The Cytoscan model E-II in intraoperative parathyroid gland identification in a rabbit model.

BACKGROUND: Intraoperative parathyroid gland identification and preservation is often a challenge even in the hands of experienced surgeons as they could be indistinguishable from fat or thyroid tissue. OBJECTIVE: The goal of this study was to demonstrate the use of the Cytoscan Model E-II, which uses orthogonal polarization spectral (OPS) imaging technology, as an intravital microscope in identifying parathyroid glands intraoperatively and differentiating the parathyroid glands from fat and thyroid tissue in a rabbit model. METHODS: The necks of 4 New England white rabbits were explored with the animals under a general anesthesia. The Cytoscan was used to obtain images of the vasculature of tissue suspected to be parathyroid, fat, and thyroid tissue. These were confirmed by histologic evaluation. RESULTS: All tissues were correctly identified by the Cytoscan and confirmed by histologic analysis. There was an obvious difference in the images obtained of fatty tissue as compared with parathyroid tissues. There was also an appreciable difference between parathyroid and thyroid tissue based on the difference in vascularity. CONCLUSIONS: OPS imaging technology can be used in identifying parathyroid glands based on the difference in vascularity from fat and the pattern and density of vessels when compared with thyroid tissue in a rabbit model. SIGNIFICANCE: The Cytoscan may play a future role in real time intraoperative identification of human parathyroid glands. Future investigation is warranted.

Coronary sinus pressure and arterial venting do not affect retrograde cardioplegia distribution.

Retrograde techniques for the administration of cardioplegia solutions are of interest because of their relative practical convenience, and because of the possibility that they provide better delivery to myocardial regions jeopardized by coronary stenosis than can be achieved with traditional antegrade techniques. This study was designed to test the following three hypotheses about how the distribution of cardioplegia by retrograde techniques might be optimized: (1) venting an occluded coronary artery improves the distribution of cardioplegia to the myocardial region originally supplied by it; (2) increasing the coronary sinus perfusion pressure makes the distribution of cardioplegia through the myocardium more uniform; and (3) increasing the driving pressure, as achieved by increasing the coronary sinus perfusion pressure or occluding a left coronary artery, improves the distribution of flow to the right ventricular free wall and interventricular septum. Tracer microspheres infused retrogradely with cardioplegia solution into canine hearts in vitro showed that the distribution of flow through the coronary sinus is consistently and significantly nonuniform, and is not significantly altered by coronary arterial occlusion and venting, or by increases in coronary sinus perfusion pressure.

The adenovirus E3-14.7K protein is a general inhibitor of tumor necrosis factor-mediated cytolysis.

We have previously described a 14,700 m.w. protein (14.7K) encoded by the E3 region of adenovirus that prevents TNF-mediated cytolysis of adenovirus-infected C3HA mouse fibroblasts. In the studies described here we have extended our analysis of TNF cytolysis of C3HA cells and the circumstances under which 14.7K protects these cells from cytolysis. C3HA cells were killed by TNF in the presence of inhibitors of protein synthesis, in the presence of cytochalasin E (which disrupts the microfilaments), and when adenovirus E1A was expressed. As described for other cell types, pretreatment of C3HA cells with TNF prevented cytolysis by TNF plus cycloheximide or TNF plus cytochalasin E, indicating that TNF induces a response that protects against these treatments. Remarkably, when 14.7K was expressed in virus-infected cells, it also prevented TNF-induced lysis whether sensitivity to TNF was induced by inhibition of protein synthesis, disruption of the cytoskeleton by cytochalasin E, or expression of adenovirus E1A. The 14.7K protein also prevented TNF lysis of cells that are spontaneously sensitive to TNF lysis. Thus, 14.7K appears to be a general inhibitor of TNF cytolysis, and as such should be an important tool in unraveling the mechanism of TNF cytolysis. There was one exception; NCTC-929 cells were spontaneously sensitive to TNF lysis and that lysis was not affected by 14.7K even though the protein was made in large quantities and was metabolically stable in these cells. This suggests that there is heterogeneity among TNF-sensitive cell lines. The 14.7K protein was found in both the nuclear and cytosol fractions of TNF resistant as well as all spontaneously sensitive cells suggesting that 14.7K may have more than one site of action within the cell.