Iv Atropine Research Articles

Risk factors for unsuccessful atropine therapy in hypertrophic pyloric stenosis.

I.v. atropine (IA) for infantile hypertrophic pyloric stenosis (IHPS) is a good alternative to pyloromyotomy but has not been broadly accepted. The lower success rate is one of the greatest disadvantages of IA. We investigated the risk factors for unsuccessful results following IA for IHPS. Medical records of patients with IHPS who were admitted to Kimitsu Chuo Hospital between 2002 and 2016 and were initially given atropine sulfate were retrospectively reviewed. Atropine was given i.v. (0.1mg/kg/day in eight divided doses). Oral feeding of milk was started with a small amount and increased in a stepwise fashion to full feed. IA therapy was defined as unsuccessful in the presence of projectile vomiting more than three times a day or intolerance to a predetermined amount of milk. Of the 48 patients with IHPS, 33 patients were successfully treated with IA and 15 patients needed surgical intervention. On univariate analysis the risk factors for unsuccessful IA therapy were younger age, lower bodyweight, and shorter duration of symptoms before diagnosis. On multivariate analysis age at diagnosis<30days was the only significant risk factor for unsuccessful IA therapy (OR, 5.7l P=0.03). Age at diagnosis<30days is a risk factor for unsuccessful IA therapy in IHPS. This might be considered when IA therapy is used for neonates with IHPS.

Effects of different target concentrations of remifentanil when combined with propofol on BIS in patients undergoing neurosurgery

Objective To investigate the effects of different target concentrations of remifentanil when combined with propofol on BIS in patients undergoing neurosurgery. Methods Fifteen ASA Ⅰ or Ⅱ patients, aged 18-64 yr, weighing 50-85 kg, scheduled for intracranial surgery, were involved in this study. The patients received propofol by target controlled infusion (TCI) at a target effect site concentration (Ce) of 3μg/ml. TCI of remifentanil was started after TCI of propofol reached the preset Ce and Ce of remifentanil was increased step by step from 2 ng/ml to 3, 4, 5, 6, 7 and 8 ng/ml. Invasive BP, MAP, HR and BIS were continuously monitored and recorded when remifentanil reached the each preset Ce. Vecuronium 0.1 mg/kg was injected iv when Ce of remifentanil reached 5 ng/ml, and then the patients were intubated and mechanically ventilated 3 min later. The changes in BP, MAP, HR and BIS were recorded. When HR < 50 bpm and/or MAP < 60 mm Hg, TCI of remifentanil was stopped and iv atropine or ephedrine was given. Results BIS was significantly decreased after TCI of remifentanil when propofol reached 3 μg/ ml compared with the baseline value ( P < 0.05 or 0.01). BIS was significantly decreased when Ce of remifentanil ≥6 ng/ml compared with that when propofol reached 3 μg/ml ( P < 0.05 or 0.01) .Conclusion Low-concentration of remifentanil when combined with propofol has no effect on BIS, but when Ce of remifentanil≥ 6 ng/ml, BIS is obviously decreased. Key words: Piperidines; Propofol; Electroencephalography; Drug delivery systems

Intracoronary Genistein Acutely Increases Coronary Blood Flow in Anesthetized Pigs through β-Adrenergic Mediated Nitric Oxide Release and Estrogenic Receptors

Various studies have suggested that the phytoestrogen genistein has beneficial cardioprotective and vascular effects. However, there has been scarce information regarding the primary effect of genistein on coronary blood flow and its mechanisms including estrogen receptors, autonomic nervous system, and nitric oxide (NO). The present study was planned to determine the primary effect of genistein on coronary blood flow and the mechanisms involved. In anesthetized pigs, changes in left anterior descending coronary artery caused by intracoronary infusion of genistein at constant heart rate and arterial pressure were assessed using ultrasound flowmeters. In 25 pigs, genistein infused at 0.075 mg/min increased coronary blood flow by about 16.3%. This response was graded in a further five pigs by increasing the infused dose of the genistein between 0.007 and 0.147 mg/min. In the 25 pigs, blockade of cholinergic receptors (iv atropine; five pigs) and alpha-adrenergic receptors (iv phentolamine; five pigs) did not abolish the coronary response to genistein, whose effects were prevented by blockade of beta(2)-adrenergic receptors (iv butoxamine; five pigs), nitric oxide synthase (intracoronary N(omega)-nitro-L-arginine methyl ester; five pigs) and estrogenic receptors (ERs; ERalpha/ERbeta; intracoronary fulvestrant; five pigs). In porcine aortic endothelial cells, genistein induced the phosphorylation of endothelial nitric oxide synthase and NO production through ERK 1/2, Akt, and p38 MAPK pathways, which was prevented by the concomitant treatment by butoxamine and fulvestrant. In conclusion, genistein primarily caused coronary vasodilation the mechanism of which involved ERalpha/ERbeta and the release of NO through vasodilatory beta(2)-adrenoreceptor effects.

Intracoronary Ghrelin Infusion Decreases Coronary Blood Flow in Anesthetized Pigs

The peptide ghrelin has been linked to the atherosclerotic process and coronary artery disease. We planned to study, for the first time, the primary effects of ghrelin on the intact coronary circulation and determine the mechanisms involved. In 24 sodium pentobarbitone-anesthetized pigs, changes in anterior descending coronary blood flow caused by intracoronary infusion of ghrelin at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. In 20 pigs, intracoronary infusion of ghrelin decreased coronary blood flow without affecting left ventricular maximum rate of change of left ventricular systolic pressure (dP/dt(max)), filling pressures of the heart or plasma levels of GH. In four pigs, this decrease was graded by step increments of infused dose of the hormone. The mechanisms of the above response were studied in the 20 pigs by repeating the experiment after coronary flow had returned to the control values observed before infusion. The ghrelin-induced coronary vasoconstriction was not affected by iv atropine (five pigs) or phentolamine (five pigs). This response was abolished by iv butoxamine (five pigs) and intracoronary N(omega)-nitro-l-arginine methyl ester (five pigs), even after reversing the increase in arterial pressure and coronary vascular resistance caused by the two blocking agents with iv infusion of papaverine. The present study showed that intracoronary infusion of ghrelin primarily caused coronary vasoconstriction. The mechanisms of this response were shown to involve the inhibition of a vasodilatory beta(2)-adrenergic receptor-mediated effect related to the release of nitric oxide.

Characterization of peptide-YY release in response to intracolonic infusion of amino acids.

Peptide-YY-(1-36) [PYY-(1-36)] is an endocrine peptide that is found primarily in the mucosal layer of the colon. We reported previously that a direct intracolonic (IC) infusion of amino acids in dogs resulted in a robust release of PYY compared to other nutrients (fat, glucose, and protein). The objective of this study was to investigate the possible mechanisms underlying the release of PYY in response to IC infusion of amino acids. Intracolonic infusion of a mixture of tryptophan and phenylalanine (Trp+Phe; 100 mM; 200 ml/h) resulted in a significant release of PYY [integrated PYY release, 74.5 +/- 14.0 ng (0-120 min)/ml], which was not affected by iv atropine, hexamethonium, or propranolol treatment. Intravenous infusion of Trp+Phe failed to release PYY [integrated PYY release, -0.6 +/- 0.9 ng (0-120 min)/ml]. Intracolonic infusion of aromatic amino acids (Trp+Phe) was more potent in releasing PYY than aliphatic (leucine and glycine) and charged (arginine) amino acids. PYY release in response to IC infusion of the deamino and decarboxylated forms of Phe was significantly (P < 0.05) decreased [integrated PYY release, 17.5 +/- 2.6 and 12.1 +/- 2.8 ng (0-120 min)/ml, respectively] compared to that in response to intact Phe [integrated PYY release, 39.4 +/- 4.3 ng (0-120 min)/ml]. These results suggest that 1) PYY release in response to IC administered amino acids is independent of ganglionic, cholinergic, and beta-adrenergic transmission; 2) PYY release in response to IC amino acids is due to a direct contact of amino acids with the luminal pole of PYY cells in the colon and is not the result of a stimulatory action of amino acids via the general circulation; and 3) the amino and carboxylic groups of an amino acid as well as the ring structures of aromatic amino acids are structural requirements for PYY release.

Intraoperative pacemaker failure in an infant

Pacemakers in children can present clinical challenges during surgery. We present a case report of an infant whose pacemaker reverted to a backup mode when electrocautery was used during surgery. The resulting bradycardia did not respond either to a magnet placed over the generator or to iv atropine. The circulation was supported by isoproterenol until the pacemaker was re-programmed by the manufacturer. Such devices require care and understanding if problems during surgery are to be avoided.

Effects of autonomic blockade on dual atrioventricular nodal pathways pattern

Fifteen patients (age: 57.6 +/- 14 years) showing dual A-V nodal pathways pattern during basal electrophysiological testing were studied following pharmacological autonomic blockade (iv propranolol 0.2 mg/Kg and iv atropine 0.04 mg/Kg). After induction of the autonomic blockade, the dual A-V nodal pathways pattern was not present in four patients due to disappearance of the slow pathway; the pattern remained in 11 (73%). The longest A2-H2 interval, the effective and functional refractory periods of the fast pathway did not change significantly following autonomic blockade. Even the electrophysiological measures of the slow pathway, in the 11 patients in whom they were comparable, did not change significantly after autonomic blockade. These data suggest that: the dual A-V nodal pathways pattern is mainly related to the intrinsic structure of the A-V node; the autonomic nervous system only affects in a variable way the refractoriness and the conduction velocity in the two pathways.

Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade.

Enhanced atrioventricular nodal conduction (EAVC) comprises a portion of the spectrum of atrioventricular node electrophysiology in which physiologic slowing of atrioventricular conduction is diminished. To evaluate the basis of EAVC in humans, we compared the effect of pharmacologic autonomic blockade on electrophysiologic characteristics of atrioventricular nodal conduction and refractoriness in 10 patients with EAVC and 12 patients without EAVC (non-EAVC). The effects of autonomic blockade (0.2 mg/kg iv propranolol and 0.04 mg/kg iv atropine) on sinus cycle length and atrial refractory period were similar in both EAVC and non-EAVC patients. After autonomic blockade, minimum atrial paced cycle length with 1:1 atrioventricular conduction lengthened in EAVC patients (control, 268 +/- 25 msec; blockade, 307 +/- 34 msec; p less than .01), but remained unchanged in non-EAVC patients (control, 392 +/- 69 msec; blockade, 382 +/- 49 msec; p = NS). Similarly, atrioventricular nodal functional refractory periods tended to lengthen in EAVC patients, while remaining unchanged or shortening in non-EAVC patients. Furthermore, although autonomic blockade reduced differences between EAVC and non-EAVC patients, both minimum cycle length with 1:1 atrioventricular conduction and atrioventricular functional refractory period remained shorter in EAVC than in non-EAVC patients (p less than .02). Thus, baseline differences in autonomic atrioventricular nodal control differ in EAVC and non-EAVC patients, but do not fully account for differences in atrioventricular nodal electrophysiologic properties in these patients. Consequently, underlying structural functional factors may play an important role in determining the range of atrioventricular nodal electrophysiologic characteristics in man.

Ontogeny of circulating gastrin and pancreatic polypeptide in the foetal sheep.

Hypoacidity and hypergastrinaemia are reported in the newborn human. To investigate the ontogeny of gastrin, plasma gastrin concentrations were measured in chronically cannulated foetal sheep from 100 days gestation to term (145 days) and up to 16 days following delivery. Plasma pancreatic polypeptide (PP) concentrations were measured as a marker of vagal activity. Compared with adult values, foetal plasma gastrin concentration was low at 101-105 days, being 7 +/- 1 pmol/l (mean +/= SEM) but greater than adult values from 130 days gestation and increased to 47 +/- 5 at 141-145 days, and 90 +/- 13 at 1-5 days post-partum. Maternal plasma gastrin level during these periods ranged between 21 and 29 pmol/l and was not related to gestational age. Similarly, maternal plasma PP levels, which varied between 220 and 400 pmol/l, did not correlate with gestational age and did not differ significantly from non-pregnant sheep. Foetal plasma PP was low, 20 +/- at 101-105 days, rose to 92 +/- 17 at 141-145 days, and increased to adult levels in the first week post-partum. Basal foetal and maternal plasma PP were inhibited by iv atropine injection. The increase in plasma PP may represent a maturity of vagal influence. Gastrin and PP have a trophic action on the gastro-intestinal tract, so the observation of significant levels of circulating gastrin and PP in the foetus suggests that they may be involved in maturation of the gastro-intestinal tract.

Baroreflex control of heart interval in conscious renal hypertensive dogs.

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.

Selective autonomic stimulation of canine trachealis with dimethylphenylpiperazinium.

The response of canine tracheal muscle to autonomic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) was studied isometrically in 39 dogs in vivo. Intra-arterial (ia) DMPP (2.5 X 10(-4) to 2.5 X 10(-2) mg/kg) caused selective dose related contraction [maximum 30.1 +/- 6.5 gram-force (gf)/cm] due to regional stimulation of parasympathetic ganglia. This contraction was blocked by regional administration of atropine 10(-3) mg/kg ia and hexamethonium 5 X 10(-2) mg/kg ia. Nonselective intravenous (iv) administration of DMPP 2.5 X 10(-2) mg/kg caused parasympathetic tracheal contraction [+13.4 +/- 1.64 gf/cm] followed by later sympathetic relaxation [-11.8 +/- 2.3 gf/cm]; 0.5 mg/kg iv atropine abolished contraction but did not affect relaxation. The role of the adrenal gland vs. direct sympathetic innervation in producing tracheal relaxation after sympathetic stimulation was also studied. Tracheal relaxation to 2.5 X 10(-2) mg/kg iv DMPP was -18.2 +/- 4.0 gf/cm before adrenalectomy (ADX) and -4.3 +/- 0.9 gf/cm afterward (P less than 0.001). In contrast, tracheal contraction resulting from alpha-adrenergic stimulation after 2.5 X 10(-2) mg/kg iv DMPP in beta-blocked (BB) dogs was not significantly altered by ADX. At 2.5 X 10(-1) mg/kg iv DMPP, the alpha-adrenergic contractile response was still 70% of the response prior to ADX. We conclude that sympathetic tracheal relaxation in dogs is predominantly mediated by circulating catecholamine from the adrenal gland, but that alpha-adrenergic contraction after BB results predominantly from direct sympathetic innervation and is not greatly augmented by adrenal secretion. We also report a new method for selective stimulation of airway cholinergic nerves in vivo without systemic effects.

Hyperglycemia and Glucagon Suppression: Possible Importance of the Vagus and Enteric Humoral Factors

Augmentation of insulin release after oral glucose by a gastrointestinal humoral mechanism is well accepted. The suggestion of a similar mechanism for suppression of glucagon release after oral glucose has not been previously tested. In this study, plasma glucagon levels have been estimated in five normal subjects after both oral and iv administration of glucose. A variable iv glucose infusion rate with frequent monitoring of blood glucose was used to match the hyperglycemia produced by the 50 g oral glucose and the iv glucose loads. Virtually complete suppression of plasma glucagon levels was seen in both cases (nadir of glucagon levels 16 +/- 6 pg/ml for oral glucose; 11.4 +/- 3 pg/ml for iv glucose). Thus, enteric humoral factors did not facilitate glucagon suppression after oral glucose ingestion in man. The vagus nerve is also involved in mediating the alpha-cell response to hypoglycemia and, thus, to examine whether hyperglycemia suppresses glucagon release through a vagal mechanism, iv atropine (15 microgram/kg) was given 20 min before administration of oral or iv glucose. Atropinization delayed the glucagon suppression after oral glucose, but this delay was probably related to delayed glucose absorption from the gut. With iv glucose, atropinization did not affect the degree of suppression of glucagon levels. It is concluded that alpha-cell suppression in response to hyperglycemia is not mediated via the vagus.