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W Jackman

Publications and source records attributed to W Jackman.

4 recordsLinked to original sources
PubMed1999

Transvenous parasympathetic cardiac nerve stimulation: an approach for stable sinus rate control.

INTRODUCTION: Epicardial electrical stimulation of parasympathetic nerves innervating the sinus node has been shown to decrease sinus rate. We investigated whether intravascular parasympathetic cardiac nerve stimulation (IPS) can be achieved over a relatively long-term period to slow the supraventricular rate. METHODS AND RESULTS: Fifteen dogs were investigated. IPS was performed with rectangular stimuli (0.05-msec duration, 20 Hz) using a catheter with an expandable electrode basket. The catheter was positioned in the superior vena cava (SVC; n = 9) or right pulmonary artery (RPA; n = 6). The basket then was expanded to hold the catheter in place. Nonfluoroscopic identification of effective IPS sites was achieved within 5 minutes in the SVC. Increasing IPS voltage resulted in a graded response of supraventricular rate slowing. A 50% prolongation of the baseline atrial cycle length was achieved with 28 V in the SVC (1,056 +/- 355 msec vs 489 +/- 154 msec; P < 0.001) and 25 V in the RPA (1,181 +/- 306 msec vs 518 +/- 138 msec; P < 0.01). The rate slowing started immediately after IPS onset, terminated abruptly after IPS cessation, and could be maintained over 10 hours. A rate slowing effect also was observed when the sinus rate was increased by isoproterenol (SVC: 304 +/- 8 msec/RPA: 341 +/- 9 msec with isoproterenol vs SVC: 635 +/- 12 msec with isoproterenol + IPS at 39 V/ RPA: 584 +/- 16 msec with isoproterenol + IPS at 38 V; n = 6). CONCLUSION: IPS results in a significant supraventricular rate slowing that is stable over a relatively long period and may be applied to slow undesirable sinus tachycardia in acute ischemic syndromes or to counteract undesirable chronotropic effects of catecholamines during treatment of cardiogenic or septic shock and acute congestive heart failure.

Animals↗
PubMed1988

Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs.

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.

Amiodarone↗
PubMedDate not supplied

Echocardiographic demonstration of coronary sinus diverticula in patients with Wolff-Parkinson-White syndrome.

Coronary sinus (CS) diverticula have been reported to be the anatomic basis of some posteroseptal accessory atrioventricular pathways. During 1 year, 53 patients with Wolff-Parkinson-White syndrome referred to our center for catheter ablation were found to have posteroseptal or left posterior accessory pathways. The accessory pathway was associated with an anomaly of the CS in seven patients (13%), including six diverticula of the CS or its branches and one aneurysmal CS. Four of the CS diverticula were visualized by transesophageal echocardiography. Diverticular appear as echolucent, contractile pouches on the epicardial surface of the posteroseptal or posterior left ventricle that connect to the CS by an isthmus. Previous reports have suggested that accessory pathways associated with CS aneurysms have rapid conduction times and may be associated with an increased risk of rapid ventricular response during atrial fibrillation and sudden death; five of our seven patients had a short preexcited R-R interval in the range of 172 to 225 msec during atrial fibrillation. In summary, many, if not the majority, of CS diverticula associated with preexcitation can be visualized by transesophageal echocardiography.

Adolescent↗