Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs

Rothe, Carl F.; Stein, P. D.; MacAnespie, C. L.; Gaddis, Monica

doi:10.1152/ajpheart.1985.249.6.h1061

Cited by 21 publications

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“…The mean and standard deviation for MCFP of 9-7 + 1-2 mmHg observed in gallamine-treated cats did not differ significantly from the values in cats breathing spontaneously under chloralose anaesthesia. It compares with values reported for the conscious rat of 7-6+007 mmHg (Samar & Coleman, 1978) and 7-9+007 mmHg (Yamamoto et al 1980), for the dog under deep pentobarbitone anaesthesia of 6-9 + 0 9 mmHg (Guyton et al 1973), for the dog under chloralose anaesthesia of 12-6 + 2-3 mmHg (Drees & Rothe, 1974) and 6-0 + 1'9 mmHg (Rothe et al 1985). The range of values from minimum to near maximum a-adrenergic stimulation (5-6-16-5 mmHg) is similar to the range of 5-16 mmHg reported by Guyton, Lindsey, Abernathy & Langston (1958) Drees & Rothe (1974) and Yamamoto et al (1980).…”

Section: Measurement Of Mcfpsupporting

confidence: 61%

“…They argued that venous return was increased principally by 8% 02 in N2 to dogs and observed that the resulting sympathetic activation increased mean circulatory filling pressure (MCFP). Cardiac output was also increased in the experiments of Smith & Crowell (1967), but not in those of Rothe et al (1985) unless CO2 was added to the gas mixture. More information has therefore been sought on the extent to which contraction of capacitance vessels in the whole animal can usefully contribute to a rise in cardiac output.…”

Section: Introductionmentioning

confidence: 83%

“…MCFP, which represents the balance between the blood volume and the total vascular capacitance, has been measured in the dog and rat by equilibration of aortic and right atrial pressures after circulatory arrest (Guyton, Polizo & Armstrong, 1954; Drees & Rothe, 1974;Samar & Coleman, 1978;Yamamoto, Trippodo, Ishise & Frohlich, 1980;Rothe et al 1985). Provided measurements were made within 7 s of arrest, there was insufficient time for reflexes to act.…”

Section: Introductionmentioning

confidence: 99%

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Mean circulatory filling pressure during splanchnic nerve stimulation and whole‐body hypoxia in the anaesthetized cat.

Bower

O’Donnell

1991

The Journal of Physiology

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SUMMARY1. Mean circulatory filling pressure (MCFP) was measured in cats under chloralose anaesthesia by obstruction of blood flow in the pulmonary artery. Pressures in the aorta, hepatic portal vein and right atrium were recorded, and MCFP was estimated from the value at which all three pressures became equal when blood was pumped from aorta to vena cava during circulatory arrest. Simultaneous equality was not attained at MCFP values below 5 mmHg.2. In cats ventilated by positive pressure after administration of gallamine, MCFP was 9-7 +0 3 mmHg (n = 14). The values of MCFP measured in six cats before and after administration of gallamine did not differ significantly. Change of blood volume altered MCFP linearly over the range 5-21 mmHg. Noradrenaline (7 5 ,ug kg-' min-') increased MCFP from 9.3 + 0 9 to 16-5 + 0-6 mmHg (n = 4), and phentolamine (2 mg kg-') reduced it to 5-6+0-3 mmHg (n = 5).3. Changes in MCFP were evoked at different circulating blood volumes by stimulation of the splanchnic sympathetic nerves and by whole-body hypoxia. Ablation of all splanchnic nerves reduced MCFP from 9-4 + 0-5 to 7-1 + 03 mmHg (n = 5) and stimulation of their distal ends at 10 Hz increased it by 4-1 +0-4 mmHg (n = 4); similar increments were obtained at different blood volumes and initial values of MCFP.4. Hypoxia increased MCFP by 0-23 mmHg per 1 mmHg fall in arterial oxygen tension below P., 0256 mmHg (r = -0-86; n = 24). Similar increments were obtained at different blood volumes and initial values of MCFP. Ablation of all splanchnic nerves reduced the increments by 60 %, and administration of phentolamine abolished them.

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Section: Measurement Of Mcfpsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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Mean circulatory filling pressure during splanchnic nerve stimulation and whole‐body hypoxia in the anaesthetized cat.

Bower

O’Donnell

1991

The Journal of Physiology

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“…Studies with dogs revealed that hypercapnia not only increased pulmonary arterial pressure but also the central venous and systemic arterial pressure and decreased heart rate (Rothe et al, 1985). Results of investigations by Anderson et al (1996) with micro pigs suggest that hypercapnia and a decreased pH participate in blood pressure regulation via increased renal sodium/hydrogen exchange and renal sodium retention.…”

Section: Discussionmentioning

confidence: 98%

Ascites and venous carbon dioxide tensions in juvenile chickens of highly selected genotypes and native strains

Scheele

Klis

Kwakernaak

et al. 2005

World's Poultry Science Journal

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A previous study by this group demonstrated that a high carbon dioxide tension in venous blood (pvCO 2 ) of juvenile broiler chickens is a reliable predictor for ascites susceptibility. In a new experiment with five highly selected genetic stocks and two ascites resistant old breeds we studied levels and variability of pvCO 2 within each stock at an early age. Effects of different selection traits (principally growth rate) between fast growing sire lines and slower growing dam lines and a commercial hybrid on blood gas (pCO 2 , pO 2 ) tensions, pH and haematocrit in venous and arterial blood were examined at different ages and compared to values found in ascites resistant breeds. All birds were housed in floor pens in a climate controlled room and subjected to an ascites-predisposing cold environment. From each stock, 16 birds with the highest (high risk: HRc) and 16 birds with the lowest (low risk: LRc) pvCO 2 values were selected at 12 days of age. These birds were marked for future blood sampling to determine changes in haematological characteristics with age and to relate these values to ascites susceptibility. At day 14, eight non-selected birds from each stock were randomly chosen for dissection to determine initial pulmonary arterial pressure index (API) values. Subsequently, all birds were allotted to 8 floor pens (13 birds per pen including two HRc and two LRc birds) per stock. Production performances from 104 birds per stock were measured from 16 to 33 days of age (feed intake (FI); feed conversion ratio (FCR); body weight (BW) at day 33). Mortality was recorded during the complete experimental period. At 5 wk of age, all HRc and LRc birds were necropsied and API values were recorded, which was used to classify the severity of the ascites syndrome. A convincing effect of pvCO 2 values in juvenile chickens on API at 5 wk of age in modern lines confirmed results obtained in the previous study. At an early age, pvO 2 values were much less predictive for high pulmonary pressure induced ascites at wk 5 than pvCO 2 values. Hypercapnia combined with low blood pH values and followed by hypoxemia (inducing high haematocrit values) provoked a marked high incidence of ascites and high API values in modern breeds. Ascites and venous carbon dioxide tensions: C.W. Scheele et al.A total absence of ascitic symptoms within native breeds corresponded with unchanged low API values during ageing from 12 to 33 days of age and with lower pCO 2 values in venous and arterial blood compared to modern breeds at all ages. The pvCO 2 difference (mean values) between HRc and LRc groups were similar for all modern lines irrespective of age and showed no relationship to growth rate. API, as a reliable indicator for ascites susceptibility, of modern breed chickens correlated with pvCO 2 values, but not with growth rate. The high correlation between pvCO 2 in juvenile chickens and API values at 5 wk of age indicated that a strong genetic selection pressure on low pvCO 2 values at an early age will be an effective method to reduce dec...

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“…[14] pointed to an increase in Q during inhalation of 7% C 0 2. In their experiments on animals, Rothe et al [15] noticed a decrease followed by an increase in the Qs, HR and Psa due to inhalation of 12% C 0 2, while Rose et al [16] stated that during acute hyper capnic acidosis the parameters of systemic hemodynamics remained unchanged. At the same time, Walley et al [17] found that, in anesthetized open-chest dogs, respira tory acidosis reduced left ventricular contractility but in creased 0 and HR with no change in blood pressure.…”

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confidence: 98%

Comparison of Respiratory and Circulatory Human Responses to Progressive Hypoxia and Hypercapnia

Serebrovskaya

1992

Respiration

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The effects of acute, progressive isocapnic hypoxia and hyperoxic hypercapnia on lung ventilation, heart rate, cardiac output and arterial blood pressure were determined simultaneously in 32 normal individuals. All subjects were exposed to hypoxia and hypercapnia in an entire range of individual tolerance. The piecewise linear approximation technique was used for analysis of the ventilatory and circulatory response curves. In all subjects, the changes in hemodynamics in the response to hypoxia paralleled those occurring in ventilation, during both the first phase of slow increase and the second phase of sharp increase. Fracture point coordinates for ventilation and circulation coincided, with the fracture being registered at an end-tidal PO₂ of 79.7 ± 3.8 mm Hg for ventilation and 79.0 ± 4.5 mm Hg (p > 0.1) for cardiac output. This may give evidence of analogous entries from the peripheral O₂-sensitive receptors to the respiratory and vascular motor bulbar centers. By contrast, a more significant rise in ventilation observed during the hypercapnic versus hypoxic drive was not accompanied by any change in the heart rate, cardiac output and arterial blood pressure until the end-tidal PCO₂ (PETCO₂) had reached a critical level. Fracture point coordinates for ventilation and circulation did not coincide, with the fracture being registered at a PETCO₂ of 51.1 ± 1.9 mm Hg for the former and 57.0 ± 2.2 mm Hg (p < 0.01) for the latter. Such differences in the response to hypoxia and hypercapnia were repeatedly observed during 5 test days. The data do not seem to show evidence in favor of an involvement of the hypercapnic challenge in the central regulation of the circulation.

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Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs

Cited by 21 publications

References 0 publications

Mean circulatory filling pressure during splanchnic nerve stimulation and whole‐body hypoxia in the anaesthetized cat.

Mean circulatory filling pressure during splanchnic nerve stimulation and whole‐body hypoxia in the anaesthetized cat.

Ascites and venous carbon dioxide tensions in juvenile chickens of highly selected genotypes and native strains

Comparison of Respiratory and Circulatory Human Responses to Progressive Hypoxia and Hypercapnia

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