Blood Respiratory Properties and the Effect of Swimming on Blood Gas Transport in the Leopard Shark Triakis Semifasciata

1990 ◽  
Vol 151 (1) ◽  
pp. 161-173 ◽  
Author(s):  
N. CHIN LAI ◽  
IEFFREY B. GRAHAM ◽  
LOUIS BURNETT

Changes in vascular pressures, blood respiratory properties and blood gas transport induced by swimming were investigated in the leopard shark Triakis semifasciata (Girard). In resting sharks, the mean ventral and dorsal aortic pressures (systolic/diastolic) were 6.8/5.6 kPa and 4.5/3.9 kPa, respectively, and only the former were increased significantly during swimming. Swimming also caused a significant decline in venous Po2 (1.6 to 0.9kPa), O2 content (0.9 to 0.4mmoill−1) and percentage O2 saturation {SO2, 39 to 18%) but the arterial variables were not affected. A significant decline in venous pH and an increase in venous Po2 also occurred during swimming but lactate concentration did not increase during or after swimming. An in vivo dissociation curve compiled from blood Po2 and So2 data for sharks in the resting, swimming and post-swimming recovery phases shows a mean P50 of 2.04 kPa, as determined by Hill transformation. The pH-bicarbonate plot for this fish shows a weak blood buffer capacity of 9.3mmoll−11pHunit−1 and during swimming the average blood pH and bicarbonateconcentration follow the buffer line which was not compensated in recovery. Neither oxygenated nor deoxygenated blood pH values were affected by CO2 equilibration, suggesting the absence of a Haldane effect. Thus, at the expense of respiratory acidosis, Triakis can aerobically sustain long (up to 60min) and moderately intense (0.45 Ls−1, where L is body length) periods of swimming by increasing cardiac output and tapping its venous reserve. Introduction Most vertebrate circulatory

1976 ◽  
Vol 40 (4) ◽  
pp. 625-629 ◽  
Author(s):  
R. L. Coon ◽  
N. C. Lai ◽  
J. P. Kampine

A newly developed, dual-function pH and PCO2 sensor was evaluated in this study. The sensors were placed in the femoral arteries of dogs anesthetized with sodium pentobarbital. Comparisons were made between systemic arterial pH and PCO2 measured using the sensor and those measured from blood samples drawn at 15-min intervals over a 7-h period using a bench instrument. The mean pH of the bench instrument measurements was 7.43. The mean difference of the sensor measurements from the bench instrument measurements for 207 comparisons was 0.0003 pH +/- 0.061 SD. The mean PCO2 of the bench instrument measurements was 40 mmHg. The mean difference of the sensor measurements from those of the bench instrument for 212 comparisons was -1.43 mmHg +/- 5.17 SD. The sensors performed equally well in the presence of metabolic or respiratory acidosis and alkalosis. The dual-function sensors evaluated in this study are useful for trend monitoring of pH and PCO2 over at least a 7-h period without recalibration. With improvement in the consistency of sensor construction, these sensors will be reliable in vivo sensing devices for blood pH and PCO2 and thus valuable research and clinical instruments.


1977 ◽  
Vol 69 (1) ◽  
pp. 173-185
Author(s):  
C. M. Wood ◽  
B. R. McMahon ◽  
D. G. McDonald

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.


1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)


1997 ◽  
Vol 273 (5) ◽  
pp. F698-F705
Author(s):  
R. Unwin ◽  
R. Stidwell ◽  
S. Taylor ◽  
G. Capasso

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7–10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux ([Formula: see text]) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([[Formula: see text]]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion ([Formula: see text]) increased threefold, but LOH[Formula: see text]was unchanged. In ARA, blood pH fell to 7.2, and blood [[Formula: see text]] rose from 28 to 34 mM; [Formula: see text] was reduced to <0.1%, but LOH[Formula: see text]was unaltered. In CRA, blood pH fell to 7.2, and blood [[Formula: see text]] increased to >50 mM, whereas[Formula: see text]decreased to <0.1%.[Formula: see text]was reduced by ∼30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH[Formula: see text]increased (by 30%) to normal. These results suggest that LOH[Formula: see text]is affected by the blood-to-tubule lumen [[Formula: see text]] gradient and[Formula: see text] backflux. When the usual perfusing solution at 20 nl/min was made[Formula: see text] free, mean[Formula: see text]was −34.5 ± 4.4 pmol/min compared with 210 ± 28.1 pmol/min plus [Formula: see text]. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 × 10−4 M, to abolish H+-dependent[Formula: see text]) was used,[Formula: see text]was −112.8 ± 5.6 pmol/min. Comparable values for[Formula: see text]at 10 nl/min were −35.9 ± 5.8 and −72.5 ± 8.8 pmol/min, respectively. These data indicate significant backflux of[Formula: see text] along the LOH, which depends on the blood-to-lumen [[Formula: see text]] gradient; in addition to any underlying changes in active acid-base transport mechanisms, [Formula: see text]permeability and backflux are important determinants of LOH[Formula: see text]in vivo.


1988 ◽  
Vol 37 (1) ◽  
pp. 77-80 ◽  
Author(s):  
J.W. Collins ◽  
D. Merrick ◽  
R.J. David ◽  
S. Ameli ◽  
E.S. Ogata

AbstractLimited data suggest that cesarean section (CS) may be the preferred method of delivery for triplets. Despite this, it is also felt that the third triplet is at great risk at delivery. We reviewed our experience of 14 triplet pregnancies at Northwestern University between 1981 and 1985. All deliveries were attended by neonatal teams in sufficient number to resuscitate each infant. Of the 14 pregnancies, two ended in previable loss. Thirty-six infants were born from 12 pregnancies of a mean gestational age of 33 weeks (28-38 weeks). The overall survival was 97.3%. Two women delivered vaginally. While the first was successful, the second resulted in vaginal delivery of the first two triplets followed by emergency CS for the third. That infant had a cord blood pH of 6.96(BE-19), was resuscitated and survived. All 10 CS were successful. The mean cord blood gas tensions and pH were normal. In addition, Apgar scores, the requirement for mechanical ventilation or supplemental oxygen, and mortality did not differ between the first and thirdborn triplet. These observations suggest that CS was beneficial. Our very low mortality rate supports the concept that CS delivery and aggressive neonatal resuscitation and therapy greatly enhances survival.


1962 ◽  
Vol 17 (5) ◽  
pp. 812-814 ◽  
Author(s):  
August G. Swanson ◽  
Harold Rosengren

Cerebrospinal fluid (CSF) in vitro has less buffering capacity than blood since it lacks serum protein and cellular hemoglobin buffers. However, during acute respiratory acidosis CSF pH falls less than blood pH, indicating a significant in vivo spinal fluid buffering capacity. The nature of this buffering capacity was studied in anesthetized and artificially ventilated cats. Carbon dioxide tensions of 70–75 mm Hg were induced by 7% CO2 breathing. Simultaneous arterial blood and cisternal CSF samples were drawn at 0, 15, 30, 60, and 120 min. pCO2 and bicarbonate were measured with a radiometer AME-1 pH meter and tonometer, using the Astrup technique. A rapid increase in CSF bicarbonate maintained spinal fluid significantly more alkaline than blood throughout CO2 breathing, even though CSF and blood CO2 tensions were nearly equal. Intravenous bicarbonate did not alter CSF bicarbonate significantly during 2 hr. It is postulated that the buffering capacity of spinal fluid increases as a result of diffusion of preformed bicarbonate from brain cells. Submitted on March 12, 1962


2022 ◽  
Vol 52 (4) ◽  
Author(s):  
Simone Marques Caramalac ◽  
Andreza Futado de Souza ◽  
Silvana Marques Caramalac ◽  
Verônica Batista de Albuquerque ◽  
Lucas Bezerra da Silva Azuaga ◽  
...  

ABSTRACT: Anesthetic protocols have been developed to obtain the most effective and safe association in wildlife. This study compared the anesthetic effects and cardiorespiratory parameters of ketamine-S (+) (10 mg/kg)/dexmedetomidine (0.020 mg/kg) (KD ) and ketamine-S (+) (10 mg/kg)/midazolam (0.5 mg/kg)/methadone (1.0 mg/kg) (KMM ) in capuchin monkeys (Sapajus apella). Eight capuchin monkeys were randomly assigned to KD (n = 4) or KMM (n = 4) to evaluate induction, immobilization, and recovery scores, heart and respiratory rate parameters, besides systolic, mean, diastolic arterial pressure and arterial blood gas. There was no difference (P = 0.56) in the quality of induction, immobilization, and anesthetic recovery between the protocols. The time for anesthetic induction was 4 ± 1 min in the KD group and 5 ± 1 min in the KMM group, and these values were statistically equal (P = 0.28). The mean immobilization time in the KD and KMM groups were 35 ± 13 and 33 ± 15 min, respectively. Heart rate was lower in animals in the KD group (P < 0.001), while respiratory rate (P = 0.03), and mean blood pressure (P = 0.046) were higher than that of the animals in the KMM group. Respiratory acidosis occurred in the KMM group, with lower pH (7.25±0.047; P = 0.0055) and higher pCO2 (51 ± 6;mmHg; P = 0.008). Both protocols exhibited good induction quality, immobilization, and anesthetic recovery, despite cardiorespiratory and blood gas alterations observed, which warrants monitoring of cardiorespiratory variables during KD or KMM chemical restraint.


1974 ◽  
Vol 2 (3) ◽  
pp. 247-250 ◽  
Author(s):  
P. L. Gaudry ◽  
C. Duffy ◽  
D. Joseph

The metabolic and respiratory components of the hydrogen ion content of A.C.D. blood was directly measured by in vitro titration at controlled partial pressures of carbon dioxide. Blood stored for periods of up to 20 days had a mean pH of 6·53. The mean metabolic hydrogen ion excess was 37 mEq/litre and the mean respiratory hydrogen ion excess (carbonic acid) was 98 mEq/litre. The pH and hydrogen ion excess were not significantly related to duration of storage. Both metabolic and respiratory acidosis may occur in recipients of these hydrogen ion loads. In addition, sodium citrate in A.C.D. solution is metabolized in vivo to sodium bicarbonate. Clinically, a variable state of acid-base imbalance may result from the transfusion of A.C.D. blood until homeostasis is restored by renal and respiratory excretion of the acid and base loads.


1996 ◽  
Vol 76 (01) ◽  
pp. 111-117 ◽  
Author(s):  
Yasuto Sasaki ◽  
Junji Seki ◽  
John C Giddings ◽  
Junichiro Yamamoto

SummarySodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1), are known to liberate nitric oxide (NO). In this study the effects of SNP and SIN-1 on thrombus formation in rat cerebral arterioles and venules in vivo were assessed using a helium-neon (He-Ne) laser. SNP infused at doses from 10 Μg/kg/h significantly inhibited thrombus formation in a dose dependent manner. This inhibition of thrombus formation was suppressed by methylene blue. SIN-1 at a dose of 100 Μg/kg/h also demonstrated a significant antithrombotic effect. Moreover, treatment with SNP increased vessel diameter in a dose dependent manner and enhanced the mean red cell velocity measured with a fiber-optic laser-Doppler anemometer microscope (FLDAM). Blood flow, calculated from the mean red cell velocity and vessel diameters was increased significantly during infusion. In contrast, mean wall shear rates in the arterioles and venules were not changed by SNP infusion. The results indicated that SNP and SIN-1 possessed potent antithrombotic activities, whilst SNP increased cerebral blood flow without changing wall shear rate. The findings suggest that the NO released by SNP and SIN-1 may be beneficial for the treatment and protection of cerebral infarction


1993 ◽  
Vol 70 (04) ◽  
pp. 676-680 ◽  
Author(s):  
H F Kotzé ◽  
V van Wyk ◽  
P N Badenhorst ◽  
A du P Heyns ◽  
J P Roodt ◽  
...  

SummaryPlatelets were isolated from blood of baboons and treated with neuraminidase to remove platelet membrane sialic acid, a process which artificially ages the platelets. The platelets were then labelled with 111In and their mean life span, in vivo distribution and sites of Sequestration were measured. The effect of removal of sialic acid on the attachment of immunoglobulin to platelets were investigated and related to the Sequestration of the platelets by the spleen, liver, and bone marrow. Removal of sialic acid by neuraminidase did not affect the aggregation of platelets by agonists in vitro, nor their sites of Sequestration. The removal of 0.51 (median, range 0.01 to 2.10) nmol sialic acid/108 platelets shortened their life span by 75 h (median, range 0 to 132) h (n = 19, p <0.001), and there was an exponential correlation between the shortening of the mean platelet life span and the amount of sialic acid removed. The increase in platelet-associated IgG was 0.112 (median, range 0.007 to 0.309) fg/platelet (n = 25, p <0.001) after 0.79 (median, range 0.00 to 6.70) nmol sialic acid/108 platelets was removed (p <0.001). There was an exponential correlation between the shortening of mean platelet life span after the removal of sialic acid and the increase in platelet-associated IgG. The results suggest that platelet membrane sialic acid influences ageing of circulating platelets, and that the loss of sialic acid may have exposed a senescent cell antigen that binds IgG on the platelet membrane. The antibody-antigen complex may then provide a signal to the macrophages that the platelet is old, and can be phagocytosed and destroyed.


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