Dorsal Aortic Blood Pressure Research Articles

Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines

Central venous blood pressure (P(ven)) increases in response to hypoxia in rainbow trout (Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including P(ven), dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (P(W)O(2) = approximately 9 kPa), where P(W)O(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure P(ven) during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, P(ven) always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.

Venous responses during exercise in rainbow trout, Oncorhynchus mykiss: α-adrenergic control and the antihypotensive function of the renin–angiotensin system

The role of the α-adrenergic system in the control of cardiac preload (central venous blood pressure; P ven) and venous capacitance during exercise was investigated in rainbow trout ( Oncorhynchus mykiss). In addition, the antihypotensive effect of the renin–angiotesin system (RAS) was investigated during exercise after α-adrenoceptor blockade. Fish were subjected to a 20-min exercise challenge at 0.66 body lengths s −1 (BL s −1) while P ven, dorsal aortic blood pressure ( P da) and relative cardiac output ( Q) was recorded continuously. Heart rate ( f H), cardiac stroke volume (SV) and total systemic resistance ( R sys) were derived from these variables. The mean circulatory filling pressure (MCFP) was measured at rest and at the end of the exercise challenge, to investigate potential exercise-mediated changes in venous capacitance. The protocol was repeated after α-adrenoceptor blockade with prazosin (1 mg kg −1 M b) and again after additional blockade of angiotensin converting enzyme (ACE) with enalapril (1 mg kg −1 M b). In untreated fish, exercise was associated with a rapid (within approx. 1–2 min) and sustained increase in Q and P ven associated with a significant increase in MCFP (0.17 ± 0.02 kPa at rest to 0.27 ± 0.02 kPa at the end of exercise). Prazosin treatment did not block the exercise-mediated increase in MCFP (0.25 ± 0.04 kPa to 0.33 ± 0.04 kPa at the end of exercise), but delayed the other cardiovascular responses to swimming such that Q and P ven did not increase significantly until around 10–13 min of exercise, suggesting that an endogenous humoral control mechanism had been activated. Subsequent enalapril treatment revealed that these delayed responses were in fact due to activation of the RAS, because resting P da and R sys were decreased further and essentially all cardiovascular changes during exercise were abolished. This study shows that the α-adrenergic system normally plays an important role in the control of venous function during exercise in rainbow trout. It is also the first study to suggest that the RAS may be an important modulator of venous pressure and capacitance in fish.

Does bradycardia or hypertension enhance gas transfer in rainbow trout ( Oncorhynchus mykiss)?

Experiments were conducted to test the hypothesis that branchial gas transfer is enhanced in rainbow trout during hypoxia or hypercarbia by bradycardia and systemic vasoconstriction. Gas transfer was indirectly assessed by continuous monitoring of arterial blood gases, PaO 2 and PaCO 2. Cardiac frequency was maximally decreased by 34.9 ± 4.3 and 8.6 ± 3.2 bpm in hypoxic and hypercarbic fish, respectively. Pre-treating fish with atropine (1 μmol kg − 1) attenuated or abolished the bradycardia during hypoxia and hypercarbia, respectively. However, there were no significant differences in the arterial blood gases between the control and atropinized fish. Dorsal aortic blood pressure was increased maximally by 11.3 ± 2.8 and 17.7 ± 2.0 mm Hg in the hypoxic and hypercarbic fish. Pre-treatment of fish with prazosin (2.4 μmol kg − 1) prevented these increases in blood pressure. Blood gases were unaltered by prazosin treatment in the hypercarbic fish. However, in the hypoxic fish, gas transfer appeared to be impaired by prazosin on the basis of lowered PaO 2 (by approximately 35 mm Hg compared to control fish) and increased PaCO 2 (by approximately 0.3 mm Hg). Because the normal hyperventilatory response to hypoxia was prevented by prazosin, it is possible that the impairment of gas transfer was related to inadequate ventilation rather than to any differences in the pressor response. The present results provide no evidence that gas transfer in rainbow trout is enhanced by bradycardia nor do they reveal any obvious benefit associated with the increases in blood pressure that accompany hypoxia and hypercarbia.

Cardiac preload and venous return in swimming sea bass (Dicentrarchus labraxL.)

Cardiac preload (central venous pressure, P(CV), mean circulatory filling pressure (MCFP), dorsal aortic blood pressure (P(DA)) and relative cardiac output (Q) were measured in sea bass (Dicentrarchus labrax) at rest and while swimming at 1 and 2 BL s(-1). MCFP, an index of venous capacitance and the upstream venous pressure driving the return of venous blood to the heart, was measured as the plateau in Pcv during ventral aortic occlusion. Compared with resting values, swimming at 1 and 2 BL s(-1) increased Q (by 15+/-1.5 and 38+/-6.5%, respectively), P(CV) (from 0.11+/-0.01 kPa to 0.12+/-0.01 and 0.16+/-0.02 kPa, respectively), MCFP (from 0.27+/-0.02 kPa to 0.31+/-0.02 and 0.40+/-0.04 kPa, respectively) and the calculated pressure gradient for venous return (DeltaP(V), from 0.16+/-0.01 kPa to 0.18+/-0.02 and 0.24+/-0.02 kPa, respectively), but not P(DA). In spite of an increased preload, the increase in Q was exclusively mediated by an increased heart rate (f(H), from 80+/-4 beats min(-1) to 88+/-4 and 103+/-3 beats min(-1), respectively), and stroke volume (Vs) remained unchanged. Prazosin treatment (1 mg kg(-1) Mb) abolished pressure and flow changes during swimming at 1 BL s(-1), but not 2 BL s(-1), indicating that other control systems besides an alpha-adrenoceptor control are involved. This study is the first to address the control of venous capacitance in swimming fish. It questions the generality that increased Q during swimming is regulated primarily through Vs and shows that an increased cardiac filling pressure does not necessarily lead to an increased Vs in fish, but may instead compensate for a reduced cardiac filling time.

Arterial hemodynamics and mechanical properties after circulatory intervention in the chick embryo

Altered blood pressure and flow impact cardiac function during morphogenesis. How the arterial system supports cardiac morphogenesis after circulatory disruptions is not well characterized. We manipulated arterial flow via left atrial ligation (LAL) or arterial load via right vitelline artery ligation (VAL) in Hamburger-Hamilton (HH) stage 21 chick embryos. Embryos were reincubated for 1 h (HH21), 14 h (HH24) or 30 h (HH27). At each stage we measured simultaneous dorsal aortic blood pressure and flow, and calculated arterial compliance, impedance and hydraulic power. LAL acutely reduced stroke volume (Vs), cardiac output (Q) and hydraulic power. Arterial pressure was preserved by a compensatory increase in characteristic impedance and decrease in compliance. Impedance parameters and compliance normalized by HH24 and all parameters normalized by HH27. VAL acutely increased arterial resistance. Embryos maintained arterial pressure by decreasing Vs and Q. These parameters remained altered through HH27. In summary, despite the intervention, compensatory alterations in Vs and arterial resistance maintained arterial pressure and fraction of oscillatory power within a narrow range. These results suggest that the maintenance of arterial pressure and circulatory energy efficiency, but not arterial flow, is critical to embryogenesis.

Cardiovascular changes and catecholamine release following anaesthesia in Chinook salmon ( Oncorhynchus tshawytscha) and snapper ( Pagrus auratus)

We investigated recovery from anaesthesia in Chinook salmon ( Oncorhynchus tshawytscha) with and without surgery. Fish either underwent light sedation on exposure to 60 ppm AQUI-S™ or surgical depth anaesthesia with 120 ppm AQUI-S. Surgical depth anaesthesia experiments were replicated using New Zealand snapper ( Pagrus auratus). During light sedation, there was no evidence of catecholamine release in salmon despite changes in heart rate and blood pressure. Following surgical anaesthesia both salmon and snapper released high concentrations of catecholamines into the circulation. Plasma half-life of adrenaline in salmon was 9.3±0.7 min ( n=7) and in snapper was 4.4±3.3 min ( n=7). There was no further release of catecholamines, despite attempts by both species to escape their enclosures. Though clearance of the catecholamines was rapid, the cardiovascular effects of anaesthesia were prolonged. Dorsal aortic blood pressure ( P DA) and heart rate (HR) were high following anaesthesia, falling by 60 min in the 60 ppm exposed salmon but remaining high in the 120 ppm group. Following anaesthesia ventral aorta blood pressure ( P VA) in snapper was positively correlated with HR, as was P DA and haematocrit in salmon. Recovery of cardiovascular control processes is prolonged in recovery from anaesthesia if the fish become hypoxic.

Baroreflex mediated control of heart rate and vascular capacitance in trout

The baroreflex was triggered by altering branchial blood pressure with pre- and post-branchial occlusions for 30 s in rainbow trout Oncorhynchus mykiss. The cardiac limb of the baroreflex was monitored by continuous heart rate (f(H)) measurements. Responses of venous capacitance vessels were assessed, immediately following either occlusion, by measuring mean circulatory filling pressure (MCFP). Arterial responses were evaluated as the change in dorsal aortic blood pressure (P(da)) before and after pre-branchial occlusion. In untreated fish pre-branchial occlusion resulted in tachycardia (62.4+/-2.4 to 69.1+/-1.7 beats min(-1)), decreased venous capacitance reflected as an increase in MCFP (0.17+/-0.03 to 0.27+/-0.03 kPa) and increased P(da) (4.0+/-0.2 kPa compared to 3.2+/-0.1 kPa before occlusion). Post-branchial occlusion somewhat reversed the responses since f(H) decreased (62.4+/-2.4 to 53.0+/-3.1 beats min(-1)), whereas MCFP remained unaltered. Treatment with the alpha-adrenergic blocker prazosin (1 mg kg(-1)) increased resting MCFP to 0.33+/-0.03 kPa and appeared to abolish both venous and arterial responses to branchial occlusion. Subsequent atropine treatment (1.2 mg kg(-1)) abolished all chronotropic responses. We present for the first time ample evidence for baroreflex-mediated control of cardiovascular homeostasis, including both the chronotropic and the vascular limb of the baroreflex in an unanaesthetized fish. Furthermore, a novel technique to cannulate and occlude the dorsal aorta, using a Fogarty thru-lumen embolectomy catheter, is explained.

Adenosinergic and cholinergic control mechanisms during hypoxia in the epaulette shark (Hemiscyllium ocellatum), with emphasis on branchial circulation

Coral reef platforms may become hypoxic at night during low tide. One animal in that habitat, the epaulette shark (Hemiscyllium ocellatum), survives hours of severe hypoxia and at least one hour of anoxia. Here, we examine the branchial effects of severe hypoxia (<0.3 mg oxygen l(-1) for 20 min in anaesthetized epaulette shark), by measuring ventral and dorsal aortic blood pressure (P(VA) and P(DA)), heart rate (fh), and observing gill microcirculation using epi-illumination microscopy. Hypoxia induced a flow of blood in two parallel blood vessels, termed longitudinal vessels, in the outer borders of the free tip of the gill filament. Hypoxia also induced significant falls in fh, P(VA) and P(DA), and a biphasic change in ventilation frequency (increase followed by decrease). Adenosine injection (1 micromol kg(-1)) also initiated blood flow in the longitudinal vessels, in addition to significant drops in P(VA), P(DA) and fh, and a biphasic response in ventilation frequency (decrease followed by increase) indicating that adenosine influences ventilation. Aminophylline (10 mg kg(-1)), an A(1) and A(2) adenosine receptor antagonist, blocked the effects of adenosine injection, and also significantly reduced blood flow in the longitudinal vessels during hypoxia. In the second part of the study, we examined the cholinergic influence on the cardiovascular circulation during severe hypoxia (<0.3 mg l(-1)) using antagonists against muscarinic (atropine 2 mg kg(-1)) and nicotinic (tubocurarine 5 mg kg(-1)) receptors. Injection of acetylcholine (ACh; 1 micromol kg(-1)) into the ventral aorta caused a marked fall in fh, a large increase in P(VA), but small changes in P(DA) (suggesting increased R(gill)). Atropine was able to inhibit the branchial vascular responses to ACh but not the hypoxic bradycardia, suggesting the presence of muscarinic receptors on the heart and gill vasculature, and that the hypoxia induced bradycardia is of non-cholinergic origin. The results suggest that adenosine mediates increases in the arterio-venous circulation in the gill during hypoxia. This may serve to increase blood supply to heart and gill tissue.

Induction of bradycardia in trout by centrally administered corticotropin-releasing-hormone (CRH)

The cardiovascular effects of centrally and peripherally administered synthetic salmon corticotropin-releasing-hormone (CRH), a member of a family of stress-related neuropeptides, were investigated in the unanesthetized trout, Oncorhynchus mykiss. In group 1, trout bearing a cannula in the dorsal aorta, neither intracerebroventricular (i.c.v.) nor intra-arterial (i.a.) injections of CRH produced any significant change in mean heart rate (HR) and mean dorsal aortic blood pressure. These results stand in contrast to the previously reported hypertensive effects of i.a. and i.c.v. injections of trout urotensin-I. In group 2, non-cannulated trout bearing two subcutaneous electrocardiographic electrodes, conditions that are considered to be less stressful to the animals, the baseline level of HR was significantly reduced compared to the corresponding value for cannulated trout. In these trout, no significant change occurred in the HR after i.c.v. administration of 1 pmol of CRH. However, i.c.v. injection of 5 pmol of CRH caused a 12% ( P<0.01) decrease in HR during the 20–25 min post-injection period. In addition, the heart rate variability (HRV), a marker of vagal input to the heart, was increased by 120%. The CRH antagonist, CRH-(9–41)-peptide alone had no effect on HR or HRV but blocked CRH-induced bradycardia. In the non-cannulated trout, i.c.v. injection of trout urotensin-I (5 pmol) produced no significant change in HR and HRV. In contrast, i.c.v. administration of angiotensin II (5 pmol) elicited a highly significant 33% ( P<0.001) increase in the mean HR as well as inducing a marked (64%) reduction in HRV. Our results suggest that picomolar doses of CRH act centrally to evoke a bradycardia by a probable mechanism that involves enhancement of the parasympathetic drive to the heart.

Cardiorespiratory adjustments during hypercarbia in rainbow trout Oncorhynchus mykiss are initiated by external CO(2) receptors on the first gill arch.

Experiments were performed to test the hypothesis that the marked ventilatory and cardiovascular responses to hypercarbia in rainbow trout Oncorhynchus mykiss arise from specific stimulation of chemoreceptors localised to the first gill arch. This was accomplished by measuring cardiorespiratory variables during acute hypercarbia (20 min at P(CO(2))=8 mmHg; 1 mmHg=0.133 kPa) in fish subjected to selective bilateral extirpation of the first gill arch. The cardiovascular responses to hypercarbia in the intact fish included a significant bradycardia (from 75.0+/-1.6 to 69.0+/-2.0 beats min(-1); means +/- S.E.M.; N=16), an increase in dorsal aortic blood pressure (from 30.8+/-1.5 to 41.9+/-2.5 mmHg; N=16) and a rise in systemic vascular resistance (from 1.1+/-0.1 to 1.4+/-0.1 mmHg ml(-1) kg(-1) min(-1); N=16). Removal of the first gill arch or pre-treatment with the muscarinic receptor antagonist atropine prevented the hypercarbic bradycardia without affecting the pressure or resistance responses. Correlation analysis, however, revealed shallow but significant inverse relationships between water P(CO(2)) and cardiac frequency in both atropinised (r(2)=0.75) and gill-extirpated (r(2)=0.90) fish, suggesting a direct mild effect of CO(2) on cardiac function. The ventilatory response to hypercarbia in the intact fish consisted of an increase in ventilation amplitude (from 0.62+/-0.06 to 1.0+/-0.13 cm; N=16) with no change in breathing frequency. Removal of the first gill arch lowered resting breathing frequency and prevented the statistically significant elevation of breathing amplitude. Gill extirpation, however, did not totally abolish the positive correlation between water P(CO(2)) and ventilation amplitude (r(2)=0.84), suggesting the presence of additional (although less important) chemoreceptive sites that are not confined to the first gill arch. Plasma catecholamine levels were elevated during hypercarbia, and this response was unaffected by prior gill extirpation. To assess whether the CO(2) chemoreceptors of the first gill arch were sensing water and/or blood P(CO(2)), bolus injections of CO(2)-enriched water or saline were made into the buccal cavity or caudal vein, respectively. Injections of CO(2)-enriched water to preferentially stimulate external receptors evoked catecholamine release and cardiorespiratory responses that closely resembled the responses to hypercarbia. As in hypercarbia, extirpation of the first gill arch prevented the bradycardia and the increase in ventilation amplitude associated with externally injected CO(2)-enriched water. Except for a slight decrease in cardiac frequency (from 73.0+/-2.8 to 70.3+/-3.5 beats min(-1); N=11), injection of CO(2)-enriched saline to preferentially stimulate internal chemoreceptors did not affect any measured variable. Taken together, these data indicate that, in rainbow trout, the bradycardia and hyperventilation associated with hypercarbia are triggered largely by external CO(2) chemoreceptors confined to the first gill arch.

Cardiovascular effects of prostaglandin F 2 α and prostaglandin E 2 in Atlantic cod ( Gadus morhua )

Little is known of the cardiovascular functions of prostaglandins in non-mammalian vertebrates. There are indications that prostaglandins may have a function in haemostasis by constricting blood vessels in filament arteries in the fish gill after injury. Our aim was to examine the cardiovascular effect of the prostaglandins F(2 alpha) (PGF(2 alpha)) and E(2) (PGE(2)) with emphasis on branchial circulation. Intra-arterial injections of PGF(2 alpha) (10, 40, 160, 400 nmol kg(-1)) in cod caused a dose-dependent increase in ventral aortic blood pressure, a reduction in cardiac output, and an increase in gill vascular resistance. A contraction of filament arteries was observed with in vivo microscopy only seconds after injection. PGF(2 alpha) may therefore possibly be involved in a haemostatic vasoconstriction. In contrast, the most significant effects of PGE(2) appeared to be on the heart. PGE(2) also reduced dorsal aortic blood pressure.

Cardiac morphology and blood pressure in the adult zebrafish.

Zebrafish has become a popular model for the study of cardiovascular development. We performed morphologic analysis on 3 months postfertilization zebrafish hearts (n > or = 20) with scanning electron microscopy, hematoxylin and eosin staining and Masson's trichrome staining, and morphometric analysis on cell organelles with transmission electron photomicrographs. We measured atrial, ventricular, ventral, and dorsal aortic blood pressures (n > or = 5) with a servonull system. The atrioventricular orifice was positioned on the dorsomedial side of the anterior ventricle, surmounted by the single-chambered atrium. The atrioventricular valve was free of tension apparati but supported by papillary bands to prevent retrograde flow. The ventricle was spanned with fine trabeculae perpendicular to the compact layer and perforated with a subepicardial network of coronary arteries, which originated from the efferent branchial arteries by means of the main coronary vessel. Ventricular myocytes were larger than those in the atrium (P < 0.05) with abundant mitochondria close to the sarcolemmal. Sarcoplasmic reticulum was sparse in zebrafish ventricle. Bulbus arteriosus was located anterior to the ventricle, and functioned as an elastic reservoir to absorb the rapid rise of pressure during ventricular contraction. The dense matrix of collagen interspersed across the entire bulbus arteriosus exemplified the characteristics of vasculature smooth muscle. There were pressure gradients from atrium to ventricle, and from ventral to dorsal aorta, indicating that the valves and the branchial arteries, respectively, were points of resistance to blood flow. These data serve as a framework for structure-function investigations of the zebrafish cardiovascular system.

Cardiovascular effects of hypercarbia in rainbow trout (Oncorhynchus mykiss): a role for externally oriented chemoreceptors.

In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO(2) on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO(2) (0.6, 1.0 or 2.0% CO(2)) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO(2) was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected. To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO(2) (Pa(CO2)) without an accompanying increase in external P(CO2) (Pw(CO2)). In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg(-1)) to inhibit CO(2) excretion, and thus raise Pa(CO2), 5-7 h prior to being exposed to an acute increase in Pw(CO2) (maximum Pw(CO2)=6.3+/-0.4 mmHg; 1 mmHg=0.133 kPa). Despite a marked increase in Pa(CO2) (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P(DA)) or systemic resistance (R(S)). The ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 35 %). A second series of experiments used a 5-7 h period of exposure to hyperoxia (Pw(O2)=643+/-16 mmHg) to establish a new, elevated baseline Pa(CO2) (7.8+/-1.1 mmHg) without any change in Pw(CO2). Despite a steadily increasing Pa(CO2) during the 5-7 h of hyperoxia, there was no associated increase in P(DA) or R(S). Ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects. These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO(2) on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.

Cardiovascular actions of centrally and peripherally administered trout urotensin-I in the trout.

The cardiovascular effects of centrally and peripherally administered synthetic trout urotensin (U)-I, a member of the corticotropin-releasing hormone family of neuroendocrine peptides, were investigated in unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular injections of U-I (5.0 and 12.5 pmol) produced a sustained increase in mean dorsal aortic blood pressure (P(DA)) without significant change in heart rate (HR). This elevation in P(DA) was associated with an increase in cardiac output, but systemic vascular resistance did not change. Intra-arterial injection of U-I (12.5-500 pmol) evoked a dose-dependent increase in P(DA), but in contrast to the hemodynamic effects of centrally administered U-I, the hypertensive effect was associated with an increase in systemic vascular resistance and an initial fall in cardiac output. HR did not change or underwent a delayed increase. Pretreatment of trout with prazosin, an alpha-adrenoreceptor antagonist, completely abolished the rise in arterial blood pressure after intra-arterial administration of U-I, which was replaced by a sustained hypotension and tachycardia. Trout U-I produced a dose-dependent (pD(2) = 7.74 +/- 0.08) relaxation of preconstricted rings of isolated trout arterial vascular smooth muscle, suggesting that the primary action of the peptide in the periphery is vasorelaxation that is rapidly reversed by release of catecholamines. Our results suggest that U-I may regulate blood pressure in trout by acting centrally as a neurotransmitter and/or neuromodulator and peripherally as a neurohormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.

Gastrointestinal blood flow in the red Irish lord, Hemilepidotus hemilepidotus: long-term effects of feeding and adrenergic control.

Cardiac output, blood flow to the coeliac and mesenteric arteries, dorsal aortic blood pressure and heart rate were recorded simultaneously at rest and postprandial for 6 days in a teleost, the red Irish lord (Hemilepidotus hemilepidotus). We anticipated that gastrointestinal blood flow would increase postprandially, supported by an increase in cardiac output. However, we had no predictions for either the exact time-course of this response, or for the regional distribution of blood flow between to the two major arteries comprising the splanchnic circulation. In resting, unfed animals, blood flow to the coeliac artery and mesenteric artery was 4.1 +/- 0.6 ml min(-1) kg(-1) and 4.9 +/-1.3 ml min(-1) kg(-1), respectively (mean +/- SEM, n = 7), which together represented 34% of cardiac output. Feeding increased blood flow to the coeliac and mesenteric arteries in a time-dependent manner. The increase in coeliac artery blood flow preceded that in the mesenteric artery, a finding that is consistent with the coeliac artery supplying blood to the liver and stomach, while the mesenteric artery supplies blood to the stomach and intestine. Coeliac blood flow had increased by 84 +/- 18% after 1 day and had a peak increase of 112 +/- 40% at day 4 postprandial. Mesenteric blood flow was not significantly elevated at day 1, but had increased by 94 +/- 19% at day 4 postprandial. Cardiac output also increased progressively, increasing by a maximum of 90 +/- 30% at day 4. Because the increase in cardiac output was adequate to meet the postprandial increase in gut blood flow, the postprandial decreases in vascular resistance for the coeliac and mesenteric circulations mirrored the increases in blood flow. Intra-arterial injections of adrenaline and noradrenaline into resting fish more than doubled coeliac and mesenteric vascular resistances, and blood flow decreased proportionately. This adrenergic vasoconstriction was totally abolished by pretreatment with the alpha-adrenoceptor antagonist phentolamine, which in itself approximately halved coeliac and mesenteric vascular resistances. These observations indicate a significant alpha-adrenergic tone in the gastrointestinal circulation of the red Irish lord, the loss of which could not entirely account for the post-prandial increase in gastrointestinal blood flow. Other control mechanisms are suggested.

Cardiovascular responses to hypoxia in the Adriatic sturgeon (Acipenser naccarii)

Summary The in vivo cardiovascular responses to hypoxia, and the intrinsic functional characteristics of the heart in vitro, were determined, and compared, in the Adriatic sturgeon (Acipenser naccarii). During exposure to hypoxia in vivo, blood oxygen content (Cao2) declined as water 02 partial pressure (Pwo2) was reduced, despite an increase in haematocrit. The main cardiovascular response was a reduction in dorsal aortic blood pressure, with a slight bradycardia, while cardiac output remained constant. Reduced oxygen content of the perfusate had significant inhibitory effects on the intrinsic performance of the heart in vitro, causing a reduction in the heart rate; a reduction in the sensitivity of responses to increased preload (Frank-Starling response), and a more rapid decline in power output and stroke volume when afterload was increased. Overall, the in vitro results suggest that hypoxia depresses the contractility of the heart (i.e. its inotropic responses). The reduction in dorsal aortic pressure in vivo may, therefore, counteract the depressive effects of hypoxia on heart contractility, and thereby avoid a hypoxic depression of cardiac output.

Cardiovascular responses to adenosine in the antarctic fish pagothenia borchgrevinki

We have investigated the effects of adenosine on the cardiovascular system of the Antarctic fish Pagothenia borchgrevinki. Continuous measurements of ventral and dorsal aortic blood pressures, heart rate (fh) and ventral aortic blood flow (cardiac output, q_dot ) were made using standard cannulation techniques and a single-crystal Doppler flowmeter. On line measurements of arterial P(O2) were made using an oxygen electrode connected to an extracorporeal loop. Adenosine (10 nmol kg(-)(1)) and the specific A(1)-receptor agonist N(6)-cyclopentyladenosine (CPA) elicited biphasic changes in the branchial and systemic resistances. While there was an initial decrease in the branchial resistance followed by an increase, the opposite was true for the systemic response. The resistance changes were significantly attenuated by aminophylline (a P(1)-receptor antagonist) and 8-cyclopentyltheophylline (CPT; an A(1)-receptor antagonist). In addition, adenosine induced an aminophylline-sensitive decrease in the arterial P(O2). The reduction was attenuated when pre-injection arterial P(O2) was low. Adenosine and CPA also caused a marked reduction in fh, with CPA being more potent. The bradycardia was blocked by aminophylline and CPT, demonstrating an involvement of A(1) receptors in this response.

The control of blood pressure during external hypercapnia in the rainbow trout (Oncorhynchus mykiss).

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13-39 %) and dorsal aortic (17-54 %) blood pressures that reflected marked increases in systemic vascular resistance (16-78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4-7 beats min(-)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(-)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (&agr;)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (&agr;)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (&agr;)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65-151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.

Altered hemodynamics in chick embryos after extraembryonic venous obstruction.

To obtain insight into hemodynamics during abnormal cardiac development, a chick model was developed recently in which a spectrum of conotruncal anomalies, in combination with abnormal semilunar valves and/or pharyngeal arch artery malformations, was induced through extraembryonic venous obstruction (venous clip) at stage 17 (70-h incubation). In chick embryos of stage 24 and stage 34 control (n = 8; n = 21) and with venous clip (n = 11; n = 18), we simultaneously measured dorsal flow velocities with a 20-MHz pulsed Doppler velocity meter and dorsal aortic (stage 24) and vitelline artery (stage 34) blood pressures with a servo-null system. After the hemodynamic recordings were collected, all 58 embryos were subjected to morphological examination. The hemodynamic data were correlated with the morphology. Statistical comparison was performed between control and experimental values. At stage 24, venous clip embryos showed impaired looping. Physiologically, only a decrease in peak acceleration was found in these embryos (p < 0.05). At stage 34, a spectrum of conotruncal malformations was seen, that consisted of a ventricular septal defect in combination with abnormal semilunar valves and/or pharyngeal arch malformations. A dextroposed aorta in combination with a ventricular septal defect was diagnosed as double-outlet right ventricle. Hemodynamically, peak systolic and mean velocities, peak systolic and mean blood flows and stroke volume were increased while the heart rate was reduced after placement of the venous clip (p < 0.05). In both stages, pressure readings showed no statistically significant differences between control and experimental embryos. Our findings suggest that the hemodynamic changes seen in venous clip embryos reflect the presence of a compensatory mechanism.

Respiratory–cardiovascular physiology and xenobiotic gill flux in the lake trout ( Salvelinus namaycush)

An in vivo respirometer–metabolism chamber was used to obtain respiratory–cardiovascular physiology under normoxic and hypoxic conditions, and xenobiotic gill absorption (flux) data on adult lake trout ( Salvelinus namaycush) over a 48-h exposure period at 11±1°C. An oral membrane was used to separate inspired and expired water flows, providing the first direct measurements of chemical flux across the gills of lake trout. Overall mean values (±S.D.) for normoxic respiratory function were: ventilation rate (V R)=53±9 # min −1, ventilation volume (Q V)=7±2 l kg −1 h −1, respiratory stroke volume (SV R)=2±1 ml, oxygen consumption (VO 2)=39±8 mg kg −1 h −1, oxygen utilization (U)=53±14%, and effective respiratory volume (Q W)=4±1 l kg −1 h −1. The resting Q V, Q W, and VO 2 seen in these lake trout were lower than seen previously in other salmonids. No significant differences ( P≥0.05) in respiratory function were detected between males and females. Trout subjected to hypoxia (30% of saturation) showed no changes in U or VO 2, while V R decreased (42±6 # min −1), Q V increased (22±6 l kg −1 h −1) and SV R increased (8±3 ml). Cardiovascular and blood gas measurements determined under normoxic conditions were heart rate (H R)=73±8 # min −1, cardiac output (Q C)=15±2 ml kg −1 min −1, cardiac stroke volume (SV H)=0.2 ml kg −1 min −1, dorsal aortic blood pressure (D BP)=34±1 mm Hg, ventral aortic blood pressure (V BP)=45±1 mm Hg, and venous oxygen partial pressure (P VO 2)=26±2 mm Hg. Initial 1-h mean±S.D. chemical gill extraction efficiencies (EE) for tetrachloroethane (TCE), pentachloroethane (PCE), and hexachloroethane (HCE) were 42±8, 58±16, and 68±17%, respectively. Forty-eight hour EE of 9±1% for TCE (log K OW=2.39) and 21±4% for PCE (log K OW=3.06) indicated they were approaching steady-state, in contrast to 54±13% for HCE (log K OW=4.04) which was not near steady-state. The EE for all three chloroethanes were significantly ( P<0.05) different from each other from 24 h to 48 h. Forty-eight hour lake trout mean cumulative chemical clearance (Cl X) values for waterborne TCE, PCE, and HCE were 64±11, 120±14, and 226±29 l kg −1, respectively. Lake trout Cl X and Q W for TCE, PCE, and HCE demonstrated an approximate 1:1 relationship indicative of water-flow limited gill absorption. Chemical gill absorption observed for the lake trout and chloroethanes was similar to the rainbow trout ( Oncorhynchus mykiss) from previous investigations and provided further support for the water-flow limited model of chemical flux across fish gills for mid-hydrophobic chemicals (log K OW=3.0–6.0).