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D P Toews

Publications and source records attributed to D P Toews.

At least 19 recordsLinked to original sources
PubMed2001

The dynamics of venous return and response to hypervolemia in the toad, Bufo marinus (L.).

BACKGROUND: Venous return from the posterior region of amphibians travels by either two renal portal veins to the kidney or a central abdominal vein that drains into the hepatic portal system. The relative proportions of blood flow in these vessels has never been measured nor has a modification of flow been determined when venous return increases by changes in blood volume during hypervolemia or during increased volume input from the posterior lymph hearts. RESULTS: Venous return from the posterior region of Bufo marinus was measured under resting conditions and in response to a systemic hypervolemia. Doppler flow probes were positioned on the renal portal and ventral abdominal veins, and flow was recorded as injections of artificial plasma equaling 100% of the animal's plasma volume were administered through the sciatic artery. Resting flow was found to be 5.54 +/- 2.03 ml min(-1) kg(-1) in the paired renal portal veins, and 7.31 +/- 0.89 ml min(-1) kg(-1) in the ventral abdominal vein. While renal portal flow was found to increase by a factor of 2.4 times during the first 10 min of hypervolemia, ventral abdominal flow only increased by a factor of 1.3. CONCLUSIONS: Our results quantify the contribution to circulation from posterior venous return in the toad Bufo marinus. A preferential movement of excess fluid through the renal portal pathway was also demonstrated, supporting the possibility of water elimination via the renal portal circulation, especially during periods of high water influx into the animals.

Abdomen↗
PubMed1997

Direct measurement of flow from the posterior lymph hearts of hydrated and dehydrated toads (Bufo marinus).

Flow from the posterior lymph hearts of Bufo marinus was measured using Doppler flow probes. These probes were placed on the posterior vertebral vein and recorded flow as lymph was ejected from the heart. In resting, hydrated toads, mean lymph flow from one of the paired posterior lymph hearts was 25.9 +/- 4.9 ml kg-1 h-1, stroke volume was 8.9 +/- 1.4 microL kg-1 and lymph heart rate was 47.5 +/- 3.7 beats min-1. We estimate that, together, the paired posterior lymph hearts are capable of generating flows that are approximately one-sixtieth of the resting cardiac output. Mean peak systolic pressure developed by the posterior lymph hearts was 1.62 +/- 0.08 kPa. Simultaneous measurements of lymph heart pressure development and flow revealed that the outflow pore of the heart opened at a pressure of 0.71 +/- 0.04 kPa, approximately 113 +/- 5 ms into systole. When toads were moderately disturbed, stroke volume increased by as much as fourfold with little change in lymph heart rate (< 5 beats min-1). When toads were dehydrated, lymph flow decreased by 70% at 12h and by 80% and 24h. Since there was only a modest non-significant decrease in lymph heart rate (30%), this reduction in flow was attributed to decreases in stroke volume (approximately 80%). Lymph heart flow and stroke volume returned to control values 30 min after adding water back into the experimental chamber. Stroke volume was clearly more important in regulating lymph flow than lymph heart rate under these conditions in Bufo marinus.

Animals↗
PubMed1992

Acid-base-electrolyte balance responses of Bufo marinus to aminoglutethimide, corticosterone, and aldosterone during hypercapnia.

Experiments were conducted to test the hypothesis that one or more interrenal steroids are active in regulatory responses to respiratory acidosis in the toad, Bufo marinus. Toads were divided into four experimental groups. The first group received sham injections. The second group received 1-3 mg of aminoglutethimide (AG) every 8 hr. AG inhibits the conversion of cholesterol to pregnenolone, thus inhibiting all steroid hormone synthesis. The third group received AG + 5 micrograms of aldosterone on the same schedule. The fourth group received AG + 25 micrograms of corticosterone on the same schedule as the other groups. All four groups were subjected to hypercapnia using 5% CO2 to induce a respiratory acidosis. The sham-operated animals displayed the normal compensatory pattern of producing a metabolic alkalosis (elevated plasma HCO3-) after 24 hr. AG-treated toads failed to elevate plasma HCO3-. Administration of interrenal steroids produced compensation in varying degrees. Aldosterone produced a small compensation while corticosterone produced a compensation similar to that seen in sham-operated animals. Analysis of steroid titers in toad plasma during hypercapnia showed that Bufo marinus does not elevate aldosterone during respiratory acidosis, but that corticosterone is elevated. AG blocked the corticosterone elevation, however. AG also produced a hyponatremia that was corrected with aldosterone or corticosterone. Normocapnic controls showed that AG does not produce deleterious effects on pH or blood gases in toads in the absence of a respiratory acidosis. We conclude that corticosterone is important in acid-base regulatory responses to respiratory acidosis in this amphibian.

Acid-Base Equilibrium↗
PubMed1992

Posterior lymph heart pressure and rate and lymph flow in the toad Bufo marinus in response to hydrated and dehydrated conditions.

Posterior lymph heart pressure, rate and flow were measured in chronically cannulated Bufo marinus during normal hydrated and dehydrated conditions. A new surgical technique was developed which allowed direct and constant measurement of the functioning of the posterior lymph hearts with minimal disruption to normal lymph drainage. The mean intra-lymph-heart systolic pressure was 2.29 +/- 0.12 kPa for hydrated animals at rest, decreasing to 1.01 +/- 0.10 kPa after 24 h of dehydration. Similarly, lymph heart rate, which was 48.2 +/- 1.7 beats min-1 under hydrated conditions, decreased to 31.8 +/- 4.6 beats min-1 after 18 h of dehydration. Lymph flow decreased almost to zero during dehydration from a hydrated rate of 1.11 +/- 0.04 ml h-1 100 g-1. This is the first study to measure directly and to correlate these variables in an amphibian and to show specifically that pressure, rate and lymph flow are significantly reduced during periods of dehydration.

Animals↗
PubMed1991

Acid-base regulation in the toad Bufo marinus during environmental hypoxia.

Gas exchange and the correlated changes in blood and tissue metabolic and acid-base status were investigated during long term exposure of the toad Bufo marinus to graded levels of hypoxia. During hypoxia, PCO2 values in blood and tissues fell, leading to a transient alkalosis in the extracellular but not in the intracellular space. A reduction in blood perfusion of the skin during hypoxia may explain why PCO2 was low in sartorius muscle under normoxia, but approached the PCO2 values found in other tissues (gastrocnemius muscle, ventricle) under hypoxia. At PO2 values below the critical PO2, lactate was formed and the decrease in total CO2 was accelerated. Lactate levels in the plasma were higher than in the intracellular space of the skeletal muscles, a finding attributed to the pH-dependent distribution of lactic acid across the cell membrane. The comparison of metabolic proton quantities with those found in the extra- and intracellular acid-base status suggests that CO2 release was accelerated by anaerobic proton formation. The alkalizing effect of decreasing PCO2 in the skeletal musculature was compensated for by a release of base equivalents into the blood. The resulting alkalosis in the blood was probably compensated for by the release of base equivalents into the environment.

Acid-Base Equilibrium↗
PubMed1990

Determination of intracellular pH and PCO2 after metabolic inhibition by fluoride and nitrilotriacetic acid.

Mean intracellular pH (pHi) and PCO2 (PiCO2) have been analysed based on pH and total CO2 measurements in tissue homogenates. Tissues were sampled from undisturbed worms (Sipunculus nudus), squid (Illex illecebrosus), trout (Salmo gairdneri), toads (Bufo marinus), and rats. Homogenate metabolism was inhibited by the addition of potassium fluoride and nitrilotriacetic acid (NTA). Model calculations revealed that the influence of dilution, medium buffers, and contamination by extracellular fluids was negligible. In white muscle tissue the resulting pHi values were virtually the same as found in studies using DMO (dimethyloxazolidinedione). If large fractions of mitochondria were present (e.g. in heart muscle), DMO derived pHi values were considerably higher, probably representing overestimates. Homogenate derived pHi values are concluded to represent the effective mean pHi by taking into account pH gradients, and the volumes and buffering of cellular compartments. High time resolution and small variability make this method especially useful to assess rapid changes in pHi, e.g. in exercising animals.

Acid-Base Equilibrium↗
PubMed1990

Compensation of progressive hypercapnia in the toad (Bufo marinus) and the bullfrog (Rana catesbeiana).

Toads (Bufo marinus L.) and bullfrogs (Rana catesbeiana Shaw) were subjected to a series of 24 h step increases in aerial CO2 (2, 4, 6 and 8%) to assess the degree of extracellular pH compensation at each CO2 level and to ascertain the importance of cutaneous ion transport in this process. Elevation of plasma [HCO3-] occurs during the 24 h period, with the bullfrogs showing a greater ability to compensate at each step. There was no indication that a [HCO3-] threshold of 30 mmol l-1 existed in either species, although bullfrogs appeared to have a greater compensatory potential when exposed to the higher levels of CO2. The results of the ion flux experiments suggest that neither the terrestrial Bufo nor the semi-aquatic Rana use their skin to any great extent for acid-base balance during hypercapnia.

Acid-Base Equilibrium↗
PubMed1988

Regulation of ventilation and acid-base status in the elasmobranch Scyliorhinus stellaris during hyperoxia-induced hypercapnia.

Exposure of the elasmobranch Scyliorhinus stellaris to environmental hyperoxia (PO2 of 500 mm Hg) resulted in a considerable rise of arterial PCO2 from 1.9 mm Hg during normoxia to about 11 mm Hg after 6 days as an expression of the primarily oxygen-oriented regulation of gill ventilation. In contrast to the typical pattern during environmental hypercapnia, however, arterial plasma pH was hardly affected by the considerable hyperoxia-induced hypercapnia. At elevated arterial PO2 values (200-300 mm Hg) gill ventilation was apparently not adjusted exclusively for the oxygen demands of the organism, but was matched to the requirements of acid-base regulation such that the rise in PCO2 could be compensated for by a net gain of bicarbonate-equivalent ions from the environment. This fine adjustment of gill ventilation to the bicarbonate-equivalent uptake rate extended the process of adaptation to about 6 days and resulted in an almost complete pH compensation during the entire process of PCO2 increase. These data suggest that during conditions of reduced oxygen-related respiratory drive the regulation of gill ventilation is primarily dependent upon the acid-base parameters.

Acid-Base Equilibrium↗
PubMed1985

The ventilatory and acid-base physiology of the toad, Bufo marinus, during exposure to environmental hyperoxia.

Bufo marinus which were exposed to a step increase of 330-350 torr O2 for a 20 h period ceased lung ventilations and buccal movements were markedly decreased. Toads which were sitting in water did not show elevations in PaCO2 or a depressed pHe but animals which were dehydrated for a 24 h period prior to high O2 exposure developed a mild acidosis, which, typical of most amphibian species, was uncompensated.

Acid-Base Equilibrium↗
PubMed1985

Partitioning of regulatory sites in Bufo marinus during hypercapnia.

Ureters were cannulated in specimens of Bufo marinus (L.) in order to partition the regulatory contributions of the kidney and skin. The in vivo roles of the kidney, skin and internal calcareous deposits in the response of these animals to chronic hypercapnia were then evaluated. There was no compensatory adjustment by the skin and only a minimal regulatory response by the kidney. Major adjustments which have been attributed to combined skin and urinary tract in previous studies must therefore come from the urinary bladder. Removal of the bladder as a regulatory site in these animals completely eliminated the compensatory elevation of HCO3- in the extracellular fluid. Mobilization of internal calcareous deposits as a source of HCO3- was found to contribute 50% of the compensatory response of these animals during hypercapnia.

Ammonia↗
PubMed1983

Acid-base and ionic balance in Ambystoma tigrinum and Necturus maculosus during hypercapnia.

The aquatic urodeles Ambystoma tigrinum and Necturus maculosus responded to hypercapnia quite differently. A. tigrinum, after 2-h exposure to 22 Torr partial pressure of CO2 (PCO2), decreased arterial pH (pHa) from 7.85 to 7.32 and increased arterial pressure of CO2 (PaCO2) to 26 Torr. Plasma [HCO-3] [( HCO-3]pl) remained constant at about 17 mM. Prolonged exposure (24 h) led to a 26% extracellular compensation as pHa rose to 7.46 while [HCO-3]pl increased to 24 mM. Plasma [K+] increased and [Cl-] decreased while [Na+] remained unchanged. Recovery in normocapnic water reversed these changes. N. maculosus did not display similar compensatory changes. Two-hour exposure to 17 Torr PCO2 resulted in a decline of pHa from 7.66 to 7.24, which was not compensated (pHa = 7.19) after 24 h. There were no significant changes in plasma [Na+], [K+], [Cl-], or [HCO-3]. The pHa decline reversed after recovery in normocapnic water, however. The fact that compensation for hypercapnic in A. tigrinum was accompanied by changes in Cl- and K+ concentrations may indicate the participation of epithelial transport mechanisms involving these ions in acid-base balance.

Acid-Base Equilibrium↗
PubMed1983

Regulation of the acid-base status during environmental hypercapnia in the marine teleost fish Conger conger.

Specimens of Conger conger (L.) were exposed to environmental hypercapnia in a closed recirculating seawater system. Arterial plasma pH, PCO2 and bicarbonate concentration, as well as the net transfer of bicarbonate and ammonia between fish and ambient seawater, were monitored for 30 h of hypercapnia. The initial hypercapnia-induced reduction of arterial pH by about 0.4 pH units was restored to near control values within 10 h of hypercapnia by compensatory elevation of plasma bicarbonate concentration. The continuous rise in extracellular bicarbonate from about 5 to 22 mM during this time was the result of two different mechanisms. Initially, there was a net bicarbonate transfer from the intracellular space to the extracellular compartment until the net uptake of bicarbonate from the seawater started. The amount of bicarbonate originally transferred to the extracellular space was then returned to the intracellular compartment and finally the changes in both extracellular and intracellular pH were compensated by bicarbonate taken up from the environmental seawater. Since the ammonia excretion was not increased during hypercapnia and the pattern of plasma electrolyte concentrations does not favour the H+/Na+ ion exchange mechanism, it is concluded that the additional bicarbonate is gained by active HCO3-/Cl- ion exchange against the electrochemical gradient between fish and seawater.

Acid-Base Imbalance↗
PubMed1982

The effects of hypercapnia on intracellular and extracellular acid-base status in the toad Bufo marinus.

Toads (Bufo marinus) were exposed to environmental hypercapnia of 5% CO2 in air, and extracellular and intracellular acid-base parameters were determined 1 and 24 h after the onset of hypercapnia. The initial drop in pH was compensated by the elevation of extracellular and intracellular bicarbonate. Relating the pH compensation to the pH drop that is expected to occur by increased PCO2 at constant bicarbonate concentration, the pH compensation in the extracellular space was 30% and reached the following values for intracellular body compartments: 65% in skeletal muscle, 77% in heart muscle and 44% in skin. The additional bicarbonate was partly produced by blood and intracellular non-bicarbonate buffers; the major portion of the remainder was related to the excretion of ammonia into the environmental water. The hypercapnia-induced changes of pH were considerably smaller in all tissue cells than in the extracellular space. Thus Bufo marinus exhibits the relative preference of intracellular over extracellular acid-base regulation that has been observed in other vertebrates.

Acid-Base Equilibrium↗
PubMed1981

Respiratory properties of blood in a strictly aquatic and predominantly skin-breathing urodele, Cryptobranchus alleganiensis.

The strictly aquatic urodele. Cryptobranchus alleganiensis, is one of the largest gill-less vertebrates in which most of the respiratory gas exchanges occur across the skin. In this study we have examined some of the gas carrying relationships in blood to determine whether certain properties are particularly adaptive to the hellbender's well oxygenated habitat and predominantly cutaneous mode of respiration. The O2 dissociation curve is sigmoidal (n = 2.9) having a P50 of 23.6 mm Hg (at pHa and PaCO2) and a Bohr factor of -0.24. A considerable amount of arterio-venous mixing prior to the ejection of blood from the heart is thought to account for a comparatively low arterial O2 1-1 .pH-1 for a hematocrit of 29%. Attention is drawn to the variability in the protein buffering related CO2 combining properties in vitro caused by hct alterations during different methods of blood sampling. Acid-base relationships between whole blood, true plasma and separated plasma are essentially the same as those described for mammalian blood. Interspecies comparison with the data from this study suggest that factors such as microhabitat, rather than water or air breathing per se, may influence the characteristics of blood O2 and CO2 carriage in amphibians.

Animals↗
PubMed1981

Respiratory, circulatory and acid-base adjustments to hypercapnia in a strictly aquatic and predominantly skin-breathing urodele, Cryptobranchus alleganiensis.

Upon initial exposure to increased ambient CO2, Cryptobranchus is titrated along an in vivo buffer line whose slope is considerably reduced from that observed when whole blood samples are equilibrated in vitro. During this time, there is no apparent reduction in the PCO2 difference between arterial blood and inspired media (PaCO2 -PICO2), despite an increase in auxiliary respiratory activities (lung and buccopharyngeal ventilation). The development of this non-compensated respiratory acidosis in the skin-breathing salamander is reminiscent of the situation seen in gill-breathing fish where the control of the acid-base balance is achieved by means other than ventilation. The increased ventilatory activities in Cryptobranchus can be interpreted as a response to the effect that the acidotic conditions have on arterial oxygenation (i.e.: CO2 Bohr effect); as a result, PaO2 increases and appears to counteract the arterial hypoxaemia which would otherwise result. More prolonged hypercapnia leads to compensatory phase of acid-base adjustment whereby plasma bicarbonate increases along a gently rising PaCO2 line to a new steady state equilibrium. This compensatory stage is slow acting and offers little by way of restoring the arterial blood pH, at least over the 36-h CO2 exposure period studied. The recovery period in air-saturated conditions is very gradual with PaCO2 levels exhibiting an exponential pattern of decline. This, together with the PaCO2 -PICO2 observations above, lends support to an accumulating body of evidence which suggests that respiratory CO2 losses across the amphibian skin are passive or at best only poorly controlled.

Acid-Base Equilibrium↗
PubMed1980

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the semi-terrestrial anuran, Bufo marinus.

Strenuous exercise results in a marked blood acid-base disturbance which is accompanied by large increases in ventilation rate, heart rate and mean arterial blood pressure. Recovery to normal resting values follows an exponential time course with a half-time of approximately 2 h for all parameters except Pa, CO2 and ventilation rate. The latter return to normal by 30 min following the exercise period. Analysis reveals that there is initially a large discrepancy between the quantity of metabolic acids buffered in the blood and the blood lactate levels. The significance of this finding is discussed. Significant changes in the concentrations of chloride, bicarbonate and lactate, in both plasma and erythrocytes, accompany the blood acid-base disturbance. Chloride and bicarbonate appear to be passively distributed between the two compartments according to a Gibbs-Donnan equilibrium whereas lactate only slowly permeates the erythrocyte.

Acid-Base Equilibrium↗