Electromagnetic interference caused by common surgical energy-based devices on an implanted cardiac defibrillator

Background

Surgical energy-based devices emit energy, which can interfere with other electronic devices (eg, implanted cardiac pacemakers and/or defibrillators). The purpose of this study was to quantify the amount of unintentional energy (electromagnetic interference [EMI]) transferred to an implanted cardiac defibrillator by common surgical energy-based devices.

Methods

A transvenous cardiac defibrillator was implanted in an anesthetized pig. The primary outcome measure was the average maximum EMI occurring on the implanted cardiac device during activations of multiple different surgical energy-based devices.

Results

The EMI transferred to the implanted cardiac device is as follows: traditional bipolar 30 W .01 ± .004 mV, advanced bipolar .004 ± .003 mV, ultrasonic shears .01 ± .004 mV, monopolar Bovie 30 W coagulation .50 ± .20 mV, monopolar Bovie 30 W blend .92 ± .63 mV, monopolar instrument without dispersive electrode .21 ± .07 mV, plasma energy 3.48 ± .78 mV, and argon beam coagulator 2.58 ± .34 mV.

Conclusion

Surgeons can minimize EMI on implanted cardiac defibrillators by preferentially utilizing bipolar and ultrasonic devices.     

Morphometric Examination of the Equine Adult and Foal Lung

To understand the mechanisms of airway inflammation associated with equine diseases such as Rhodococcus equi infection, we must identify baseline “normal” structural characteristics of the horse lung. To develop a detailed understanding of the morphology of the horse lung, we adapted and applied stereological methods to the lungs from healthy adult horses (N = 4) and 1‐day (N = 5) and 30‐day (N = 5) old foals. The left lung was fixed in situ by intrabronchial instillation of glutaraldehyde/paraformaldehyde fixative at 25 cm H₂O column and sampled using a fractionator design followed by embedding in glycol methacrylate. The lung was characterized into parenchyma and non‐parenchyma, where median parenchymal density was 81.0% in 1‐day‐old foals, 84.4% in 30‐day‐old foals and 93.7% in adult lungs. The median volume density of alveolar airspace per lung was 45.9% in 1‐day‐old, 55.5% in 30‐day and 66.9% in adult horse lungs. The median alveolar surface area increased with age, from 205.3 m², 258.2 m², and 629.9 m² in 1‐day‐old foals, 30‐day‐old foals, and adults, respectively. While the median alveolar surface density decreased with age, the mean linear intercept (mean free distance within acinar airspaces) increased with age. Alveolar surface area was greater than endothelial surface area within each lung. The ratio between alveolar and endothelial surface density remains unchanged with age. The median endothelium surface area was 106.2 m² in 1‐day, 147.5 m² in 30‐day, and 430 m² in adult lungs. The data suggest the foal lung is functionally developed and postnatal lung development and remodelling is driven by alveolar expansion paralleled with angiogenesis. Anat Rec, 297:1950–1962, 2014. © 2014 Wiley Periodicals, Inc.     

Specific recognition of influenza virus polymerase protein (PB1) by a murine cytotoxic T-cell clone

Cytotoxic T-cell clones were raised in CBA mice that recognised both A/X31 and A/JAP/305/1957 influenza virus. Here, we describe one CTL clone that recognises target cells infected with a recombinant vaccinia virus expressing influenza PB1.     

Calmodulin antagonist trifluoperazine inhibits polyamine biosynthesis and liver regeneration

Polyamines are essential for cell growth and differentiation. Trifluoperazine (TFP) is a potent, competitive inhibitor of the calcium-calmodulin complex. TFP, when given to rats after partial hepatectomy, causes a significant decrease in DNA synthesis. The purpose of this study was to examine the effects of TFP on polyamine biosynthesis and on liver regeneration after partial hepatectomy. TFP (60 mg/kg, bodyweight) or saline control was administered to 80 male Sprague-Dawley rats 2 h before, 2 h after, or at the time of hepatectomy. Polyamines (putrescine, spermidine and spermine) were measured at the time of hepatectomy, and at 6, 24, 48, and 72 h after hepatectomy. TFP, when it was administered either 2 h before or at time of hepatectomy, blocked increases in putrescine that are seen normally at 6 h after hepatectomy. When TFP was given at the time of partial hepatectomy, putrescine was increased at 24 h, and then returned to normal levels at 72 h. Spermidine was inhibited at 24 h, but not at 48 and 72 h. Spermine was not significantly altered at any time. The administration of TFP 2 h after hepatectomy did not significantly alter concentrations of polyamines. The weight of regenerating liver was decreased by TFP at 48 h (23 per cent) and 72 h (22 per cent) after hepatectomy. These findings provide evidence that the calcium-calmodulin complex is required for the synthesis of liver polyamines before liver regeneration can proceed.