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L N Torres

Publications and source records attributed to L N Torres.

3 recordsLinked to original sources

Expression of connexins 26 and 43 in canine hyperplastic and neoplastic mammary glands.

Gap junctions are the only communicating junctions found in animal tissues and are composed of proteins known as connexins. Alterations in connexin expression have been associated with oncogenesis; reported studies in rodent and human mammary glands, which normally express connexins 26 and 43, confirm these alterations in malignancies. Mammary neoplasms represent the second most frequent neoplasm in dogs, and since there are no reports on the study of connexins in canine mammary glands, the present study investigated the expression of connexins 26 and 43 in normal, hyperplastic, and neoplastic mammary glands of this species, to verify if altered patterns of connexin staining are related to higher cell proliferation and malignant phenotypes. A total of 4 normal, 8 hyperplastic mammary glands, 9 benign, and 51 malignant mammary gland neoplasms were submitted for the immunostaining of connexins 26 and 43, E-cadherin, and proliferating cell nuclear antigen (PCNA). Normal, hyperplastic, and benign neoplastic mammary glands showed a punctate pattern for connexin 26 and 43 staining and an intercellular E-cadherin staining. Malignant neoplasms, especially the most aggressive cases with high cell proliferation rates, presented either fewer gap junction spots on the cell membranes or increased cytoplasmic immunostaining. Malignant tumors also expressed a less intense immunostaining of E-cadherin; the expression of this adhesion molecule is important for the transportation of connexins to cell membranes and in forming communicating gap junctions. Deficient expression of E-cadherin could be related to the aberrant connexin localization and may contribute to the malignant phenotype. In conclusion, the expression and distribution of connexins and E-cadherin are inversely correlated to cell proliferation in malignant mammary neoplasms of dogs and may well be related to their more aggressive histologic type and biologic behavior.

Animals↗

Effects of hypertonic saline solution on mesenteric microcirculation.

We evaluated systemic and microvascular effects of hypertonic NaCl solution on normovolemic and hemorrhaged animals. Forty-three Wistar rats (186 +/- 4 g, mean +/- SEM) were anesthetized with pentobarbital and cannulated for mean arterial pressure (MAP), heart rate (HR), and mean pulse pressure (MPP) monitoring and blood withdrawal. Diameters of 126 arterioles and 88 venules of the exteriorized mesentery were studied by using intravital microscopy. Microvascular blood flow was calculated from diameter and red blood cell velocity measurements. The protocol consisted of 15 min control, 30 min hypotension (MAP = 52.9 +/- 0.9 mmHg, hemorrhaged vol. = 17.1 +/- 0.7 mL/kg) and 60 min post-infusion of either normal (0.9%) or hypertonic saline (7.5%, 4 mL/kg). Normovolemic animals showed no systemic or microvascular effects of hypertonic saline. Hemorrhagic hypotension resulted in HR fall that was not changed after infusions. Hypertonic infusion reversed MPP decrease during hypotension but only partially restored MAP and microvascular blood flow. Venules did not change diameter during protocols. During hypotension, 24% of arterioles displayed vasomotion (38% of the rats) with low- and high-frequency components present in 74% and 87% of arterioles, respectively. Arterioles with vasomotion during hypotension had larger control diameters (28.9 +/- 2.0 microm) and contracted more (30.8 +/- 4.1%) than arterioles without vasomotion (18.7 +/- 1.2 microm and 8.1 +/- 1.5%, respectively). Mean arteriolar diameter did not change after infusions. After hypertonic solution, the number of vessels showing vasomotion increased 80%, frequency of vasomotion was unchanged, and amplitude increased. These findings may help to explain some of the mechanisms underlying resuscitation effects of hypertonic infusions during hemorrhagic hypotension.

Animals↗

Determination of macromolecular exchange and PO2 in the microcirculation: a simple system for in vivo fluorescence and phosphorescence videomicroscopy.

We have developed a system with two epi-illumination sources, a DC-regulated lamp for transillumination and mechanical switches for rapid shift of illumination and detection of defined areas (250-750 microm(2)) by fluorescence and phosphorescence videomicroscopy. The system permits investigation of standard microvascular parameters, vascular permeability as well as intra- and extravascular PO2 by phosphorescence quenching of Pd-meso-tetra (4-carboxyphenyl) porphine (PORPH). A Pechan prism was used to position a defined region over the photomultiplier and TV camera. In order to validate the system for in vivo use, in vitro tests were performed with probes at concentrations that can be found in microvascular studies. Extensive in vitro evaluations were performed by filling glass capillaries with solutions of various concentrations of FITC-dextran (diluted in blood and in saline) mixed with different amounts of PORPH. Fluorescence intensity and phosphorescence decay were determined for each mixture. FITC-dextran solutions without PORPH and PORPH solutions without FITC-dextran were used as references. Phosphorescence decay curves were relatively unaffected by the presence of FITC-dextran at all concentrations tested (0.1 microg/ml to 5 mg/ml). Likewise, fluorescence determinations were performed in the presence of PORPH (0.05 to 0.5 mg/ml). The system was successfully used to study macromolecular extravasation and PO2 in the rat mesentery circulation under controlled conditions and during ischemia-reperfusion.

Animals↗