Pulmonary vasoconstrictor responses to graded decreases in precapillary blood PO2 in intact-chest cat

The effects of graded changes in pulmonary lobar arterial blood PO2 and ventilatory hypoxia were investigated in the intact-chest cat under conditions of controlled lobar blood flow. A reduction in precapillary PO2 from systemic arterial levels to below 60 Torr increased lobar arterial pressure. Ventilation with 10% O2 increased lobar arterial pressure, and responses to ventilatory hypoxia and precapillary hypoxemia were independent but additive. The magnitude of the pressor response to precapillary hypoxemia was similar in experiments in which the lung was autoperfused with right atrial blood or cross-perfused with aortic blood from a donor cat breathing 10% O2. During retrograde perfusion of the ventilated lung, a reduction in pulmonary venous PO2 to 40 Torr did not affect inflow pressure. The present data suggest that sensor sites upstream to the alveolar-capillary region in segments of lobar artery unexposed to alveolar gas sense a reduction in precapillary blood PO2 and elicit a pulmonary vasoconstrictor response. The sensor site in the precapillary segment is independent of sensors in the alveolar-capillary-exposed segment region, and the effects of stimulation of both sensors on the pulmonary vascular bed are additive. In addition, the present data indicate that sensors in the pulmonary veins do not sense a reduction in PO2 in venous blood and elicit a vasoconstrictor response. These data suggest that the mixed venous blood PO2 may exert an important regulatory role in controlling pulmonary arterial pressure and pulmonary vascular resistance in the cat under normal and pathological conditions.

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Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis

Clinical Science ◽

10.1042/cs0570385 ◽

1979 ◽

Vol 57 (5) ◽

pp. 385-388 ◽

Cited By ~ 1

Author(s):

R. D. Latimer ◽

G. Laszlo

Keyword(s):

Whole Blood ◽

Base Excess ◽

Venous Blood ◽

Main Pulmonary Artery ◽

Mixed Venous Blood ◽

Arterial Blood ◽

Significant Difference ◽

Venous Pco2 ◽

Pulmonary Arterial ◽

Gas Pressures

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.

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Respiratory measurements of cardiac output: from elegant idea to useful test

Journal of Applied Physiology ◽

10.1152/japplphysiol.01074.2001 ◽

2004 ◽

Vol 96 (2) ◽

pp. 428-437 ◽

Cited By ~ 41

Author(s):

Gabriel Laszlo

Keyword(s):

Cardiac Output ◽

Human Subjects ◽

Venous Blood ◽

The Body ◽

Mixed Venous Blood ◽

Indirect Determination ◽

Arterial Blood ◽

Pulmonary Capillary ◽

Pulmonary Arterial ◽

Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

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Evidence that the Pco2 of mixed venous blood is not a regulator of ventilation during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1963.18.2.345 ◽

1963 ◽

Vol 18 (2) ◽

pp. 345-348 ◽

Cited By ~ 5

Author(s):

Winnifred F. Storey ◽

John Butler

Keyword(s):

Venous Blood ◽

Muscular Exercise ◽

Mixed Venous Blood ◽

Arterial Blood ◽

Cardiac Lesions ◽

Pulmonary Arterial ◽

Mixed Venous

We studied 10 patients with intracardiac left-to-right shunt and 13 patients with other cardiac lesions during exercise. The hyperpnea of muscular exercise was independent of the mixed venous Pco2. In the 13 patients without shunt both the pulmonary arterial Pco2 and the ventilation increased during exercise. In the 10 patients who had shunts ventilation increased during exercise even when the Pco2 in the pulmonary arterial blood did not rise. Submitted on July 5, 1962

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Thromboxane does not mediate pulmonary hypertension in phorbol ester-induced acute lung injury in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.1.345 ◽

1990 ◽

Vol 69 (1) ◽

pp. 345-352 ◽

Cited By ~ 5

Author(s):

A. H. Stephenson ◽

R. S. Sprague ◽

T. E. Dahms ◽

A. J. Lonigro

Keyword(s):

Pulmonary Hypertension ◽

Acute Lung Injury ◽

Lung Injury ◽

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Pressor Response ◽

H2 Receptor Antagonist ◽

Arterial Blood ◽

Pulmonary Arterial ◽

The Relationship

Thromboxane (Tx) has been suggested to mediate the pulmonary hypertension of phorbol myristate acetate- (PMA) induced acute lung injury. To test this hypothesis, the relationship between Tx and pulmonary arterial pressure was evaluated in a model of acute lung injury induced with PMA in pentobarbital sodium-anesthetized male mongrel dogs. Sixty minutes after administration of PMA (20 micrograms/kg iv, n = 10), TxB2 increased 10-fold from control in both systemic and pulmonary arterial blood and 8-fold in bronchoalveolar lavage (BAL) fluid. Concomitantly, pulmonary arterial pressure (Ppa) increased from 14.5 +/- 1.0 to 36.2 +/- 3.5 mmHg, and pulmonary vascular resistance (PVR) increased from 5.1 +/- 0.4 to 25.9 +/- 2.9 mmHg.l-1.min. Inhibition of Tx synthase with OKY-046 (10 mg/kg iv, n = 6) prevented the PMA-induced increase in Tx concentrations in blood and BAL fluid but did not prevent or attenuate the increase in Ppa. OKY-046 pretreatment did, however, attenuate but not prevent the increase in PVR 60 min after PMA administration. Pretreatment with the TxA2/prostaglandin H2 receptor antagonist ONO-3708 (10 micrograms.kg-1.min-1 iv, n = 7) prevented the pressor response to bolus injections of 1-10 micrograms U-46619, a Tx receptor agonist, but did not prevent or attenuate the PMA-induced increase in Ppa. ONO-3708 also attenuated but did not prevent the increase in PVR. These results suggest that Tx does not mediate the PMA-induced pulmonary hypertension but may augment the increases in PVR in this model of acute lung injury.

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Effect of lung inflation and hypoxia on pulmonary arterial blood volume

Journal of Applied Physiology ◽

10.1152/jappl.1977.43.1.8 ◽

1977 ◽

Vol 43 (1) ◽

pp. 8-13 ◽

Cited By ~ 8

Author(s):

E. J. Quebbeman ◽

C. A. Dawson

Keyword(s):

Blood Flow ◽

Pulmonary Artery ◽

Arterial Pressure ◽

Pressor Response ◽

Transpulmonary Pressure ◽

The Other ◽

Lung Inflation ◽

Arterial Blood ◽

Pulmonary Arterial ◽

Arterial Blood Volume

Isolated cat lungs were perfused with constant blood flow. During control conditions (Pa02, 100 Torr), pulmonary artery pressure increased as the lungs were inflated. Hypoxia (Pa02, 22 Torr) increased arterial pressure. However, as the lungs were inflated arterial pressure fell. Thus, the magnitude of the hypoxic pressor response was reduced by inflation. During control conditions, arterial volume (ether bolus method) increased with increasing transpulmonary pressure. Hypoxia decreased arterial volume, and the increase in arterial volume with inflation was somewhat less than that during control conditions. When the influences of vascular and transpulmonary pressures were examined independently by changing one while holding the other constant, increasing transpulmonary pressure increased arterial volume beyond that which could be accounted for by changes in the differences between arterial and pleural pressure. However, this influence of transpulmonary pressure did not appear to be altered by hypoxia. Thus, while hypoxia decreased arterial volume at all levels of lung inflation, it had relatively little effect on the influence of interdependence between the pulmonary arterial bed and the surrounding lung tissue.

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Pulmonary hypertension with muscular exercise in the newborn calf

Journal of Applied Physiology ◽

10.1152/jappl.1965.20.2.249 ◽

1965 ◽

Vol 20 (2) ◽

pp. 249-252 ◽

Cited By ~ 1

Author(s):

John T. Reeves ◽

James E. Leathers

Keyword(s):

Pulmonary Hypertension ◽

Arterial Pressure ◽

Pulmonary Arterial Pressure ◽

Pressor Response ◽

Muscular Exercise ◽

Arterial Oxygen ◽

Mixed Venous Blood ◽

Fetal Life ◽

Pulmonary Vasoconstriction ◽

Pulmonary Arterial

Two types of pulmonary hypertension occur with muscular exercise (walking) in the calf on the day of birth: a) Pulmonary arterial pressure increased in all calves during exercise. The increase was greatest in the youngest calves. Pulmonary arterial pressures did not rise to systemic levels and arterial oxygen saturations remained normal. Pulmonary hypertension subsided in 2 min after stopping exercise. Pulmonary arterial pressure rose again when exercise was repeated. Both an increased pulmonary flow and pulmonary vasoconstriction may have contributed to the increased pulmonary arterial pressure during exercise. b) Pulmonary hypertension was observed in five calves for 30-50 min after exercise ceased. When pulmonary arterial pressure exceeded aortic pressure, arterial oxygen unsaturation occurred. This pulmonary hypertension which occurred only once per calf resembled"spontaneous" pulmonary vasoconstriction observed in resting calves on the day of birth. It is postulated that some substance remaining in the lung after fetal life, rather than the acutely reduced oxygenation of mixed venous blood, initiated this pressor response. hypoxia; pulmonary vasoconstriction Submitted on May 11, 1964

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The effects of inhalation salbutamol administration on systemic and pulmonary hemodynamic, pulmonary mechanics and oxygen balance during general anaesthesia in the horse

Veterinární Medicína ◽

10.17221/2984-vetmed ◽

2010 ◽

Vol 55 (No. 9) ◽

pp. 445-456 ◽

Cited By ~ 7

Author(s):

M. Patschova ◽

R. Kabes ◽

S. Krisova

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

General Anaesthesia ◽

Venous Blood ◽

Pulmonary Mechanics ◽

Mixed Venous Blood ◽

Oxygen Balance ◽

Arterial Blood ◽

Pulmonary Hemodynamic ◽

Pulmonary Arterial

This research aimed to determine the effect of aerosolized salbutamol administration on systemic and pulmonary hemodynamic, pulmonary mechanics and oxygen balance in healthy horses during general anaesthesia. Six healthy Thoroughbreds (body weight range 471–587 kg) underwent two general anaesthesias in dorsal recumbency with and without aerosolized salbutamol administration in randomized order with a one month washout period. The anaesthesia was induced by 1.1 mg/kg of xylazine, 0.02 mg/kg of diazepam and 2.2 mg/kg of ketamine, maintained with isoflurane in oxygen and air and horses were mechanically ventilated. Measurement of arterial and pulmonary arterial blood pressures, cardiac output and arterial and mixed venous blood gas analysis was carried out. Spirometry was performed using a Horse-lite. After achieving a steady state, baseline (T0) values of cardiac output, systemic and pulmonary arterial blood pressures, heart rate, dynamic compliance, airway resistance and arterial and mixed venous blood gas values and pH were recorded in both groups. In the S-group (salbutamol), 2 µg/kg of aerosolized salbutamol were administered synchronously with inspirium into the tracheal tube. In both groups data were recorded at 15, 30, 45 and 60 min (T15, T30, T45, T60) after the baseline. PaO2/FiO2 ratio, oxygen consumption (VO2), oxygen delivery (DO2), pulmonary shunt values were calculated. Data were tested for normality and compared within each group: T0 value with T15, T30, T45, T60 values using Wilcoxon's test with Bonferoni correction (significance level 0.0125). For each time point, comparisons were made between the S- and C-groups (control) using Wilcoxon's test. In the S-group, there was a significant increase in values (mean ± SD) of cardiac output (l/min), T0 (38 ± 7), a peak at T15 (64 ± 25.5), significantly higher values persisted throughout the period of anaesthesia; heart rate (beats/min), T0 (32 ± 2), T15 (40 ± 6), T30 (38 ± 5); DO2 (l/min), T0 (5.8 ± 0.8), a peak at T15 (9.6 ± 3.2), significantly higher values persisted until the end of anaesthesia and VO2 (l/min), T0 (1.1 ± 0.5), T30 (1.6 ± 0.7) and T45 (1.8 ± 0.5). In the C-group, there was a significant decrease in values of PaO2/FiO2 ratio from T0 (176 ± 67) to a minimum at T60 (114 ± 36) and in DO2 from T0 (6 ± 2.3) to a minimum at T60 (4.3 ± 1.2). A comparison of the S- and C-groups did not reveal any difference in the baseline data. Subsequently, significantly higher values of cardiac output, heart rate, DO2, and the PaO2/FiO2 ratio were found in the S-group compared to the C-group. Pulmonary arterial blood pressure was significantly lower in the S-group. Aerosolized salbutamol administration in healthy horses during general anaesthesia caused hemodynamic changes which resulted in an elevation of oxygen delivery. It can have a positive effect on arterial oxygenation, but the effect varies between individuals.

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Pulmonary diffusion in the dog lung

Journal of Applied Physiology ◽

10.1152/jappl.1962.17.6.885 ◽

1962 ◽

Vol 17 (6) ◽

pp. 885-892 ◽

Cited By ~ 7

Author(s):

Albert H. Niden ◽

Charles Mittman ◽

Benjamin Burrows

Keyword(s):

Carbon Monoxide ◽

Pulmonary Artery ◽

Experimental Animal ◽

Venous Blood ◽

Whole Body ◽

Mixed Venous Blood ◽

Pulmonary Diffusion ◽

Perfused Lung ◽

Pulmonary Arterial ◽

Mixed Venous

Methods have been presented for assessing pulmonary diffusion by the “equilibration technique” in the experimental intact dog and perfused lung while controlling ventilation with a whole body respirator. No significant change in diffusion of carbon monoxide was noted between open and closed chest anesthetized animals, with duration of anesthesia in the intact dog, or with duration of perfusion of the isolated dog's lung. There was no demonstrable difference in diffusion when arterialized blood was used as the perfusate in place of mixed venous blood in the lung perfusions suggesting that within the range studied the Po2, Pco2, and pH of pulmonary artery blood does not directly affect the diffusion of carbon monoxide. Retrograde perfusions of dogs' lungs did not significantly alter diffusion, suggesting that pulmonary venous resistance was not significantly lower than pulmonary arterial resistance in the perfused dog lung at the flows and pressures studied. The equilibration technique for measuring pulmonary diffusion and assessing the uniformity of diffusion was well suited to the study of pulmonary diffusing characteristics in the experimental animal. Submitted on January 8, 1962

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Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.6.2136 ◽

1986 ◽

Vol 61 (6) ◽

pp. 2136-2143 ◽

Cited By ~ 5

Author(s):

D. C. Curran-Everett ◽

K. McAndrews ◽

J. A. Krasney

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Pulmonary Blood Flow ◽

Pulmonary Arterial Pressure ◽

Pressor Response ◽

Superior Vena ◽

Acute Hypoxia ◽

Vena Cava ◽

Normobaric Hypoxia ◽

Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

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Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.273.3.r1126 ◽

1997 ◽

Vol 273 (3) ◽

pp. R1126-R1131 ◽

Cited By ~ 1

Author(s):

Y. X. Wang ◽

J. T. Crofton ◽

S. L. Bealer ◽

L. Share

Keyword(s):

Blood Flow ◽

Vascular Resistance ◽

Regional Blood Flow ◽

Pressor Response ◽

Peripheral Resistance ◽

Female Rats ◽

Sexually Dimorphic ◽

Arterial Blood ◽

Vasoconstrictor Response ◽

Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

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