Hatchery and wild larval lake sturgeon experience effects of captivity on stress reactivity, behavior and predation risk.

Reintroduction programs are important tools for wildlife conservation. However, captive rearing environments may lead to maladaptive behavior and physiological alterations that reduce survival probability after release. For captive rearing programs that raise individuals captured from the wild during early ontogeny for later release, there is a lack of information about when during ontogeny the detrimental effects of captive rearing may become evident. In this study we compared cortisol levels, predation rates and swimming behavior between hatchery-produced and wild-caught larval lake sturgeon (Acipenser fulvescens), a threatened fish species, at three times over 9 days. Cortisol levels did not indicate that hatchery-produced individuals were more stressed, but cortisol reactivity to an acute stressor disappeared for both hatchery-produced and wild-caught larvae after 9 days in the hatchery. Swimming activity levels decreased over time for hatchery-produced larvae but increased over time for wild-caught larvae, suggesting that behavioral trajectories may be programmed prior to the larval stage. Neither increasing nor decreasing activity levels was advantageous for survival, as predation rates increased over time in captivity for larvae from both treatments. Results suggest that physiological and behavioral phenotypes may not accurately predict survival for individuals released from reintroduction programs and that the captive environment may inhibit transition to the wild even if cortisol levels do not indicate high stress. Findings emphasize that even a short amount of time in captivity during early ontogeny can affect phenotypes of individuals captured from wild populations, which may impact the success of reintroduction programs.

The effects of angiotensin II on the coupled microstructural and biomechanical response of C57BL/6 mouse aorta.

RATIONALE: Abdominal aortic aneurysm (AAA) is a complex disease that leads to a localized dilation of the infrarenal aorta, the rupture of which is associated with significant morbidity and mortality. Animal models of AAA can be used to study how changes in the microstructural and biomechanical behavior of aortic tissues develop as disease progresses in these animals. We chose here to investigate the effect of angiotensin II (AngII) in C57BL/6 mice as a first step towards understanding how such changes occur in the established ApoE(-/-) AngII infused mouse model of AAA. OBJECTIVE: The objective of this study was to utilize a recently developed device in our laboratory to determine how the microstructural and biomechanical properties of AngII-infused C57BL/6 wildtype mouse aorta change following 14 days of AngII infusion. METHODS: C57BL/6 wildtype mice were infused with either saline or AngII for 14 day. Aortas were excised and tested using a device capable of simultaneously characterizing the biaxial mechanical response and load-dependent (unfixed, unfrozen) extracellular matrix organization of mouse aorta (using multiphoton microscopy). Peak strains and stiffness values were compared across experimental groups, and both datasets were fit to a Fung-type constitutive model. The mean mode and full width at half maximum (FWHM) of fiber histograms from two photon microscopy were quantified in order to assess the preferred fiber distribution and degree of fiber splay, respectively. RESULTS: The axial stiffness of all mouse aorta was found to be an order of magnitude larger than the circumferential stiffness. The aortic diameter was found to be significantly increased for the AngII infused mice as compared to saline infused control (p=0.026). Aneurysm, defined as a percent increase in maximum diameter of 30% (defined with respect to saline control), was found in 3 of the 6 AngII infused mice. These three mice displayed adventitial collagen that lacked characteristic fiber crimp. The biomechanical response in the AngII infused mice showed significantly reduced circumferential compliance. We also noticed that the ability of the adventitial collagen fibers in AngII infused mice to disperse in reaction to circumferential loading was suppressed. CONCLUSIONS: Collagen remodeling is present following 14 days of AngII infusion in C57BL/6 mice. Aneurysmal development occurred in 50% of our AngII infused mice, and these dilatations were accompanied with adventitial collagen remodeling and decreased circumferential compliance.

Cardiac patch constructed from human fibroblasts attenuates reduction in cardiac function after acute infarct.

The current experiments used a scaffold-based, three-dimensional, human dermal fibroblast culture (3DFC) as a cardiac patch to stimulate revascularization and preserve left ventricular (LV) function of the infarcted LV in severe combined immunodeficient (SCID) mice. The 3DFC contains viable cells that secrete angiogenic growth factors and has been previously shown to stimulate angiogenesis. The hypothesis tested was that a 3DFC cardiac patch would attenuate a reduction in LV function of infarcted hearts. Five groups of mice were studied, including normal SCID mice (n = 13), normal SCID mice with 3DFC (n = 6), infarcted SCID mice (n = 6), infarcted mice with nonviable 3DFC (n = 6), and infarcted SCID mice with 3DFC (n = 6). An occlusion of a branch of the left anterior descending (LAD) coronary artery was performed by thermal ligation, and 3DFC was sized to the damaged area and implanted onto the epicardium at the site of tissue injury. Fourteen days postsurgery, LV mechanics were characterized with the Millar conductance catheter system (CCS). The data demonstrated that 3DFC-treated infarcted myocardium had significantly higher ejection fractions (EFs) compared with infarct-only mice (58.9 +/- 10.8 versus 31.0 +/- 5.8%, respectively; p < 0.05). Preload recruitable stroke work (PRSW) parameters were significantly higher in 3DFC-treated mice compared with infarct-only mice (64.6 +/- 11.9 versus 36.8 +/- 6.4 mmHg, respectively; p < 0.05). These results show that the 3DFC as a cardiac patch functioned to attenuate further loss of LV function accompanying acute myocardial infarct and that this may be related in part to myocardial revascularization.