Assessment of River Herring and Striped Bass in the Connecticut River: Abundance, Population Structure, and Predator/Prey Interactions

Populations of anadromous alewife Alosa pseudoharengus and blueback herring A. aestivalis, collectively referred to as river herring, have declined in the Connecticut River. An explanatory hypothesis for these declines is that predation pressures have increased as a result of recent increases in abundance of sympatric striped bass Morone saxatilis. We sampled river herring and striped bass from the stretch of the Connecticut River between Wethersfield, CT and Holyoke, MA during the vernal migration seasons of 2005-2008. The objectives of the sampling program were to assess abundance, temporal/spatial distribution, and population structure of both river herring and striped bass, as well as striped bass food habits. Blueback herring population structure has changed over recent decades. Contemporary runs feature younger, smaller fish that are less likely to complete multiple spawning runs over their lifetime. These temporal shifts are indicative of elevated mortality rates operating on older, larger herring. Striped bass predation is a significant source of mortality for adult blueback herring in the Connecticut River. River herring comprise a significant portion of striped bass diets in the Connecticut River during May-June, and striped bass congregate in locations where they are successful in capturing herring. The estimated seasonal consumption of blueback herring by striped bass in our study stretch is comparable to the numbers of herring passed annually at the Holyoke fish lift prior to the onset of recent declines. Future studies will incoporate estimates of predation mortality described here into structured population models that can be used to hindcast the impact of striped bass predation on river herring run size in recent decades, and examine the potential for amelioration of river herring mortality via changes to management of striped bass fisheries

Band assignments for the liver tissue spectra.

<p>Band assignments for the liver tissue spectra.</p

Second derivative spectra from Fig. 3 for liver tissue: hydrated tissue ATR spectrum (blue), formalin fixed transmission spectrum (black), desiccator dried transmission spectrum (pink) and ethanol dehydrated transmission spectrum (green).

<p>Second derivative spectra from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0116491#pone.0116491.g003" target="_blank">Fig. 3</a> for liver tissue: hydrated tissue ATR spectrum (blue), formalin fixed transmission spectrum (black), desiccator dried transmission spectrum (pink) and ethanol dehydrated transmission spectrum (green).</p

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<p>Cardiopulmonary bypass (CPB) induced systemic inflammation significantly contributes to the development of postoperative complications, including respiratory failure, myocardial, renal and neurological dysfunction and ultimately can lead to failure of multiple organs. Ghrelin is a small endogenous peptide with wide ranging physiological effects on metabolism and cardiovascular regulation. Herein, we investigated the protective effects of ghrelin against CPB-induced inflammatory reactions, oxidative stress and acute organ damage. Adult male Sprague Dawley rats randomly received vehicle (n = 5) or a bolus of ghrelin (150 μg/kg, sc, n = 5) and were subjected to CPB for 4 h (protocol 1). In separate rats, ghrelin pre-treatment (protocol 2) was compared to two doses of ghrelin (protocol 3) before and after CPB for 2 h followed by recovery for 2 h. Blood samples were taken prior to CPB, and following CPB at 2 h and 4 h. Organ nitrosative stress (3-nitrotyrosine) was measured by Western blotting. CPB induced leukocytosis with increased plasma levels of tumor necrosis factor-α and interleukin-6 indicating a potent inflammatory response. Ghrelin treatment significantly reduced plasma organ damage markers (lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase) and protein levels of 3-nitrotyrosine, particularly in the brain, lung and liver, but only partly suppressed inflammatory cell invasion and did not reduce proinflammatory cytokine production. Ghrelin partially attenuated the CPB-induced elevation of epinephrine and to a lesser extent norepinephrine when compared to the CPB saline group, while dopamine levels were completely suppressed. Ghrelin treatment sustained plasma levels of reduced glutathione and decreased glutathione disulphide when compared to CPB saline rats. These results suggest that even though ghrelin only partially inhibited the large CPB induced increase in catecholamines and organ macrophage infiltration, it reduced oxidative stress and subsequent cell damage. Pre-treatment with ghrelin might provide an effective adjunct therapy for preventing widespread CPB induced organ injury.</p

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<p>Cardiopulmonary bypass (CPB) induced systemic inflammation significantly contributes to the development of postoperative complications, including respiratory failure, myocardial, renal and neurological dysfunction and ultimately can lead to failure of multiple organs. Ghrelin is a small endogenous peptide with wide ranging physiological effects on metabolism and cardiovascular regulation. Herein, we investigated the protective effects of ghrelin against CPB-induced inflammatory reactions, oxidative stress and acute organ damage. Adult male Sprague Dawley rats randomly received vehicle (n = 5) or a bolus of ghrelin (150 μg/kg, sc, n = 5) and were subjected to CPB for 4 h (protocol 1). In separate rats, ghrelin pre-treatment (protocol 2) was compared to two doses of ghrelin (protocol 3) before and after CPB for 2 h followed by recovery for 2 h. Blood samples were taken prior to CPB, and following CPB at 2 h and 4 h. Organ nitrosative stress (3-nitrotyrosine) was measured by Western blotting. CPB induced leukocytosis with increased plasma levels of tumor necrosis factor-α and interleukin-6 indicating a potent inflammatory response. Ghrelin treatment significantly reduced plasma organ damage markers (lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase) and protein levels of 3-nitrotyrosine, particularly in the brain, lung and liver, but only partly suppressed inflammatory cell invasion and did not reduce proinflammatory cytokine production. Ghrelin partially attenuated the CPB-induced elevation of epinephrine and to a lesser extent norepinephrine when compared to the CPB saline group, while dopamine levels were completely suppressed. Ghrelin treatment sustained plasma levels of reduced glutathione and decreased glutathione disulphide when compared to CPB saline rats. These results suggest that even though ghrelin only partially inhibited the large CPB induced increase in catecholamines and organ macrophage infiltration, it reduced oxidative stress and subsequent cell damage. Pre-treatment with ghrelin might provide an effective adjunct therapy for preventing widespread CPB induced organ injury.</p

The representative histological and angiographic findings of the 2 rats in which the coronary artery was ligated 2 mm distal to the LAA (A-C and D-F).

<p>Both cases showed myocardial infarction localized to anterior territory with intact LCX and septal artery. The size of myocardial infarction was 33% <b>(A)</b>, and 26% <b>(C)</b>, respectively. Abbreviations, see Figs <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183323#pone.0183323.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183323#pone.0183323.g002" target="_blank">2</a>.</p

There are 3 branching patterns of LCX, which arose distally from a long LMCA (A, B), proximally from a short LMCA (C, D), or the septal artery (E, F).

<p>Abbreviations, see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0183323#pone.0183323.g001" target="_blank">Fig 1</a>, LMCA = left main coronary artery.</p

Relationship between the size of myocardial infarction and LV end-diastolic dimension (A), LV end-systolic dimension (B), and LV ejection fraction (C).

<p>The black circles indicate the models in which the coronary artery was ligated 2 mm distal to the LAA and the white circles indicate the models in which the LAD was ligated immediately below LAA.</p

Scatter plot showing size of myocardial infarction (A), LV end-systolic dimension (B), and LV ejection fraction (C) in the models in which the LCA was ligated distally versus proximally.

<p>Scatter plot showing size of myocardial infarction (A), LV end-systolic dimension (B), and LV ejection fraction (C) in the models in which the LCA was ligated distally versus proximally.</p

Influence of coronary architecture on the variability in myocardial infarction induced by coronary ligation in rats - Fig 1

<p>The left coronary artery was permanently ligated 2 mm distal to <b>(A)</b> or immediately below <b>(B)</b> the LAA. A catheter with an internal diameter of 0.89 mm was inserted from the right carotid artery into the aortic root <b>(C)</b>. The septal artery invariably branched off either from proximal part of the LCA (n = 30, 60%) <b>(D)</b> or RCA (n = 20, 40%) <b>(E)</b>. Representative histological images of left and right ventricular cavities at the level of the papillary muscles in normal rats <b>(F)</b>. Abbreviations: LV = left ventricle, LAA = left atrial appendage, CCA = carotid coronary artery, PI = peripherally inserted, LCA = left coronary artery, RCA = right coronary artery, RV = right ventricle, LAD = left anterior descending artery, LCX = left circumflex artery, APM = anterior papillary muscle, PPM = posterior papillary muscle.</p