.8 ± 1.3 min; P < 0.0001), had the same efficacy to achieve hemodynamic parameters, without increasing adverse effects. The summed stress scores obtained by automatic analysis were similar in both protocols (6.3 ± 6.3 vs. 6.8 ± 6.3; P = NS) as well as the summed difference scores (2.5 ± 3.6 vs. 2.7 ± 3.4; P = NS). Early atropine injection during dobutamine stress protocol shortens stress duration. Our results suggest that patient safety and accuracy of MPS are unaltered, when compared to the conventional protocol, but further, larger studies are still necessary.

Endogenous orexin-A in the brain mediates 2-deoxy-d-glucose-induced stimulation of gastric motility in freely moving conscious rats

Increasing evidence has indicated that brain orexin plays a vital role in the regulation of gastrointestinal (GI) physiology such as gastric acid secretion and GI motility. The aim of this study was to elucidate the effects and mechanisms of orexin on gastric motility in non-fasted rats. In this study, we recorded intraluminal gastric pressure waves in freely moving conscious rats with a manometric catheter located in the antrum. We assessed the area under the manometric trace as the motor index (MI), and compared its values for 1 h before and after drug administration. Intracisternal (ic) injection of orexin-A (10 μg) significantly increased the MI, but intraperitoneal (ip) injection did not have any effect. Pretreatment of ip injection of atropine significantly blocked the orexin-A-induced stimulation of gastric motility. Intravenous injection of 2-deoxy-D-glucose (2-DG, 200 mg/kg), a central vagal stimulant, significantly increased the MI. The ic injection of SB-334687 (40 μg), a selective orexin-A antagonist, did not modify the basal MI, but this antagonist significantly suppressed the stimulant action of 2-DG. These results suggest that endogenous orexin-A in the brain is involved in the vagal-dependent stimulation of gastric contractions.

A comparison of patients’ heart rate variability and blood flow variability during surgery based on the Hilbert–Huang Transform

Previous studies have indicated that heart rate variability (HRV) is considered to be one of the effective parameters for assessing autonomous nervous system activity. Therefore, HRV can be used to detect the state of patients during surgery, even for estimating depth of anaesthesia (DOA). However, the heartbeat can be affected by anaesthesia drugs, breathing rate and electric influence during surgery, which can result in inaccurate information about the patient. To contend with this problem, blood flow variability (BFV) is proposed in this paper as an indicator to monitor the patient's status when HRV is not appropriate. In our experiments, thirty patients undergoing ear, nose, and throat (ENT) surgery with different anaesthetics are used to compare the efficiency and validity between the fast Fourier transform (FFT) and the Hilbert–Huang transform (HHT). Of another thirty patients, twenty patients accepted ENT surgery, of which ten have received Atropine, while the others have not. The other ten patients who have accepted abdominal surgery with an electric knife were compared with the previously mentioned ten patients who did not receive an Atropine injection for ENT surgery. As a result, the FFT that is applied in this study was replaced with the HHT for analysing the data in a particular frequency range of sympathetic and parasympathetic divisions, because of the lesser response of the results that were analysed by FFT for intubation. Also, BFV is proven to be a useful indicator for assisting doctors to assess the state of the patients instead of HRV during the operation in comparison with HRV under drugs (i.e., Atropine and Glycopyrrolate) and diathermy effects (i.e., high frequency interference from electric knife).

Abstract P081: Voltage-Gated TTX-Sensitive Nav1.1 Brain Sodium Channels Are Important for Cardiac Contractile Function

Background: Mutations in voltage gated brain sodium channel Nav1.1 have been linked to many disorders, including Generalized Epilepsy with Febrile Seizures Plus (GEFS+) and Severe Myoclonic Epilepsy of Infancy (SMEI). Recent studies have identified TTX- sensitive Nav1.1 brain sodium channels in the SA node and ventricular T-tubules of the heart, though their role in cardiac function is still controversial. We tested the functional significance of Nav1.1 sodium channels in the heart by creating a novel knock-in of human epilepsy GEFS+ mutation SCN1A-R1648H at the Scn1a locus of a C57BL/6J X 129 mouse. Method: In vivo 2-D echocardiography was performed on 2 week old (juvenile) and 8 week old (adult) wild-type and heterozygote (Scn1aRH/+) mice after extracardiac neuronal block through intraperitoneal injections of atropine and propranolol (2.5mg/kg each). Calcium and contractility studies on adult ventricular cardiomyocytes isolated from the wild type and Scn1aRH/+ mice paced at 0.5Hz were followed by administration of TTX (100nM, a brain sodium channel inhibitor) and pacing at 2Hz. qRT-PCR and Western blot of the isolated cells and whole heart samples was also done. Results: A decrease in Nav1.1 gene expression in the Scn1aRH/+ juvenile (by 31%, 0.69 of 1) and adult (by 60%, 0.4 of 1) whole heart samples and isolated cells (p&lt;0.05) was seen. Echocardiography revealed concentric hypertrophy in the juvenile Scn1aRH/+ mice by a significant increase in LV mass, LV mass/body weight ratio, and relative wall thickness (p&lt;0.05). In the adult Scn1aRH/+ mice, systolic isovolumic contraction time (IVCT) was reduced (p=0.03) and decrease in diastolic function was evident through significant decreases in isovolumic relaxation time (IVRT) and E’/A’ ratio, and increase in E/E’ ratio. Isolated adult ventricular Scn1aRH/+ cardiomyocytes showed significant reduction in percent sarcomere shortening, maximum rate of contraction and relaxation, and time to peak contraction, exaggerated with TTX and pacing at 2Hz (p&lt;0.5). Conclusions: Our study demonstrates the importance of voltage gated TTX-sensitive Nav1.1 brain sodium channels in cardiac contractile function and their possible role in cardiac complications in epilepsy.

Usefulness of atropine in patients with chronotropic incompetence and poor exercise capacity during treadmill stress testing

Atropine, an anticholinergic agent, has been shown to increase heart rate and enhance the sensitivity of dobutamine stress echocardiography in the detection of CAD in patients with chronotropic incompetence; however, the addition of atropine to exercise stress testing EST, in these types of patients has not been well studied previously. Investigating the usefulness and accuracy of atropine in decreasing the number of inconclusive results of EST in patients with chronotropic incompetence and poor exercise capacity. Thirty patients (16 males and 14 females with the age range of 40:73 years with mean of 55 ± 8) out of 180 patients who preformed EST were chosen as having chronotropic incompetence or poor exercise capacity by Borg scale. Atropine was administered during the exercise phase in doses of 0.5 mg per minute until test conclusion or the maximum dose of 2 mg was reached. All patients were subjected to stress myocardial perfusion imaging SMPI to confirm accuracy. Conclusive test results were achieved in 29 patients (97%). Heart rate and blood pressure were markedly increased with statically highly significant difference ( P value <0.001), patients on b-blocker treatment had lower maximum heart rate compared to other patients with significant difference. Twenty-three (79%) patients had negative test results and six (21%) patients had positive test results, and if compared to SMPT results, EST was considered better positive than negative test, with higher specificity than sensitivity and accuracy. Atropine injection during EST significantly reduced the inconclusive test results in patients with chronotropic incompetence and poor exercise capacity.

The Bainbridge and the “Reverse” Bainbridge Reflexes

Francis A. Bainbridge demonstrated in 1915 that an infusion of saline or blood into the jugular vein of the anesthetized dog produced tachycardia. His findings after transection of the cardiac autonomic nerve supply and injection of the cholinergic blocking drug atropine demonstrated that the tachycardia was reflex in origin, with the vagus nerves constituting the afferent limb and a withdrawal of vagal tone the primary efferent limb. Subsequent investigators demonstrated that the increase in venous return was detected by stretch receptors in the right and left atria. In the 1980s, it was shown convincingly that the Bainbridge reflex was present in primates, including humans, but that the reflex was much less prominent than in the dog. This difference may be due to a more dominant arterial baroreceptor reflex in humans. A "reverse" Bainbridge reflex has been proposed to explain the decreases in heart rate observed under conditions in which venous return is reduced, such as during spinal and epidural anesthesia, controlled hypotension, and severe hemorrhage. The Bainbridge reflex is invoked throughout the anesthesia literature to describe the effect of changes in venous return on heart rate in patients in the surgical and critical care settings, but a critical analysis of the experimental and clinical evidence is lacking. Our main objectives in this review are to summarize the history of the Bainbridge reflex, to describe its anatomy and physiology, and to discuss the evidence for and against it having an influence on heart rate changes observed clinically. The interaction of the Bainbridge reflex with the arterial baroreceptor and Bezold-Jarisch reflexes is discussed.

Hypoxic alligator embryos: Chronic hypoxia, catecholamine levels and autonomic responses of in ovo alligators

Hypoxia is a naturally occurring environmental challenge for embryonic reptiles, and this is the first study to investigate the impact of chronic hypoxia on the in ovo development of autonomic cardiovascular regulation and circulating catecholamine levels in a reptile. We measured heart rate (f H) and chorioallantoic arterial blood pressure (MAP) in normoxic (‘N21’) and hypoxic-incubated (‘H10’; 10% O 2) American alligator embryos ( Alligator mississippiensis) at 70, 80 and 90% of development. Embryonic alligator responses to adrenergic blockade with propranolol and phentolamine were very similar to previously reported responses of embryonic chicken, and demonstrated that embryonic alligator has α and β-adrenergic tone over the final third of development. However, adrenergic tone originates entirely from circulating catecholamines and is not altered by chronic hypoxic incubation, as neither cholinergic blockade with atropine nor ganglionic blockade with hexamethonium altered baseline cardiovascular variables in N21 or H10 embryos. In addition, both atropine and hexamethonium injection did not alter the generally depressive effects of acute hypoxia — bradycardia and hypotension. However, H10 embryos showed significantly higher levels of noradrenaline and adrenaline at 70% of development, as well as higher noradrenaline at 80% of development, suggesting that circulating catecholamines reach maximal levels earlier in incubation for H10 embryos, compared to N21 embryos. Chronically elevated levels of catecholamines may alter the normal balance between α and β-adrenoreceptors in H10 alligator embryos, causing chronic bradycardia and hypotension of H10 embryos measured in normoxia.

A new method for induction of atrioventricular nodal reentrant tachycardia in non-inducible cases

In some patients with clinical paroxysmal supraventricular tachycardia (PSVT), who are candidates for radiofrequency (RF) catheter ablation, attempts for the induction of arrhythmia during the electrophysiological study (EPS) fail despite different stimulation protocols even during the isoproterenol infusion and atropine injection. The presence of an atrial-His interval (AH) jump during decremental pre-mature atrial stimulation is the only clue for slow pathway ablation in these patients; in occasional patients, however, the AH jump is an accidental finding and the real arrhythmia is not atrioventricularnodal reentrant tachycardia (AVNRT). We aimed to introduce a new method for the induction of AVNRT in these patients. Ten patients (50% male, mean age=44.40 ± 12.80 years) with clinical PSVT who were referred to our department for the EPS and RF catheter ablation were selected. These patients had documented clinical PSVT with non-inducible arrhythmia during the EPS with different stimulation protocols even during the isoproterenol infusion and atropine injection but they only showed an AH jump. To induce AVNRT, low-watt (15-20), low-temperature (40-45°C) RF currents were delivered into the slow pathway area for a maximum of 40 s. Atrioventricularnodal reentrant tachycardia was inducible in five cases (50%, three male, mean age=45.80 ± 9.65 years). Induction of AVNRT occurred either during the RF current application after the occurrence of junctional ectopic beats or after another stimulation protocol. A low-watt, low-temperature RF current application into the slow pathway area can be a provocative method for the induction of AVNRT probably by AV-junction warming and conduction-velocity augmentation.

Organophosphate poisoning in pregnancy

Organophosphate poisoning during pregnancy is rarely reported in the literature. In our retrospective study, we report the outcome of 21 cases of organophosphate poisoning during pregnancy. All patients received atropine injection until the tracheobronchial tree is cleared of the secretions and most secretions were dried. In addition, ventilatory care was needed in five women. Two patients (9.52%) died of the organophosphorus poisoning during the acute stage of poisoning and three patients were lost to follow-up. One woman had a spontaneous abortion. The remaining 15 women had no significant complication during pregnancy or labour and delivery. There was no congenital abnormality and no neurological deficit in any baby. However, long-term follow-up of neonates was lacking in our study population.