Objective-Modified lipoproteins, particularly oxidized LDLs, are believed to evoke an inflammatory response which participates in all stages of atherosclerosis. Disposal of these particles is mediated through receptors which may trigger proinflammatory signaling pathways leading to vascular injury. This study was aimed at assessing the role in atherogenesis of one of these receptors, galectin-3. Methods and Results-Galectin-3-deficient and wild-type mice were fed an atherogenic diet or standard chow for 8 months. Lesion area and length were higher in galectin-3-deficient versus wild-type mice. At the level of the aortic sinus, wild-type animals showed only fatty streaks, whereas galectin-3-deficient mice developed complex lesions, associated with extensive inflammatory changes. This was indicated by the presence of T lymphocytes with activated Th1-phenotype and by more marked monocyte-macrophage infiltration, inflammatory mediator expression, vascular cell apoptosis, and proinflammatory transcription factor activation. Increased accumulation of oxidixed LDLs and lipoxidation products and upregulation of other receptors for these compounds, including the proinflammatory RAGE, were detected in galectin-3-deficient versus wild-type mice. Conclusions-These

SummaryOrotracheal intubation in mice is a complicated technique because of the peculiar oropharyngeal anatomy and the dif culty in visualizing the laryngis aditus. Here we report a new and simple method for rapid endotracheal intubation by using a small bore, straight bre-optic arthroscope. Under endoscope-assisted visualization of the laryngis aditus, a polyethylene cannula, inserted on a guide-wire in order to facilitate the introduction of the tip across the vocal cords, was advanced in the trachea. The success rate of intubation was 100%. We were also able to re-intubate the mice 4 and 8 weeks later without any major complications. We conclude that this method can be easily and safely used for studies where controlled pulmonary ventilation is necessary.

In the aortic banding-induced model of LVH: (i) the antihypertrophic effect of propranolol is independent of its beta-adrenergic blocking activity; and Iii) since disopyramide and D-propranolol also proved to be able to antagonize banding-induced LVH, the hypothesis is proposed that membrane-stabilizing activity, among the ancillary properties of propranolol, most likely accounts for the antihypertrophic effect of this drug.

We investigated the effects of isoflurane on the rabbit cardiovascular system at several end-tidal concentrations. Furthermore, because isoflurane has been reported to produce tachycardia while reducing sympathetic nervous activity and baroreflex function, we evaluated whether the chronotropic effects of isoflurane could be due to a vagal withdrawal. ECG, mean arterial pressure (MAP), and heart rate (HR) were obtained in rabbits the conscious, unsedated state and during isoflurane anesthesia by telemetric device. Measurements of pH, oxygen, carbon dioxide, plasma catecholamines, baroreflex sensitivity, and spectral analysis of HR variability were made in nonanesthetized and anesthetized animals. Isoflurane caused an increase in HR at 0.5, 1, and 1.5 minimum alveolar concentration (MAC) and a decrease in systolic and diastolic blood pressure (SBP, DBP) and MAP at 1 and 1.5 MAC. Biochemical analysis showed that isoflurane-mediated cardiovascular effects were not accompanied by any significant changes in plasma norepinephrine (NE) and epinephrine (Epi) levels. Neither were any significant differences in plasma catecholamine levels noted between anesthetized and awake animals. The analysis of spectral components of HR variability and baroreflex function indicated that isoflurane induced a marked reduction in the low- and high-frequency spectral power of HR variability and in baroreflex sensitivity. Tachycardia under isoflurane was suppressed dose dependently by the administration of clonidine or atenolol and was not influenced by bilateral vagotomy. Collectively, our results indicate that cardiovascular effects induced by isoflurane in smaller animals such as rabbits are similar to those observed in humans and other animal species. We showed that isoflurane-induced tachycardia is mainly the result of vagal withdrawal rather than a baroreflex response, even though a marginal role of baroreflex in heart response to higher concentrations of isoflurane cannot be excluded.

This review takes into consideration the main mechanisms involved in cellular remodeling following an ischemic injury, with special focus on the possible role played by non-genomic estrogen effects. Sex differences have also been considered. In fact, cardiac ischemic events induce damage to different cellular components of the heart, such as cardiomyocytes, vascular cells, endothelial cells, and cardiac fibroblasts. The ability of the cardiovascular system to counteract an ischemic insult is orchestrated by these cell types and is carried out thanks to a number of complex molecular pathways, including genomic (slow) or non-genomic (fast) effects of estrogen. These pathways are probably responsible for differences observed between the two sexes. Literature suggests that male and female hearts, and, more in general, cardiovascular system cells, show significant differences in many parameters under both physiological and pathological conditions. In particular, many experimental studies dealing with sex differences in the cardiovascular system suggest a higher ability of females to respond to environmental insults in comparison with males. For instance, as cells from females are more effective in counteracting the ischemia/reperfusion injury if compared with males, a role for estrogen in this sex disparity has been hypothesized. However, the possible involvement of estrogen-dependent non-genomic effects on the cardiovascular system is still under debate. Further experimental studies, including sex-specific studies, are needed in order to shed further light on this matter.