Gas Exchange in Rainbow Trout (Salmo gairdneri) with Varying Blood Oxygen Capacity

1970 ◽  
Vol 27 (6) ◽  
pp. 1069-1085 ◽  
Author(s):  
James N. Cameron ◽  
John C. Davis
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Peripheral Resistance ◽  
Hemoglobin Concentration ◽  
Salmo Gairdneri ◽  
Compensatory Mechanism ◽  
Blood Oxygen ◽  
Phenylhydrazine Hydrochloride ◽  
Oxygen Capacity ◽  
Oxygen Tensions

The effects of large changes in hemoglobin concentration were studied in rainbow trout in fresh water between 8 and 14 C. Anemia was produced by injecting phenylhydrazine hydrochloride or by replacing blood with either saline or plasma.No significant changes were observed in the rate of oxygen consumption, arterial or venous oxygen tensions, ventilation volume, inspired and expired water oxygen tensions, or dorsal aortic blood pressure. The primary compensatory mechanism invoked was an increase in the cardiac output, which was accomplished almost entirely by increases in stroke volume. Although the viscosity of the blood was reduced, there must also be large changes in the peripheral resistance to blood flow, since greatly increased cardiac output was achieved without significant increase in blood pressure.The change in blood oxygen capacity and increase in cardiac output caused significant lowering of the ventilation–perfusion ratio, but the capacity–rate ratio of water to blood varied only a little. A small rise occurred at low hematocrit values, due to small changes in a number of parameters.The experiments illustrate what happens when blood oxygen capacity is reduced, but do not elucidate the mechanism for control of stroke output of the heart. They also indicate that a species' hemoglobin level is maintained at a level that allows cardiac output to vary over an optimal range of its efficiency curve.

Hematological Aspects of the Thermoacclimatory Process in the Rainbow Trout, Salmo gairdneri

1967 ◽  
Vol 24 (11) ◽  
pp. 2267-2281 ◽  
Author(s):  
Mary Anne DeWilde ◽  
A. H. Houston
Keyword(s):  
Rainbow Trout ◽  
General Problem ◽  
Carrying Capacity ◽  
Packed Cell Volume ◽  
Salmo Gairdneri ◽  
Blood Oxygen ◽  
Hemoglobin Content ◽  
Oxygen Capacity ◽  
Higher Temperature ◽  
Oxygen Carrying Capacity

The blood oxygen capacity of the rainbow trout has been investigated as a function of thermal acclimation in terms of erythrocyte abundance, packed cell volume, hemoglobin concentrations, and mean erythrocytic volume and hemoglobin content. Fish at the lower acclimation temperatures employed (3, 7 C) were characterized by relatively low erythrocyte counts, hematocrits, and hemoglobin levels. Mean erythrocyte volumes tended to be relatively high, whereas mean erythrocytic hemoglobin content was somewhat below that typical of the higher temperature groups. In general, animals held at intermediate temperatures (11, 14, 17 C) showed significant increases in oxygen-carrying capacity by comparison with cold-acclimated fish. Finally trout at 21 C typically had larger numbers of somewhat smaller red cells, more hemoglobin, and higher levels of hemoglobin per erythrocyte than either the low- or intermediate-temperature fish. Significant differences were observed between summer and fall–winter series of trout, particularly with respect to hemoglobin levels. The results are discussed in relation to the general problem of respiratory thermoadaptation.

Circulatory and Ventilatory Responses of Rainbow Trout (Salmo gairdneri) to Artificial Manipulation of Gill Surface Area

1971 ◽  
Vol 28 (10) ◽  
pp. 1609-1614 ◽  
Author(s):  
John C. Davis
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Surface Area ◽  
Salmo Gairdneri ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Gill Area ◽  
Gill Surface Area ◽  
The Brain

Reductions in surface area of the gill were artificially produced by ligating various gill arches and occluding their blood supply. Rainbow trout (Salmo gairdneri) responded to a 40–57% reduction in gill area, by increasing cardiac output and ventilation volume, and probably by redistributing blood within the remaining functional gill area. Fish with blood flow to gill arches one and three only, could maintain arterial PO2 at 90–100 mm Hg, whereas, in those with blood flow to arches three and four only, arterial PO2 fell to around 40 mm Hg. The presence of a chemoreceptor site for the regulation of arterial PO2 associated with the efferent blood vessels of arch number one is discussed. Such a receptor may be located in the pseudobranch or in the portion of the brain supplied with arterial blood from the first gill arch.

Cardiovascular responses to diving and their relation to lung and blood oxygen stores in vertebrates

1988 ◽  
Vol 66 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Warren Burggren
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Lung Perfusion ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Resistance Reduction ◽  
Lower Vertebrates ◽  
Oxygen Stores ◽  
Cardiovascular Performance

Air-breathing vertebrates generally respond to apnea during diving by adjusting cardiovascular performance (e.g., bradycardia, selective increases in peripheral resistance, reduction and redistribution of cardiac output). In mammals, and to a lesser extent in birds, the major O2 stores at the beginning of a dive reside within blood and tissues rather than in lung gas. Consequently, there is limited respiratory benefit during apnea in either maintaining or transiently restoring extensive lung perfusion to predive levels, and so cardiac output (and thus lung perfusion) remains low during the dive. In contrast, in most amphibians and reptiles the major O2 stores at the beginning of a dive reside within lung gas rather than in blood and tissues. Recent experiments on frogs and turtles reveal that pulmonary blood flow during diving can transiently increase to or above predive levels when it becomes necessary during the dive to transfer O2 from lung gas to arterial blood. In this regard, cardiovascular responses to diving in lower vertebrates are qualitatively different from those of higher vertebrates.

Consultation with the Specialist

1992 ◽  
Vol 13 (10) ◽  
pp. 379-380
Author(s):  
William B. Strong
Keyword(s):  
Cardiac Output ◽  
Oxygen Saturation ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Cyanotic Congenital Heart Disease ◽  
Compensatory Mechanism ◽  
Peripheral Tissues ◽  
Arterial Blood ◽  
Infant And Young Child ◽  
Oxygen Carrying Capacity

What is the likely pathophysiology of this event? What are the more common complications of hypoxemia in the older infant and young child? This clinical scenario is uncommon, but it represents one of the two feared central nervous system complications of cyanotic congenital heart disease, (ie, cerebrovascular accident and brain abscess). A uniform response to hypoxemia of cardiac etiology is the production of erythropoietin to produce more red blood cells. This is a compensatory mechanism to maintain oxygen delivery to the peripheral tissues. Normally, hemoglobin is about 96% saturated with oxygen. Therefore, the oxygen-carrying capacity of blood with a normal hemoglobin concentration of 15 g/dL is approximately 20.3 mL of oxygen per 100 mL of blood (ie, 15 g of hemoglobin x 1.35 mL of O2 per g of hemoglobin = 20.3). The oxygen content of blood equals the oxygen-carrying capacity multiplied by the oxygen saturation. At a normal oxygen saturation of 96%, the O2 content of arterial blood (Hgb 15 g/dL) equals 19.5 mL/dL (96% x 20.3 mm3/dL) or 195 mL per liter of cardiac output. The arterial O2 content of this child, assuming an average arterial saturation of 85%, will be 11.1 mL/dL. Therefore, every liter (10 dL) of cardiac output will carry 111 mL of O2 or 84 mL of O2 less than the child with a 15 g/dL hemoglobin level.

Use of phenylhydrazine in the detection of responsive changes in haemoglobin isomorph abundances

1988 ◽  
Vol 66 (3) ◽  
pp. 758-762 ◽  
Author(s):  
Annette P. Byrne ◽  
A. H. Houston
Keyword(s):  
Gene Expression ◽  
Rainbow Trout ◽  
Environmental Change ◽  
Globin Gene ◽  
Salmo Gairdneri ◽  
Respiratory Response ◽  
Phenylhydrazine Hydrochloride ◽  
Total Hemoglobin ◽  
Response To Environmental Change ◽  
Globin Gene Expression

The possible masking of responsive adjustments in hemoglobin isomorph abundances was examined in rainbow trout, Salmo gairdneri. Comparison of untreated animals with specimens recovering from anemia induced by phenylhydrazine hydrochloride at 14 °C under normoxic circumstances revealed significant differences in the relative abundances of 8 of 12 isomorphs representing over half of the total hemoglobin complement. Comparisons with trout similarly treated after normoxic acclimation to 20 °C led to very similar findings. Observed differences do not appear to be attributable to direct phenylhydrazine effects on globin gene expression or to acute anemic hypoxia. It is suggested that prior induction of anemia may provide a means for improving detection of changes in hemoglobin isomorph complement during respiratory response to environmental change.

Estimation of Circulation Time in Rainbow Trout, Salmo gairdneri

1970 ◽  
Vol 27 (10) ◽  
pp. 1860-1863 ◽  
Author(s):  
John C. Davis
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Blood Volume ◽  
Water Flow ◽  
Mean Value ◽  
Arterial System ◽  
Circulation Time ◽  
Dorsal Aorta ◽  
Salmo Gairdneri ◽  
Receptor Sites

Circulation time in rainbow trout, Salmo gairdneri (mean weight 211.9 g) at 10 C was estimated by injecting Cardio-Green dye into the dorsal aorta and timing its reappearance at the site of injection. Circulation times ranged from 48 to 96 sec in the nine fish studied and had a mean value of 64.1 ± 16.4 sec. These circulation times are consistent with the known blood volume and cardiac output for rainbow trout.Such circulation times provide useful information on the theoretical positioning of receptors for the regulation of circulation and ventilation. Responses of trout to hypoxia or reduced gill water flow are too rapid to be initiated solely by a venous receptor considering these circulation times. Receptor sites must therefore be located in the arterial system or on the gills themselves.

scholarly journals Cardiac Output and Regional Blood Flow in Gills and Muscles after Exhaustive Exercise in Rainbow Trout (Salmo Gairdneri)

1983 ◽  
Vol 105 (1) ◽  
pp. 1-14
Author(s):  
PETER NEUMANN ◽  
GEORGE F. HOLETON ◽  
NORBERT HEISLER
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Muscle Blood Flow ◽  
Recovery Period ◽  
Flow Distribution ◽  
Strenuous Exercise ◽  
Salmo Gairdneri ◽  
Diffusion Resistance ◽  
Blood Flow Distribution

Rainbow trout (Salmo gairdneri) were electrically stimulated to exhausting activity and the changes in cardiac output and blood flow distribution to gills and systemic tissues resulting from the developing severe lactacidosis were repeatedly measured by the microsphere method (15 μm). Determination of cardiac output by application of the Fick principle resulted in values not significantly different from cardiac output measured by the indicator dilution technique, suggesting that cutaneous respiration, oxygen consumption, and arterio-venous shunting were insignificant under these conditions. Following muscular activity, cardiac output was elevated by up to 60%. In the gills, the blood flow distribution in the gill arches showed a consistent pattern, even during lactacidosis, with a higher perfusion in gill arches II and III, and in the middle sections of individual gills. Blood flow to white and red muscle was increased much more than cardiac output (+230 and +490%, respectively) such that blood flow to other tissues was actually reduced. We conclude that the elimination of lactate from muscle cells during the recovery period from strenuous exercise is delayed, not as a result of an impaired post-exercise muscle blood flow, but probably as a result of a high diffusion resistance in the cell membrane. Note: Deceased.

Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs

1977 ◽  
Vol 43 (5) ◽  
pp. 784-789 ◽  
Author(s):  
J. F. Borgia ◽  
S. M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Carrying Capacity ◽  
Hemoglobin Concentration ◽  
Severe Hypoxia ◽  
Systemic Hypertension ◽  
Anesthetized Dogs ◽  
Oxygen Tensions ◽  
Oxygen Carrying Capacity

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.

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