Branchial and systemic roles of adenosine receptors in rainbow trout: an in vivo microscopy study

1996 ◽  
Vol 271 (3) ◽  
pp. R661-R669 ◽  
Author(s):  
L. Sundin ◽  
G. E. Nilsson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Water Immersion ◽  
Cardiovascular Effects ◽  
Secondary System ◽  
A1 Receptor

The purinergic branchial vasomotor control in rainbow trout (Oncorhynchus mykiss) was studied using an epi-illumination microscope equipped with a water-immersion objective. Cardiac output (Q), heart rate, and dorsal (PDA) and ventral (PVA) aortic pressures were recorded simultaneously. Prebranchial injection of adenosine or the A1-receptor agonist N6-cyclopentyl-adenosine (CPA) constricted the distal portion of the filament vasculature, which coincided with an increase of PVA. The A2-receptor agonist PD-125944 was without effect. After adenosine and CPA injection, an overflow of blood to the secondary system was repeatedly observed unless blood flow came to a complete stop. The lack of a concomitant reduction of Q suggested a redistribution of blood to the secondary system and to more proximal parts of the filament. The branchial effects of adenosine and CPA were completely blocked by the unspecific adenosine receptor antagonist amino-phylline and the specific A1-receptor antagonist N6-cyclopen-tyltheophylline. The results suggest that A1-receptors alone mediate the branchial vasoconstriction observed. Thus the responses of the branchial vasculature to adenosine include a vasoconstriction of the filament vasculature mediated via specific A1 receptors and a redistribution of blood flow to the secondary system and to proximal parts of the filament. Additional cardiovascular effects of adenosine included decreased systemic vascular resistance and heart rate.

scholarly journals Influence of the coronary circulation on thermal tolerance and cardiac performance during warming in rainbow trout

2017 ◽  
Vol 312 (4) ◽  
pp. R549-R558 ◽  
Author(s):  
Andreas Ekström ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Jeroen Brijs ◽  
Erik Sandblom
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Cardiac Function ◽  
Thermal Tolerance ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Cardiac Performance ◽  
Juvenile Trout

Thermal tolerance in fish may be related to an oxygen limitation of cardiac function. While the hearts of some fish species receive oxygenated blood via a coronary circulation, the influence of this oxygen supply on thermal tolerance and cardiac performance during warming remain unexplored. Here, we analyzed the effect in vivo of acute warming on coronary blood flow in adult sexually mature rainbow trout ( Onchorhynchus mykiss) and the consequences of chronic coronary ligation on cardiac function and thermal tolerance in juvenile trout. Coronary blood flow at 10°C was higher in females than males (0.56 ± 0.08 vs. 0.30 ± 0.08 ml·min−1·g ventricle−1), and averaged 0.47 ± 0.07 ml·min−1·g ventricle−1 across sexes. Warming increased coronary flow in both sexes until 14°C, at which it peaked and plateaued at 0.78 ± 0.1 and 0.61 ± 0.1 ml·min−1·g ventricle−1 in females and males, respectively. Thus, the scope for increasing coronary flow was 101% in males, but only 39% in females. Coronary-ligated juvenile trout exhibited elevated heart rate across temperatures, reduced Arrhenius breakpoint temperature for heart rate (23.0 vs. 24.6°C), and reduced upper critical thermal maximum (25.3 vs. 26.3°C). To further analyze the effects of coronary flow restriction on cardiac rhythmicity, electrocardiogram characteristics were determined before and after coronary occlusion in anesthetized trout. Occlusion resulted in reduced R-wave amplitude and an elevated S-T segment, indicating myocardial ischemia, while heart rate was unaffected. This suggests that the tachycardia in ligated trout across temperatures in vivo was mainly to compensate for reduced cardiac contractility to maintain cardiac output. Moreover, our findings show that coronary flow increases with warming in a sex-specific manner. This may improve whole animal thermal tolerance, presumably by sustaining cardiac oxygenation and contractility at high temperatures.

scholarly journals In vivo imaging with a water immersion objective affects brain temperature, blood flow and oxygenation

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Morgane Roche ◽  
Emmanuelle Chaigneau ◽  
Ravi L Rungta ◽  
Davide Boido ◽  
Bruno Weber ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Temperature ◽  
Water Immersion ◽  
Phosphorescence Lifetime ◽  
Cranial Window ◽  
Hemoglobin Saturation ◽  
Tissue Po2 ◽  
Physiological Values ◽  
Water Immersion Objective

Previously, we reported the first oxygen partial pressure (Po2) measurements in the brain of awake mice, by performing two-photon phosphorescence lifetime microscopy at micrometer resolution (Lyons et al., 2016). However, this study disregarded that imaging through a cranial window lowers brain temperature, an effect capable of affecting cerebral blood flow, the properties of the oxygen sensors and thus Po2 measurements. Here, we show that in awake mice chronically implanted with a glass window over a craniotomy or a thinned-skull surface, the postsurgical decrease of brain temperature recovers within a few days. However, upon imaging with a water immersion objective at room temperature, brain temperature decreases by ~2–3°C, causing drops in resting capillary blood flow, capillary Po2, hemoglobin saturation, and tissue Po2. These adverse effects are corrected by heating the immersion objective or avoided by imaging through a dry air objective, thereby revealing the physiological values of brain oxygenation.

Hemodynamic effects of leukotriene C4 in ovine fetus

1990 ◽  
Vol 259 (6) ◽  
pp. E851-E855
Author(s):  
B. A. Meyer ◽  
S. W. Walsh ◽  
V. M. Parisi
Keyword(s):  
Blood Flow ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
In Vivo Studies ◽  
Leukotriene C4 ◽  
Blood Flows ◽  
Before And After ◽  
Placental Blood ◽  
Near Term

Leukotrienes are synthesized during pregnancy and produce cardiovascular effects in adults. We hypothesized that leukotriene C4 would cause vasoconstriction in the fetus and placenta. Eight near-term, unanesthetized ovine fetuses were studied before and after infusion of 10 micrograms leukotriene C4 (LTC4) into the fetal vena cava. Cardiovascular monitoring of maternal and fetal arterial pressures and heart rates was performed. Fetal blood flows were measured by the radioactive-microsphere technique. Sustained elevations in systolic and diastolic blood pressure and decreased fetal heart rate began by 1 min and returned to baseline by 30 min. Arterial pH fell from 7.33 +/- 0.01 to 7.29 +/- 0.01 at 15 min (P less than 0.05) and to 7.29 +/- 0.01 at 30 min (P less than 0.05), with a significant increase in base deficit from 0.7 +/- 0.7 to 3.5 +/- 0.7 at 15 min (P less than 0.05) and to 2.9 +/- 1.0 at 30 min (P less than 0.05). Fetal PO2 and PCO2 were unchanged. Significant decreases in blood flow and resistance were seen in the umbilical placental circulation as well as in fetal skeletal muscle and intestine. Blood flow and resistance were unchanged in the renal and adrenal vascular beds. Fetal administration of LTC4 caused no changes in maternal cardiovascular parameters. These findings represent the first in vivo studies of the effects of a lipoxygenase metabolite on fetal-placental blood flow.

scholarly journals Importance of the coronary circulation for cardiac and metabolic performance in rainbow trout ( Oncorhynchus mykiss )

2018 ◽  
Vol 14 (7) ◽  
pp. 20180063 ◽  
Author(s):  
Andreas Ekström ◽  
Michael Axelsson ◽  
Albin Gräns ◽  
Jeroen Brijs ◽  
Erik Sandblom
Keyword(s):  
Heart Rate ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Metabolic Rate ◽  
Oxygen Supply ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Coronary Ligation ◽  
Metabolic Performance

Cardiac oxygenation is achieved via both coronary arterial and luminal venous oxygen supply routes in many fish species. However, the relative importance of these supplies for cardiac and aerobic metabolic performance is not fully understood. Here, we investigated how coronary artery ligation in rainbow trout ( Oncorhynchus mykiss ), implanted with heart rate loggers, affected cardiorespiratory performance in vivo . While coronary ligation significantly elevated resting heart rate, the standard metabolic rate was unchanged compared to sham-treated controls. However, coronary ligation reduced the maximum metabolic rate while heart rate remained unchanged following enforced exercise. Thus, coronary ligation reduced metabolic and heart rate scopes by 29% and 74%, respectively. Our findings highlight the importance of coronary oxygen supply for overall cardiorespiratory performance in salmonid fish, and suggest that pathological conditions that impair coronary flow (e.g. coronary arteriosclerosis) constrain the ability of fish to cope with metabolically demanding challenges such as spawning migrations and environmental warming.

Contribution of adenosine to isoproterenol-stimulated prostacyclin production in rabbit heart

1992 ◽  
Vol 263 (1) ◽  
pp. H218-H225
Author(s):  
C. Cano ◽  
Z. Qureshi ◽  
S. Carter ◽  
K. U. Malik
Keyword(s):  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Rabbit Heart ◽  
Mechanical Function ◽  
Cgs 21680 ◽  
A1 Receptor ◽  
Prostacyclin Production ◽  
Prostacyclin Synthesis ◽  
A2 Receptors ◽  
Krebs Henseleit Buffer

This study investigated adenosine's contribution to isoproterenol-stimulated prostacyclin production, measured as 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) output, and mechanical function in the isolated rabbit heart perfused with Krebs-Henseleit buffer. The isoproterenol-induced increase in 6-keto-PGF1 alpha was diminished by adenosine (10 microM), the A1 receptor antagonist 1,3-dipropyl, 8-cyclopentylxanthine (DPCPX 0.06 microM), and the A2 receptor agonist CGS-21680 (0.6 microM); CGS-21680 did not decrease heart rate (HR) or myocardial contractility (dP/dt(max)). The isoproterenol-induced increase in 6-keto-PGF1 alpha was potentiated by the A1 receptor agonist 1-deaza,2-chloro,N6-cyclopentyladenosine (DCCA, 0.6 microM) and the A2 receptor antagonist 3,7-dimethyl,1-propargylxanthine (DMPX, 6 microM). The isoproterenol-induced increase in dP/dt(max) and HR was diminished by adenosine, DCCA, and DMPX. DPCPX enhanced dP/dt(max) and HR and prevented the decrease by adenosine and DCCA of the isoproterenol-induced increase in HR and dP/dt(max); the increase by DCCA but not the decrease by adenosine in 6-keto-PGF1 alpha output was abolished. DMPX abolished the effect of adenosine and CGS-21680 to reduce isoproterenol-stimulated 6-keto-PGF1 alpha. These data suggest that adenosine generated in response to isoproterenol attenuates its effect on HR and dP/dt(max) through A1 receptors and on prostacyclin synthesis via A2 receptors.

Cardiovascular effects of dobutamine during exercise in dogs

1989 ◽  
Vol 257 (3) ◽  
pp. H954-H960
Author(s):  
G. C. Haidet ◽  
T. I. Musch ◽  
D. B. Friedman ◽  
G. A. Ordway
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Maximal Exercise ◽  
Cardiovascular Effects ◽  
Receptor Reserve ◽  
Concomitant Reduction ◽  
Stimulation Of

To test the hypothesis that stimulation of adrenergic receptors in the heart is maximal during maximal exercise, and to determine whether generalized stimulation of adrenergic receptors during strenuous exercise produces significant alterations in the normal regional distribution of blood flow that occurs during exercise, we evaluated the cardiovascular effects of the infusion of dobutamine (40 micrograms.kg-1.min-1) in mongrel dogs during treadmill running. During maximal exercise, the dobutamine infusion resulted in a significant (P less than 0.05) increase in heart rate. Exercise capacity, total body O2 consumption (VO2), and maximal arteriovenous O2 difference, however, each were reduced during the infusion of this drug. A concomitant reduction in maximal blood flow to locomotive skeletal muscle occurred. The infusion of dobutamine also resulted in an increase in heart rate at a strenuous level of submaximal exercise. However, unlike during maximal exercise, VO2 was unchanged. Blood flow to locomotive skeletal muscle increased, and there was a concomitant reduction in arteriovenous O2 difference. Blood flow reductions that normally occur in splanchnic circulations during strenuous and during maximal exercise were generally somewhat attenuated during the infusion of this drug. Thus, dobutamine, a sympathomimetic agent, produces significant cardiovascular effects when infused in high doses during exercise. Our results demonstrate that beta-adrenergic receptor reserve exists in the heart during maximal exercise in dogs. In addition, the peripheral responses that occur during the infusion of the drug provide additional evidence that different degrees of adrenergic receptor reserve normally appear to be present within different regional circulations during strenuous and during maximal exercise.

Inhibition of tubuloglomerular feedback during adenosine1 receptor blockade

1990 ◽  
Vol 258 (3) ◽  
pp. F553-F561 ◽  
Author(s):  
J. Schnermann ◽  
H. Weihprecht ◽  
J. P. Briggs
Keyword(s):  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Tubuloglomerular Feedback ◽  
Receptor Blockade ◽  
Peritubular Capillary ◽  
Maximum Change ◽  
A1 Receptor ◽  
Afferent Arterioles ◽  
Flow Pressure ◽  
Stop Flow

Experiments were performed in anesthetized rats to study the effect of the selective adenosine1 (A1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX) on tubuloglomerular feedback (TGF) responses assessed as the maximum change of stop-flow pressure (PSF). Compared with control, PSF responses were reduced during luminal application of CPX at 10(-4) and 10(-5)M (-4.9 +/- 0.44 vs. + 0.9 +/- 0.42 mmHg and -6.8 +/- 0.69 vs. -1.4 +/- 0.7 mmHg, respectively), during peritubular administration of CPX at 10(-4)M (-6.2 +/- 0.44 vs. -2.8 +/- 0.42 mmHg), and during infusion of CPX at 10(-4) M into the lumen of a neighboring nephron (-5.6 +/- 0.6 vs. -1.98 +/- 0.51 mmHg). Selectivity of CPX was tested by studying its effect on the PSF reduction produced by the A1-receptor agonist N6-cyclohexyladenosine (CHA). CHA at 10(-5)M reduced PSF when infused into the peritubular blood (-11.8 +/- 3.7 mmHg), and this effect was blunted by luminal application of CPX (-1.5 +/- 0.6 mmHg). CHA also reduced PSF when infused into a neighboring nephron, and this effect was blunted by infusing CPX at 10(-4)M into the same neighboring nephron, a different neighboring nephron, or a peritubular capillary. These results are consistent with the concept that activation of A1-receptors on vascular cells of the afferent arterioles participates in the mediation of TGF responses.

Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats

1993 ◽  
Vol 264 (2) ◽  
pp. R345-R349
Author(s):  
K. Shimizu ◽  
J. Schwartz ◽  
B. P. McGrath
Keyword(s):  
Heart Rate ◽  
Receptor Agonist ◽  
Pressor Response ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Pressor Responses ◽  
Autonomic Blockade ◽  
V2 Receptor ◽  
Intact Rats

Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V1 or V2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or [Phe2,Orn8]oxytocin, a potent, selective V1-receptor agonist, in the absence and presence of infusion of [Val4,D-Arg8]VP, a selective V2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and [Phe2,Orn8]oxytocin were similarly increased. Infusion of the V2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V1 agonist, in either intact or autonomically blocked rats. In the presence of the V2 agonist, the decrease in heart rate induced by the V1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V1 and not V2 receptors. However, V2 receptors may be involved in modulating the heart rate response to AVP.

Cardiovascular effects of acute hemorrhage in fetal lambs

1981 ◽  
Vol 240 (1) ◽  
pp. H45-H48 ◽  
Author(s):  
P. L. Toubas ◽  
N. H. Silverman ◽  
M. A. Heymann ◽  
A. M. Rudolph
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Blood Volume ◽  
Age Groups ◽  
Blood Gases ◽  
Cardiovascular Effects ◽  
Carbon Dioxide Tension ◽  
Acute Hemorrhage ◽  
Arterial Blood ◽  
Placental Blood

The effects of acute hemorrhage were studied in two groups each with six fetal lambs (100-116 amd 128-147 days gestation) 3-4 days after we implanted catheters. Fetal blood pressures, heart rate, arterial blood gases and pH, and combined ventricular output and its distribution (radionuclide-labeled microsphere technique) were measured before and 5 min after removal of 15% of fetal-placental blood volume measured by 125I-albumin dilution. Because there were no differences in responses in the two age groups, the data were pooled. Fetal arterial mean pressure fell significantly (50.7 +/- 2.5 to 45.5 +/- 2.6 mmHg) as did heart rate (186 +/- 6 to 151 +/- 13 beats/min) and arterial blood pH (7.39 +/- 0.02 to 7.30 +/- 0.02); arterial blood carbon dioxide tension rose (39.7 +/- 29 to 44.1 +/- 4.4). Combined ventricular output fell from 610 +/- 58 to 448 +/- 45 ml . kg-1 . min-1 (P < 0.05). Blood flow to the umbilical-placental circulation, as well as to the fetal body, fell significantly. Blood flow to the kidneys, gastrointestinal tracts, and lungs also fell, but flow to other organs was maintained. Blood volume reduction in the fetus markedly influences blood gas exchange, because it results in a reduction of umbilical-placental blood flow associated with the fall in arterial pressure.

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