Fourier Transform Emission Spectroscopy of the A2Delta-X2Pi Transition of SiH and SiD.

The emission spectra of the A2Delta-X2Pi transition of SiH and SiD have been observed at high resolution using a Fourier transform spectrometer. The molecules were excited in a Si hollow cathode lamp by passing a discharge through a mixture of Ne and a trace of H2 or D2. The present data, combined with the previous infrared vibration-rotation measurements, have been used to determine improved molecular constants for the ground and excited states of SiH and SiD. Copyright 1998 Academic Press.

Salicylate reduces ventricular dysfunction and arrhythmias during reperfusion in isolated rat hearts.

Recent studies have shown the ability of salicylic acid (SA) to trap hydroxyl radicals (OH.) generated during reperfusion in ischemic myocardium. Since OH. is implicated in the pathogenesis of reperfusion injury, we examined the effect of SA on reperfusion-induced arrhythmias and postischemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with Krebs-Henseleit buffer containing SA for 10 min. Hearts were then made ischemic for 30 min, followed by 30 min of reperfusion. In a separate group, SA was administered only at the onset of reperfusion. The left ventricular contractile functions, left ventricular developed pressure (LVDP) and its first derivative (LV dP/dt), coronary flow (CF), and creatine kinase (CK) release were determined before and after ischemia. Epicardial electrocardiogram (ECG) was also recorded to analyze the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP, LV dp/dt, and CF recovery and reduced CK release compared to the control group. The incidence of VT and VF during reperfusion was also significantly reduced by SA. Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces myocardial reperfusion injury and attenuates ventricular arrhythmias by trapping OH. radicals upon reperfusion in isolated rat hearts.

Characterization of the anaphylatoxin inactivator and chemotactic factor inactivator activities during cardiopulmonary bypass.

Complement activation productive of phlogistic products has been suggested as one of the major mechanisms of the pump lung syndrome associated with cardiopulmonary bypass (CPB) surgery. Recent studies have demonstrated the presence of circulating C3a antigens in the serum of patients undergoing CPB and have suggested that the vasoactive nature of C3a may contribute directly to the interstitial edema and vascular changes seen in pump lung syndrome. In an effort to unravel the underlying mechanisms of pump lung syndrome, we undertook investigations to determine whether CPB and associated complement activation would alter the serum levels of the major regulators of both C3a and C5a complement split products. These serum regulators designated chemotactic factor inactivator (CFI) and anaphylatoxin inactivator (AI) were measured in the serum of patients undergoing CPB. In these studies, we demonstrated that during CPB a rapid and dramatic drop in the anaphylatoxin inactivator activities occurred within the first 10 minutes of CPB. These lowered AI levels were maintained throughout the CPB but AI levels returned to normal within 24 hours postsurgery. CFI levels were generally maintained throughout the CPB surgery with only minimal depressions in CFI levels during or after CPB surgery. These studies clearly demonstrate that the major regulator system of the complement-derived vasopermeability factors (C3a and C5a) is dramatically depressed during cardiopulmonary bypass and may suggest that the mechanisms of interstitial edema associated with pump lung syndrome may at least, in part, be related to the loss of the serum regulator enzyme carboxypeptidase N, also designated AI.

Optogalvanic effect in a hollow cathode discharge with nonlaser sources.

Several atomic emission sources were investigated for their potential to induce optogalvanic signals in hollow cathode lamps. The sources included an inductively coupled argon plasma, a H(2)-O(2) flame, a high-temperature furnace, electrodeless microwave discharge lamps, and hollow cathode lamps. Successful results were obtained with argon emission from the inductively coupled plasma focused into an argon-filled hollow cathode tube and with atomic emission from one hollow cathode discharge focused into a hollow cathode tube containing the same element. Very low level optogalvanic signals were observed from the other sources but could not be unambiguously ascribed to emission from a specific element. A problem encountered was the presence of a background signal due to photoelectric emission and possibly radiative heating of the cathode.

Optogalvanic double-resonance spectroscopy: experimental observations.

Conjunctive effects are observed when two lasers are used to induce impedance changes in a hollow-cathode discharge and when there is an intermediate energy level common to both induced transitions. These conjunctive effects are useful for determining and confirming spectral assignments and for energy-transfer studies.

Hyperfine structure and isotope shift of the 1.3-microm transition of (129)I.

High resolution Fourier transform spectra of the 1.3-microm emission from (127)I and (129)I electrodeless discharge lamps are presented and analyzed. The hyperfine splitting constants of (129)I are: A = 18.35 +/- 0.01 mK and B = 26.55 +/- 0.07 mK for the J = 3/2 ground state and A = 146.32 +/- 0.02 mK for the J = (1/2) excited state. The validity of the theoretical intensity and isotope relationships is confirmed. The isotope shift between (129)I and (127)I for the 1.3-microm transition was measured to be <1 mK.

Left ventricular venting during cardioplegic arrest.

A technique is described for venting the left ventricle during ischemic arrest without cannulation of the ventricle. This approach is ideally suited for coronary revascularization.

Electrophysiologic observations in a patient with bradycardia-dependent atrioventricular block.

In a patient with atrioventricular (A-V) block distal to the His bundle (H), 1:1 A-V conduction with right bundle branch block and H-V interval of 70 msec was established with atrial pacing at rates of 120 to 150/min, suggesting that the A-V block was bradycardia-dependent. Advanced second degree A-V block distal to the H deflection occurred with atrial pacing at 160/min after completion of A-V nodal Wenckebach periodicity proximal to the H deflection because of the long H-H encompassing the blocked P wave. Atrial extrastimulus testing coupled with sinus rhythm (with A-V block) demonstrated that critical H1-H2 intervals of less than 545 msec allowed conduction to the ventricles. The H2-V2 interval shortened progressively from 290 to 70 msec with shortening of these critical H1-H2 intervals. Atrial extrastimulus testing coupled with an atrial driven cycle lenght of 500 mesc (with intact A-V conduction) revealed block of the H2 deflection with an H1-H2 interval longer than 540 msec. In conclusion, at critical diastolic intervals, impulses were blocked, creating a state of decreased responsiveness. If a cycle length of subsequent impulses was shorter than the critical diastolic blocking interval, membrane responsiveness gradually improved and conduction resumed. If a cycle length of subsequent impulses was longer than the critical blocking diastolic interval, A-V block was sustained. Blocked impulses continually penetrated to the site of block and reset the state of membrane responsiveness.