Interaction of anesthetics and catecholamines on conduction in the canine His-Purkinje system.

The findings in papillary muscles that epinephrine facilitates conduction at Purkinje fiber-muscle junctions and in the endocardium are consistent with older observations that activation of myocardial beta-adrenergic receptors speeds conduction and activation in the heart and thereby increases the synergy of contraction (46,47). The cellular mechanism underlying this action is probably increased cell-to-cell coupling between muscle fibers secondary to elevation of cyclic AMP (19,48). However, the findings that epinephrine alone or with halothane transiently slows conduction in the Purkinje layer while simultaneously improving conduction across Purkinje-muscle junctions and in the endocardium may represent proarrhythmic actions.

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. II. Effects of enflurane and isoflurane during exposure to epinephrine with and without muscarinic blockade.

Background: Atrial dysrhythmias precede ventricular dysrhythmias during epinephrine-anesthetic sensitization, and may be caused by an altered relationship between automaticity of primary and subsidiary pacemakers. The following hypotheses were tested: (1) epinephrine-induced pacemaker shifts with enflurane or isoflurane require intact vagal reflexes and (2) these anesthetics sensitize the atrial myocardium to epinephrine-induced dysrhythmias.

Methods: Eight dogs were instrumented for chronic electrophysiologic investigation, including electrodes at the SA node, atrial appendages, right ventricle, and His bundle, and along the sulcus terminalis.

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. I. Methodology, conscious state, and halothane anesthesia: comparison with and without muscarinic blockade during exposure to epinephrine.

Background: Supraventricular dysrhythmias are common during anesthesia, but have been incompletely investigated. Mechanisms may involve altered automaticity of subsidiary pacemakers and participation of vagal reflexes. The following hypotheses were tested: (1) shifts from the sinoatrial (SA) node to subsidiary pacemakers require intact vagal reflexes and (2) halothane sensitizes the heart to epinephrine-induced atrial pacemaker shifts.

Effects of epidural and systemic lidocaine on sympathetic activity and mesenteric circulation in rabbits.

Background: The mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. This study examines the sympathetic block and splanchnic venodilatation that result from extensive thoracolumbar epidural anesthesia in rabbits using direct measurements of sympathetic efferent nerve activity (SENA) and mesenteric vein diameter (VD).

Methods: Epidural catheters were inserted in rabbits anesthetized with alpha-chloralose, paralyzed with vecuronium, and receiving mechanical ventilation.

Anesthetics and automaticity in latent pacemaker fibers. IV. Effects of isoflurane and epinephrine or norepinephrine on automaticity of dominant and subsidiary atrial pacemakers in the canine heart.

Background: Anesthesia and surgery may be associated with atrioventricular junctional or ventricular rhythm disturbances. These may be caused by alteration of automaticity of primary and subsidiary pacemakers.

Methods: The direct effects of isoflurane, alone or in combination with epinephrine (E) and norepinephrine (NE), as well as single effects of E and NE, were examined on automaticity of primary and subsidiary atrial pacemakers (SAP) using a perfused canine right atrial preparation (n = 29).

Differential sensitivity of proximal and distal coronary arteries to a nitric oxide donor following reperfusion injury or inhibition of nitric oxide synthesis.

Objective: The effect of the nitric oxide donor, SIN-1, in proximal and distal coronary arteries with normal endothelium was characterised before and after inhibition of NO synthesis with L-nitroarginine methyl ester (L-NAME). The effect of reperfusion injury in vivo in similar vessels on the response to SIN-1 was also assessed.

Methods: In vitro reactivity of preconstricted coronary arterial rings was studied in control dogs (group 1), and dogs in which the left circumflex coronary artery was subjected in vivo to four acute occlusions of 5 min duration, with three intervening reperfusion periods of 5 min and a final reperfusion period of 60 min (group 2).

The effects of halothane and isoflurane on slowly inactivating sodium current in canine cardiac Purkinje cells.

The effects of halothane (0.45 and 0.9 mM, equivalent to 0.

Effects of nifedipine with isoflurane, halothane, or enflurane on automaticity, conduction, and contractility in isolated guinea pig hearts.

Background: Calcium channel blockers and volatile anesthetics have depressant effects on cardiac function. Both groups of drugs appear to exert both qualitatively and quantitatively different effects on electrophysiologic and mechanical function. The aim of this study was to compare the direct cardiac effects of the calcium channel blocker nifedipine in the absence and presence of isoflurane, halothane, or enflurane.

Potassium channel openers attenuate atrioventricular block by bupivacaine in isolated hearts.

Our purpose was to test if pinacidil and bimakalim (EMD 52692 or SR 44866), which are ATP-sensitive K+ (K+ATP) channel openers, can attenuate bupivacaine-induced atrioventricular (AV) block. Bupivacaine-induced AV block was studied in 24 isolated guinea pig hearts with or without either pinacidil or bimakalim. Hearts were perfused at 55 mm Hg with a modified Krebs' perfusate.

Inhibition by enflurane of baroreflex mediated mesenteric venoconstriction in the rabbit ileum.

Background: Halothane and isoflurane are known to attenuate neurally mediated regulation of mesenteric vein diameter. The current study evaluated the effects of enflurane on baroreflex control of small mesenteric veins.

Methods: Changes in mesenteric vein diameter, intravenous pressure, mean arterial pressure, and heart rate in response to bilateral carotid occlusion, aortic nerve stimulation, and celiac ganglion stimulation were measured in 23 chloralose-anesthetized rabbits before, during, and after 1% and 2% inhaled enflurane administration.

Does isoflurane alter mesenteric venous capacitance in the intact rabbit?

Volatile anesthetics act at a number of sites to alter cardiovascular function and the response of the cardiovascular system to barostatic reflexes. We examined the effects of isoflurane on reflex regulation of mesenteric venous capacitance vessels. To determine whether isoflurane alters mesenteric venous capacitance, continuous direct observations of mesenteric vein diameter, intravenous pressure, and mesenteric sympathetic efferent nerve activity (SENA) were made in 31 chloralose-anesthetized New Zealand white rabbits.

Recovery of contractile function of postischemic, reperfused myocardium: influence of 2,3-butanedione-2-monoxime.

Inhibition of mechanical activity during ischemia could improve recovery of stunned myocardium. In this study, the effect of 2,3-butanedione-2-monoxime (BDM), an agent that disrupts excitation-contraction coupling, on the time course of recovery of contractile function of postischemic reperfused myocardium was studied in open-chest anesthetized dogs. Ischemia was produced by occluding the left anterior descending coronary artery (LAD) for 15 mins.

Actions of volatile anesthetics on ischemic and nonischemic Purkinje fibers in the canine heart: regional action potential characteristics.

The effects of halothane, isoflurane, and enflurane on proximal (false tendon) and distal (apical) Purkinje fibers were measured in vitro in infarcted canine hearts to assess their effects on action potentials of fibers located within the nonischemic and ischemic regions, respectively. High- and low-dose anesthetic effects were evaluated in three groups of eight preparations and compared to changes occurring at identical times in eight infarcted control preparations. Under control conditions in all groups, the action potential duration at 90% repolarization (APD90, mean +/- SEM) of ischemic distal fibers (396 +/- 9 ms) was longer (P < or = 0.

Actions of halothane and isoflurane on Purkinje fibers in the infarcted canine heart: conduction, regional refractoriness, and reentry.

The actions of halothane (HAL) and isoflurane (ISO) on conduction and regional refractoriness were studied in infarcted canine hearts to compare their effects on reentry in vitro. In two anesthetic groups of 8 hearts, high and low dose effects were assessed using action potentials recorded from Purkinje fibers located in the nonischemic and ischemic regions. An extrastimulus technique was used to determine the relationship between delay of conduction of premature impulses into the more refractory ischemic region and induction of reentrant responses.

Reperfusion with adenosine and nitroprusside improves preservation of isolated guinea pig hearts after 22 hours of cold perfusion with 2,3 butanedione monoxime.

The function of isolated guinea pig hearts treated with 2,3 butanedione monoxime (BDM) before, during, and initially after 22 h of hypothermic perfusion was examined during 4 h of normothermic reperfusion. BDM is a vasodilatory and negative inotropic agent that reversibly decreases sensitivity of contractile proteins to Ca2+. Also examined were the effects of adenosine (ADE) and nitroprusside (NP) in improving coronary flow (CF) and contractile function when given with BDM during rewarming and during the initial period of normothermic reperfusion.

Transient negative dromotropic effects of catecholamines on canine Purkinje fibers exposed to halothane and isoflurane.

The time-dependent effects of catecholamines in combination with volatile anesthetics on conduction velocity of canine Purkinje fibers were investigated to evaluate a controversial older hypothesis that the arrhythmogenic interaction between epinephrine and halothane may involve abnormal conduction. Two groups of 12 in vitro preparations were stimulated at 150 beats/min. In the first group, 5 microM epinephrine by itself did not alter conduction velocity over a 10-min period from a control mean value of 1.

Effects of 2,3-butanedione monoxime in isolated hearts: protection during reperfusion after global ischemia.

The cardiac effects of 2,3-butanedione monoxime on electrical and mechanical function, rhythm, oxygen utilization, and coronary flow responsiveness, particularly during severe ischemia and reperfusion, have not been studied. After perfusing hearts at 55 mm Hg, coronary perfusion was interrupted for 30 minutes and was then reestablished at the control perfusion pressure for 40 minutes. Hearts were divided into four groups (n = 10 each) treated with 0, 3, 5, or 10 mmol/L of 2,3-butanedione monoxime added to the perfusate for 10 minutes before and during ischemia and for the first 10 minutes of reperfusion.

Enflurane, halothane, and isoflurane attenuate contractile responses to exogenous and endogenous norepinephrine in isolated small mesenteric veins of the rabbit.

Background: Volatile anesthetics exert both direct and indirect (neurally mediated) effects to produce splanchnic venodilation. These effects may result in clinically relevant hemodynamic changes. The present study examined the direct effects of isoflurane, halothane, and enflurane on rabbit mesenteric venous smooth muscle.

Halothane reduces release of adenosine, inosine, and lactate with ischemia and reperfusion in isolated hearts.

We investigated the protective effects of halothane on cardiac function of isolated hearts during global hypoperfusion and reperfusion by examining halothane's effects on altering coronary flow, myocardial oxygen utilization (MVO2), and release of adenosine (ADE), inosine (INO), and lactate (LAC). Isolated perfused guinea pig hearts were divided into three groups of perfusion at 25% (14 mm Hg), 10% (5.5 mm Hg), and 0% (no perfusion) from control perfusion pressure (PP, 55 mm Hg).