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Rapid fluctuations of the oxygen content of both natural and anthropogenic origin are relatively common in freshwater environments. Fish adaptation to these conditions implies tolerance of both low levels of oxygen availability and reoxygenation. Hypoxia tolerance in fish has been widely studied, but the involvement of mitochondria in the response of fish to rapid hypoxia/reoxygenation stress is less known. Zebrafish, a floodplain species, is likely facing significant changes in dissolved oxygen in its natural environment and displays a moderate ability to tolerate hypoxia. In the present study, we report the effects of an acute hypoxia/reoxygenation stress (H/R) protocol on mitochondrial functionality (respiration, complex activities, rate of H2O2 release) and redox state (level of HPs and protein oxidation) of muscle tissue. In parallel, the animal metabolic performance (routine metabolism, nitrogen excretion and swimming performance) was measured. Additionally, the recovery from H/R was tested 20 h after treatment. A significant stimulation by H/R of muscle mitochondrial respiration and H2O2 release was observed, which was only in part counteracted by stimulation of the antioxidant system, resulting in an increased level of lipid peroxides and protein carbonyls. In parallel, H/R increased the animal oxygen consumption and urea excretion rate and reduced routine activity. A significant strong reduction of endurance at 80% Ucrit was also observed. Most of the altered parameter did not recover 20 h after reoxygenation. These data indicate a significant alteration of zebrafish muscle mitochondrial state after acute H/R, associated with changes in tissue redox state and locomotor performance.

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In both 3,5,3-triiodothyronine (T(3))-induced hyperthyroidism and cold-induced functional hyperthyroidism, the heart displays an increased susceptibility to oxidative challenge in vitro. Hearts from T(3)-treated rats also exhibit an increased susceptibility to ischaemia-reperfusion, a condition that raises free radical production. The present study was designed to establish whether cold-exposed rats exhibit an increased cardiac susceptibility to ischaemia-reperfusion which can be attenuated by vitamin E. The following four groups of animals were used: C, control rats (n = 8, temperature 24°C); C+VE, vitamin E-treated rats (n = 8, temperature 24°C); CE, cold-exposed rats (n = 8, temperature 4°C); and CE+VE, cold-exposed vitamin E-treated rats (n = 8, temperature 4°C). Langendorff preparations from these animals were submitted to 20 min ischaemia followed by 25 min reperfusion. At the end of the ischaemia-reperfusion protocol, homogenates and mitochondria were prepared and used for analytical procedures. With respect to control hearts, cold hearts showed a lower inotropic recovery and a higher oxidative stress, as inferred by higher levels of oxidized proteins and lipids and lower reduced glutathione levels. These changes were prevented when cold rats were treated with vitamin E. Evidence was also obtained that mitochondria are involved in the tissue derangement of cold hearts. Indeed, they display a faster production of reactive oxygen species, which causes mitochondrial oxidative damage and functional decline that parallel the tissue dysfunction. Moreover, vitamin E-linked improvement of tissue function was associated with a lower oxidative damage and a restored function of mitochondria. Finally, the mitochondrial population composition and Ca(2+)-induced swelling data indicate that the decline in mitochondrial function is in part due to a decrease in the amount of the highly functional heavy mitochondria linked to their higher susceptibility to oxidative damage and swelling. In conclusion, our work shows that vitamin E treatment attenuates harmful side-effects of the cardiac response to cold, such as oxidative damage and susceptibility to oxidants, thus preserving mitochondrial function and tissue recovery from ischaemia-reperfusion.

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Acute stress may affect metabolism and nitrogen excretion as part of the adaptive response that allows animals to face adverse environmental changes. In the present paper the acute effects of different salinities and temperatures on routine metabolism, spontaneous activity and excretion of ammonia and urea were studied in two freshwater fish: gambusia, Gambusia affinis and zebrafish, Danio rerio, acclimated to 27 degrees C. The effects on gill morphology were also evaluated. Five salinities (0 per thousand, 10 per thousand, 20 per thousand, 30 per thousand and 35 per thousand) were tested in gambusia, while four salinities were used in zebrafish (0 per thousand, 10 per thousand, 20 per thousand and 25 per thousand). Each salinity acute stress was tested alone or in combination with an acute temperature reduction to 20 degrees C. In gambusia, both salinity and temperature acute stress strongly stimulated urea excretion. Routine oxygen consumption was barely affected by acute salinity or temperature stress, and was reduced by the combined effects of temperature and high salinity. Gills maintained their structural integrity in all stressing conditions; hyperplasia and hypertrophy of mitochondria-rich cells were observed. In zebrafish, temperature and salinity acute changes, both alone and in combination, scarcely affected any parameter tested. The major effect observed was a reduction of nitrogen excretion at 20 degrees C-25 per thousand; under these extreme conditions a significant structural disruption of gills was observed. These results confirm the high tolerance to acute salinity and temperature stress in gambusia, and demonstrate the involvement of urea excretion modulation in the stress response in this species.

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A method for perfusion of the isolated trout heart coronary circulation with red blood cells (RBCs) was developed. The method was used to analyse the influence of RBC perfusion on myocardial O(2) supply and O(2) consumption and to test the hypothesis that nitrite is converted to vasoactive nitric oxide in the RBC-perfused coronary circulation. Perfusion with RBCs significantly increased myocardial O(2) supply and O(2) consumption by increasing the incoming O(2) concentration and the O(2) extraction. Coronary flow did not differ between RBC perfusion and saline perfusion, but RBC perfusion established a strong linear increase in myocardial O(2) consumption with coronary flow. Nitric oxide was measured in the atrial effluent of the preparation. Perfusion with saline under hypoxic conditions was associated with NO production. The nitric oxide synthase inhibitor L-NA obliterated this NO production and significantly decreased coronary flow, showing that the NO was vasoactive and probably of endothelial origin. RBC perfusion at low P(O(2)) similarly caused an L-NA-inhibitable NO production. The change in NO production upon subsequent nitrite addition, by contrast, was not inhibited by L-NA. Nitrite entered trout erythrocytes independent of degree of oxygenation, but the O(2) saturation of RBCs showed a major decrease in the coronary circulation, and [NO(2)(-)] decreased while methaemoglobin rose, suggesting that deoxyHb-mediated reduction of nitrite to NO may have occurred. However, other possibilities (e.g. NO(2)(-)-->NO conversion in myocardial cells) cannot be excluded. The NO formation associated with nitrite had no effect on coronary flow, possibly because NO was produced after the resistance vessels.

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In mammals, the in vivo coronary blood flow and myocardial oxygen consumption are closely related via changes in coronary resistance in response to the metabolic demands of the myocardium. A fine neurohumoral regulation of coronary resistance holds true also in fish, and particularly in teleosts, where several vasoconstrictive and vasodilative mechanisms have been described, with numerous putative effectors, including prostanoids, acetylcholine, adrenaline, serotonin, adenosine, steroid hormones. Here, a resume is reported of the available evidence on the involvement of nitric oxide (NO) in the control of coronary resistance in teleosts and particularly in salmonids. Most of the evidence reported is from a comprehensive study performed on a Langedorff-type preparation of the isolated trout heart. Using a physio-pharmacological approach, the experiments performed on this preparation have demonstrated that trout coronary resistance is reduced by l-arginine (NOS substrate), nitroprusside and SNAP (NO donors) and is increased by the NOS inhibitors l-NNA and l-NAME. The vasodilation induced by nitroprusside is blocked by the guanylate cyclase inhibitor methylene blue. l-arginine increases NO release in the perfusate, while l-NNA reduces the release. NO release is inversely related with the coronary resistance. l-NNA inhibits the vasodilatory effects of acetylcholine, serotonin and adenosine. The vasodilation induced by adenosine is accompanied by NO release and involves stretch receptors. Hypoxia induces vasodilation and both adenosine and NO release in the preparation; the NO release under hypoxia is blocked by theophylline. On the whole these data indicate that NO plays a central role in the control of coronary resistance in trout. In particular, a main role for NO as an amplifier of the adenosine-mediated vasodilation under hypoxia can be hypothesized.

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We investigated the role of nitric oxide (NO) in the mitochondrial derangement associated with the functional response to ischemia-reperfusion of hyperthyroid rat hearts. Mitochondria were isolated at 3000 g from hearts subjected to ischemia-reperfusion, with or without N(omega)-nitro-L-arginine (L-NNA, an NO synthase inhibitor). During reperfusion, hyperthyroid hearts displayed tachycardia and low functional recovery. Their mitochondria exhibited O(2) consumption similar to euthyroid controls, while H(2)O(2) production, hydroperoxide, protein-bound carbonyl and nitrotyrosine levels, and susceptibility to swelling were higher. L-NNA blocked the reperfusion tachycardic response and increased inotropic recovery in hyperthyroid hearts. L-NNA decreased mitochondrial H(2)O(2) production and oxidative damage, and increased respiration and tolerance to swelling. Such effects were higher in hyperthyroid preparations. These results confirm the role of mitochondria in ischemia-reperfusion damage, and strongly suggest that NO overproduction is involved in the high mitochondrial dysfunction and the low recovery of hyperthyroid hearts from ischemia-reperfusion. L-NNA also decreased protein content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000 g. This and previous results suggest that the above fraction contains, together with light mitochondria, damaged mitochondria coming from the heaviest fraction, which has the highest cytochrome oxidase activity and capacity to produce H(2)O(2). Therefore, we propose that the high mitochondrial susceptibility to swelling, favoring mitochondrial population purification from H(2)O(2)-overproducing mitochondria, limits hyperthyroid heart oxidative stress.

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This study was designed to investigate the short-term effects of cortisol and 17-beta-estradiol on the intact coronary tree of rainbow trout (Oncorhynchus mykiss). A non-working, isolated, and perfused heart preparation was used. The coronary pressure was monitored together with the coronary flow in order to calculate the coronary resistance. The drug effects were expressed as percent change in coronary resistance. At concentrations higher than 10(-5) mol l(-1), cortisol elicited a significant vasoconstriction (p<0.001) within 10 min of perfusion. The simultaneous administration of cortisol and adenosine (both at 10(-4) mol l(-1)) induced a significant reduction (p<0.001) of the coronary tree response elicited by each drug alone. The perfusion of the intact coronary trout system with 20 ng ml(-1) of 17-beta-estradiol elicited a significant vasodilative response (p<0.001) within 5-15 min of perfusion. This vasodilation did not involve nitric oxide, because no significant effect of Nomega-nitro-L-arginine (L-NA, a nitric oxide synthase inhibitor) in presence of the estrogen was observed. 17-beta-estradiol was also able to reduce the vasoconstriction induced by 10(-3) mol l(-1) acetylcholine. From these results it is possible to suggest that the steroid hormones, cortisol and 17-beta-estradiol, expound their action on the trout coronary tree through a non-genomic mechanism.

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Basal performance, volume loading response and oxygen consumption were determined in a resistance-headed preparation of the isolated trout heart. Two groups of hearts were used: the +CF group, in which the coronary vascular tree was perfused with a flow directly related to the pressure generated by the heart, and the -CF group, in which the coronary flow was set to zero. As a criterion for setting basal performance, the atrial input pressure was set in order to induce the ventricle to produce a cardiac output of 15 ml min(-1) kg(-1). Once basal conditions were obtained, the preparation was perfused for 30 min, and atrial and aortic pressure, cardiac output, heart rate, coronary pressure and coronary flow were determined at 5 min intervals. At the onset of perfusion, there was no difference in the basal performance between the two groups: the same preload was necessary to get the same cardiac output in both perfusion groups. None of the other performance parameters determined were different. However, after only 5 min of perfusion, the -CF hearts displayed significant adjustments, with increased atrial preload and ventricular preload (mean atrial pressure), and a significant decrease in cardiac output. At the end of the 30 min basal perfusion period, hearts were challenged with a stepwise increase in preload in order to obtain maximal stroke work (volume loading). The effect of coronary perfusion on the heart's response to volume loading was highly significant: the stroke work-preload relationship was significantly shifted towards higher preload values in the -CF group. Also, the maximal work produced by the heart under the experimental conditions used was lower in the -CF group. Rate of oxygen consumption of the heart increased significantly with volume loading, from a basal value of approximately 20 microl O2 min(-1) g(-1) to approx. 40 microl O2 min(-1) g(-1), but was not significantly affected by the absence of coronary perfusion. Mechanical efficiency under basal conditions was approximately 17%, but was not affected by either volume loading or coronary perfusion. Taken as a whole, these data represent direct evidence of the effect of coronary perfusion on the mechanical performance of the trout heart, but also show that these effects are limited by significant self-adjustments that occur in the heart.

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The effects of low-intensity, prolonged swimming on functional recovery of the rat heart (Langendorff preparations) from ischaemia-reperfusion (I/R) were investigated. Three groups of rats (120 days old) were used: sedentary rats (S) and rats exercised by a single bout of swimming lasting 5 (E5) or 8 h (E8), respectively. The effect of exercise on the response to I/R was related to an index of oxidative damage such as lipid peroxidation, as well as to the tissue antioxidant capacity and the response of heart tissue to in vitro oxidative stress. The intrinsic performance of E5 Langendorff preparations paced at 220 beats x min(-1) was also determined. A group of sedentary animals was used for H2O2-treated preparations. The effect of antioxidant treatment on inotropic recovery during reperfusion was studied on preparations from 5 or 8 h swimming vitamin E-treated (EVT5 and EVT8 and 5 or 8 h swimming untreated (EVU5 and EVU8) rats. Hearts from exercised animals displayed a reduced preischaemic inotropism, which in E5 rats was accompanied by an increase in the intrinsic heart rate. The lower intrinsic cardiac inotropism of E5 animals was confirmed in the paced preparations. The reduced contractility found in control hearts after addition of H2O2 to perfusion medium suggested that the low inotropism of E5 and E8 hearts was due to an exercise-induced increase in reactive oxygen species. Inotropic recovery during reperfusion was low in the S hearts, was significantly increased in the E5 hearts, and was again reduced to the S level in the E8 hearts. In the E8 hearts the indexes of cellular damage (LDH release) and oxidative stress increased, and antioxidant capacity decreased, while in E5 hearts there was no evidence of significant changes in such parameters. Performance and reperfusion recovery of hearts from 5 h swimming rats was not affected by vitamin E treatment, while those of hearts from 8 h swimming rats was the highest observed. We suggest that the higher inotropic recovery during reperfusion in the hearts from the E5 rats is related to the negative inotropic effect of exercise. The fall in recovery following the 8 h exercise was instead related to the increased oxidative stress.

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We recently reported that hyperthyroidism affects the heart response to ischemia/reperfusion. A significant tachycardia during reperfusion was associated with an increase in the oxidative stress of hearts from T3-treated animals. In the present study we checked the possible role of nitric oxide (NO) in this major stress induced by the hyperthyroid state. We compared the functional recovery from ischemia/reperfusion of Langendorff preparations from euthyroid (E) and hyperthyroid (H, ten daily intraperitoneal injections of T3, 10 microg/100 g body weight) rats, in the presence and in the absence of 0.2 mM Nomega-nitro-L-arginine (L-NNA). At the end of the ischemia/reperfusion protocol (10 min preischemic perfusion, 20 min global ischemia, 30 min reperfusion) lipid peroxidation, antioxidant capacity (CA) and susceptibility to in vitro oxidative stress were determined on heart homogenates. The main effect of hyperthyroidism on the reperfusion functional response was confirmed to be a strong tachycardic response (154% recovery at 25 min reperfusion) accompanied by a low recovery in both left ventricular diastolic pressure (LVDP) and left ventricular dP/dtmax. This functional response was associated with a reduction in CA and an increase in both lipid peroxidation and susceptibility to oxidative stress. Perfusion of hearts with L-NNA per se had small but significant negative chronotropic and positive inotropic effects on preischemic performance of euthyroid rat hearts only. More importantly, L-NNA perfusion completely blocked the reperfusion tachycardic response in the hyperthyroid rats. Concomitantly, myocardium oxidative state (lipid peroxidation, CA and in vitro susceptibility to oxidative stress) of L-NNA perfused hearts was similar to that of E animals. These results suggest that the higher reperfusion-induced injury occurring in hyperthyroid animals is associated with overproduction of nitric oxide.

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Hyperthyroidism has been reported to decrease heart antioxidant capacity and increase its susceptibility to in vitro oxidative stress. This may affect the heart response to ischemia-reperfusion, a condition that increases free radical production. We compared the functional recovery from in vitro ischemia-reperfusion (Langendorff) of hearts from euthyroid (E), hyperthyroid (H, ten daily intraperitoneal injections of T3, 10 microg/100g body weight), vitamin E-treated (VE, ten daily intramuscular injections, 20 mg/100g body weight) and hyperthyroid vitamin E-treated (HVE) rats. We also determined lipid peroxidation, tissue antioxidant capacity and the tissue capability to face an oxidative stress in vitro. A significant tachycardia was displayed during reperfusion following 20 min ischemia by the hyperthyroid hearts, together with a low recovery of left ventricular developed pressure (LVDP) and left ventricular dP/dt(max). When H hearts were paced at 300 beats/min, the functional recovery (LVDP and dP/dt(max)) was close to 100% and significantly higher than in E paced hearts. At the end of the ischemia-reperfusion protocol, myocardium antioxidant capacity was significantly lower, whereas lipid peroxidation and the susceptibility to in vitro oxidative stress were higher in the T3 treated (H) than in euthyroid rats. The in vitro tachycardic response, the reduction in the antioxidant capacity and the increase in lipid peroxidation were prevented by treatment of hyperthyroid rats with vitamin E (HVE). These results suggest that the tachycardic response to reperfusion following chronic T3 pretreatment was associated with the reduced capability of the heart to face oxidative stresses in hyperthyroidism.

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The rat heart protection offered by vitamin E against oxidative stress after ischaemia-reperfusion was studied by using a new methodological approach. Functional recovery of hearts from ischaemia-reperfusion was correlated with a traditional index of oxidative stress such as lipid peroxidation and with antioxidant capacity and susceptibility to oxidants of the tissue evaluated by enhanced chemiluminescence techniques. Rats were treated with ten daily i.m. injections of 100 mg/kg body weight of vitamin E. The functional recovery during reperfusion (20 min, following 45 min ischaemia) of Langendorff preparations from control (vehicle-injected) and vitamin E treated rats was evaluated in terms of heart rate, left ventricular developed pressure (LVDP), double product (= heart rate. LVDP) and coronary flow recovery. Vitamin E treatment significantly improved functional recovery of heart rate, LVDP, double product and coronary flow. It also increased the level of vitamin E and reduced the levels of both malondialdehyde and hydroperoxides in the heart tissue at the end of the ischaemia-reperfusion protocol. In contrast, it did not affect the antioxidant capacity and the response of heart homogenates to in vitro oxidative stress measured after ischaemia-reperfusion. These results show a protective action of vitamin E treatment against lipid peroxidation and cardiac dysfunction associated with ischaemia-reperfusion. Although the precise mechanism of this protection is not evident, our model in part suggests a role of vitamin E other than as a free radical scavenger.

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The involvement of the central cholinergic system in predatory performance, and on the recall of individual and observational memory in Octopus vulgaris was studied by treating the animals with the muscarinic antagonist scopolamine (2 mg/kg). The absence of the effects of the injection of scopolamine on blood circulation was also checked. Scopolamine did not affect the ability of octopuses to prey on live crabs. However, it interfered significantly with memory recall. In fact, the ability to solve the jar problem was impaired within the first hour after injection (short-term effects) and was only partially recovered after 24 h (long-term). Moreover, both individual and observational learning of a visual discrimination were significantly reduced at the short- and long-term testing. These results support a role of the cholinergic system in the processes of memory recall of O. vulgaris.

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A vasoconstrictory response to adenosine has been reported in coronary rings from fish. Since the reactivity of the large coronary arteries and the microcirculation may differ, the present study was undertaken to determine the role of adenosine in the intact coronary system of trout under constant pressure or flow using an isolated and non-working heart preparation. The involvement of nitric oxide (NO) and the interaction with noradrenaline were also studied. At 10(-9) to 10(-8 )mol l-1, adenosine caused a vasoconstrictory response, whereas between 10(-7) and 10(-5 )mol l-1 the response was predominantly vasodilative. Theophylline abolished both these responses to adenosine. The vasodilation induced by adenosine (at 10(-5 )mol l-1) was significantly reduced when the preparation was perfused under constant-flow than rather under constant-pressure conditions. The nitric oxide synthase inhibitor N-nitro-l-arginine (l-NA, 10(-4 )mol l-1) partially reduced the vasodilation induced by adenosine (at 10(-5 )mol l-1) under constant-pressure but not under constant-flow conditions. Perfusion of the intact coronary system with l-arginine or with adenosine significantly increased the rate of nitrite (NO2-) release, while perfusion with l-NA or theophylline reduced NO2- release. Chemical denudation of the coronary endothelium by CHAPS resulted in the loss of both the l-arginine- and adenosine-mediated vasodilation and the l-arginine-induced increase in the rate of NO2- release. Adenosine (10(-5 )mol l-1) offset and overrode the vasoconstriction induced by 10(-7 )mol l-1 noradrenaline. l-NA inhibited only the adenosine-induced vasodilation but not the ability to offset noradrenaline vasoconstriction, excluding the involvement of NO in the interaction between adenosine and noradrenaline.

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Channichthyid icefishes of Antarctica are unique among adult vertebrates. All icefish species lack hemoglobin and red blood cells in their circulating blood. All icefishes examined to date also lack the intracellular oxygen-binding protein myoglobin (Mb) in their oxidative skeletal muscles. However, some icefish species do express Mb in their heart ventricles. It is unknown whether Mb in those species in which it is present represents an evolutionary relic or has functional significance. To address this problem, we compared mechanical performance of isolated, perfused hearts from two species of icefish in which Mb is either present (Chionodraco rastrospinosus) or is absent (Chaenocephalus aceratus). Hearts were challenged with increasing afterload (2.5-4.0 kPa) under conditions of defined basal flow (approximately 100 ml.min-1.kg-1), in both the presence and absence of 5 mM sodium nitrite, a Mb poison. Unlike hearts from C. aceratus, which were unable to maintain a constant cardiac output under pressure loading, those from C. rastrospinosus retained a constant flow up to 3.5 kPa afterload. At the upper range of power outputs, hearts of Mb-lacking C. aceratus display greater oxygen utilization than those of Mb-containing C. rastrospinosus. Poisoning of Mb significantly impaired the ability of C. rastrospinosus hearts to face pressure loading without reduction in flow, whereas those of C. aceratus were refractory to the treatment. The results strongly support a functional role for Mb in the former species.

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Dietary polyunsaturated fatty acids (PUFA) of the n-3 series that have beneficial effects on mammalian heart function are typically found at high levels in fish tissues. The effects of dietary fatty acid composition on cardiac function were investigated in the sturgeon. When compared with sturgeon maintained for 1 yr on a diet enriched with saturated fatty acids (SFA) (the coconut oil-supplemented diet, COD), sturgeon maintained on a diet enriched with n-3 PUFA (the fish oil-supplemented diet, FOD) had higher myocardial 20:5(n-3) and lower 20:4(n-6) content with a consequent decrease in the n-6-to-n-3 ratio (from 0.86 to 0.25) and a lower intrinsic in vitro heart rate (22.0 +/- 1.5 vs. 29.9 +/- 1.0 beats/min) and cardiac power output (PO) (0.33 +/- 0.08 vs. 0.48 +/- 0.03 mW/g), but had a greater in vitro scope for cardiac work (almost twice the maximal-to-basal PO ratio). Reducing the oxygen supply to the hearts significantly decreased, by approximately 40%, the maximal in vitro PO in the COD group of animals but had no effect in the FOD group. These differences in performance were not reflected in heart rate or blood pressure in vivo, either in normoxia or hypoxia. Addition of vitamin E as an antioxidant to the diets reduced intrinsic heart rate by approximately 25% but did not influence the effects (dietary fatty acid composition on in vitro cardiac performance. The results indicate that dietary n-3 PUFA can have beneficial effects on the resistance of the fish heart to environmental stressors such as hypoxia.

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Despite the great interest of Cephalopods in learning studies, behavioral pharmacological experiments using these animals are scanty. The purpose of this study was to find an appropriate method of injection of substances for studying their effects on the behavior of octopuses. We injected into the branchial heart a known volume of seawater to test the effect of cold anaesthesia and of different types of manipulation on the predatory performance of Octopus vulgaris. An injection procedure that is simple, reliable, and does not require anaesthesia is proposed. The article also addresses ethical and manipulation requirements of modern behavioral pharmacology.

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The Channichthyidae or "icefish" represent an intriguing example of extreme adaptation to the stable low temperature and high oxygen content of the Antarctic waters. The lack of respiratory pigments (hemoglobin and myoglobin) in these teleosts is associated with relatively low oxygen consumption and relevant cardio-circulatory adjustments which include large blood volume, increased relative heart weight (cardiomegaly), and very high cardiac output. The heart has the ability to displace large systolic volumes at a low rate and relatively low pressure, with large ventricular fillings (high ventricular compliance), whereas it is incapable of facing increased afterloads. These functional aspects of mechanical flexibility and restrictions of the cardiac pump have been tentatively related to some constructional aspects of the icefish cardiomegaly, particularly, at the whole ventricular level, to the trabeculate type of myo-architecture, and, at the subcellular level, to the conflict in space economy between the exceptionally high mitochondrial densities and the consequent severe reduction in myofibrillar volume. On the basis of this morphodynamic approach, we suggest that the icefish may illustrate how a certain feature (I.e., an architectural cardiac design) common to the suborder and to most teleosts, and apparently with "irrelevant" properties, can become useful for a specialized purpose (i.e., volume pump design); and how, in contrast, the internal machinery construction, because of structural and ultrastructural constraints, may prevent these stenothermal sedentary teleosts from conquering niches requiring more active locomotory habits.

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The Channichthyidae or "icefish" represent an intriguing example of extreme adaptation to the stable low temperature and high oxygen content of the Antarctic waters. The lack of respiratory pigments (hemoglobin and myoglobin) in these teleosts is associated with relatively low oxygen consumption and relevant cardio-circulatory adjustments which include large blood volume, increased relative heart weight (cardiomegaly), and very high cardiac output. The heart has the ability to displace large systolic volumes at a low rate and relatively low pressure, with large ventricular fillings (high ventricular compliance), whereas it is incapable of facing increased afterloads. These functional aspects of mechanical flexibility and restrictions of the cardiac pump have been tentatively related to some constructional aspects of the icefish cardiomegaly, particularly, at the whole ventricular level, to the trabeculate type of myo-architecture, and, at the subcellular level, to the conflict in space economy between the exceptionally high mitochondrial densities and the consequent severe reduction in myofibrillar volume. On the basis of this morphodynamic approach, we suggest that the icefish may illustrate how a certain feature (i.e., an architectural cardiac design) common to the suborder and to most teleosts, and apparently with "irrelevant" properties, can become useful for a specialized purpose (i.e., volume pump design); and how, in contrast, the internal machinery construction, because of structural and ultrastructural constraints, may prevent these stenothermal sedentary teleosts from conquering niches requiring more active locomotory habits.

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Fishes show the highest diversity among vertebrates. Defined differences in ventricular myoarchitecture exist in fish. There are two main types of cardiac ventricle in fish: a spongy type and a mixed type. In the spongy ventricle, the muscle trabeculae form a sponge-like network, the spongiosa. In the mixed ventricle, one or more superficial layers of compact tissue (compacta) enclose an inner spongiosa. The spongiosa and compacta are respectively associated with a lacunary and a vascularized supply of blood. Interspecies differences exist in the proportion of compacta and the extent of vascularization. Here the mechanical limits and flexibility of the different types of ventricular organization are examined. The spongy type (found only in teleosts) seems to be particularly suitable for performing volume work. An example is the icefish heart. The main characteristics of this fish are the absence of hemoglobin in the blood and the very large volume of blood. The cardiac ventricle of the icefish is characterized by a cardiomegaly of the spongy type with myocardial pseudohypertrophy. It functions as a specialized volume pump which moves large stroke volumes at a low heart rate, but is not able to produce high pressures. The most active teleosts have mixed heart ventricles with different thicknesses of compacta. The presence of compacta gives these types of heart the potential to act as pressure pumps: they move small volumes at a relatively high rate and high pressure. The tuna heart is an extreme example of the mixed type. It has the highest relative mass and proportion of compacta (40-70%) among fishes.(ABSTRACT TRUNCATED AT 250 WORDS)

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