Decreased ventilatory response to hypoxia during acute polycythemia in the calf

Bisgard, G. E.; Alvarez, Hector; Grover, Robert F.

doi:10.1016/0034-5687(69)90020-6

Cited by 13 publications

(5 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For these reasons there must be some reservation regarding the ultimate significance of the effects of carbon monoxide on ventilation. Recent studies from our laboratory indicate that in awake cattle augmentation of oxygen transport produced by transfusion-induced increases in hematocrit decreased the ventilatory response to hypoxia (36). Yet studies by Eisele, Pegg, and Severinghaus (37 )in anesthetized dogs showed no diminution in hypoxic drive following production of polycythemia.…”

Section: Methodsmentioning

confidence: 82%

Hypoxic ventilatory drive in normal man

Weil¹,

Byrne-Quinn²,

Sodal³

et al. 1970

J. Clin. Invest.

Self Cite

382

174

View full text Add to dashboard Cite

A B S T R A C TFor purposes of quantitation these curves are approximated by a simple hyperbolic function, the parameters of which are evaluated by a least squares fit of the data. The parameter A denotes curve shape such that the higher the value of A, the greater the increase in ventilation for a given decrease in PAO2 and hence the greater the hypoxic drive. Curves are highly reproducible for each subject and curves from different subjects are similar. In 10 normal subjects at resting PAcO2, A = 180.2 +14.5 (SEM). When PACO, is adjusted to levels 5 mm Hg above and below control in six subjects A = 453.4 ±103 and 30.2 ±6.8 respectively. These latter values differed significantly from control (P < 0.05). These changes in curve shape provide a clear graphic description of interaction between hypercapnic and hypoxic ventilatory stimuli. At normal PACo2 the VE-PAO2 curve has an inflection zone located over the same P02 range as the inflection in the oxygenhemoglobin dissociation curve. This indicated that ventilation might be a linear function of arterial oxygen saturation or content. Studies in four subjects have

show abstract

Section: Methodsmentioning

confidence: 82%

Hypoxic ventilatory drive in normal man

Weil¹,

Byrne-Quinn²,

Sodal³

et al. 1970

J. Clin. Invest.

Self Cite

382

174

View full text Add to dashboard Cite

show abstract

“…Note the expanded rough endoplasmic reticulum (ER), enlarged dense-cored vesicles (DCV), and increased number of mitochondria in the CP cells. Nucleus (1); perivascular space (2); dilated, abundant rough ER (3); DCV (4); mitochondrion (5). Original scale bars = 500 nm.…”

Section: Resultsmentioning

confidence: 99%

“…The CP mice were clearly very different than WT in terms of their ventilatory and carotid-body phenotypes, despite demonstrating only a moderate increase in hemoglobin and hematocrit. The latter is unlikely to have been a confounding influence, since other animal studies have demonstrated that the hypoxic ventilatory response is inhibited (3) or unchanged (7) acutely by polycythemia.…”

Section: Discussionmentioning

confidence: 99%

The von Hippel-Lindau Chuvash mutation in mice causes carotid-body hyperplasia and enhanced ventilatory sensitivity to hypoxia

Slingo

Turner

Christian

et al. 2014

Journal of Applied Physiology

View full text Add to dashboard Cite

The hypoxia-inducible factor (HIF) family of transcription factors coordinates diverse cellular and systemic responses to hypoxia. Chuvash polycythemia (CP) is an autosomal recessive disorder in humans in which there is impaired oxygen-dependent degradation of HIF, resulting in long-term systemic elevation of HIF levels at normal oxygen tensions. CP patients demonstrate the characteristic features of ventilatory acclimatization to hypoxia, namely, an elevated baseline ventilation and enhanced acute hypoxic ventilatory response (AHVR). We investigated the ventilatory and carotid-body phenotype of a mouse model of CP, using whole-body plethysmography, immunohistochemistry, and electron microscopy. In keeping with studies in humans, CP mice had elevated ventilation in euoxia and a significantly exaggerated AHVR when exposed to 10% oxygen, with or without the addition of 3% carbon dioxide. Carotid-body immunohistochemistry demonstrated marked hyperplasia of the oxygen-sensing type I cells, and the cells themselves appeared enlarged with more prominent nuclei. This hypertrophy was confirmed by electron microscopy, which also revealed that the type I cells contained an increased number of mitochondria, enlarged dense-cored vesicles, and markedly expanded rough endoplasmic reticulum. The morphological and ultrastructural changes seen in the CP mouse carotid body are strikingly similar to those observed in animals exposed to chronic hypoxia. Our study demonstrates that the HIF pathway plays a major role, not only in regulating both euoxic ventilatory control and the sensitivity of the response to hypoxia, but also in determining the morphology of the carotid body.

show abstract

“…Unfortunately, the animals were made anemic, thus adding to the objections above those of iatrogenic alterations of oxygen delivery such as decreased end-capillary Po2 (18), altered cardiac output, and a possible shift towards anaerobic metabolism in low-P50 animals (19). Not surprisingly, conflicting results have also come from models employing polycythemia (20)(21)(22)(23), which has complex effects on oxygen delivery (24).…”

Section: Resultsmentioning

confidence: 99%

Hypoxic ventilatory response in subjects with normal and high oxygen affinity hemoglobins.

1977

View full text Add to dashboard Cite

A B S T R A C T It has still not been shown unequivocally whether a decrement of arterial oxygen content or tension governs the ventilatory response to hypoxia. In an attempt to discriminate between the two possibilities, we have measured the ventilatory response to isocapnic progressive hypoxia in two healthy children with a high oxygen affinity hemoglobin (Hb AndrewMinneapolis) and in their age-and sex-matched normal siblings. Hypoxic ventilatory response was identical in all subjects, there being no difference in minute ventilation at PAO2 = 40 mm Hg or in k (decrement of Po2 required to increase ventilation by a factor of 2.718). In contrast, at PAO2 = 40 mm Hg, hemoglobin oxygen saturation decreased markedly in controls but only slightly in high affinity subjects. Furthermore, the increase in heart rate at PAO2 = 40 mm Hg was significantly less in high affinity subjects, suggesting a concomitant difference in oxygen delivery. Thus, with identical decrements in PAO2 but widely divergent changes in arterial oxygen content and oxygen delivery, controls and high affinity subjects showed virtually identical ventilatory response to hypoxia. We conclude

show abstract

Decreased ventilatory response to hypoxia during acute polycythemia in the calf

Cited by 13 publications

References 19 publications

Hypoxic ventilatory drive in normal man

Hypoxic ventilatory drive in normal man

The von Hippel-Lindau Chuvash mutation in mice causes carotid-body hyperplasia and enhanced ventilatory sensitivity to hypoxia

Hypoxic ventilatory response in subjects with normal and high oxygen affinity hemoglobins.

Contact Info

Product

Resources

About