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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hyberbaric nitrogen on the responses of ventilation and central inspiratory activity (CIA) to progressive hypercapnia were studied in eight subjects rebreathing a) O2 at an ambient pressure of 1.3 bar (control), and b) air at 6.1 bar (PO2 = 1.3 bar, PN2 = 4.8 bar). Inspiratory occlusion pressure (P0.1), pulmonary ventilation, and end-tidal PCO2 were used for the computation of individual CIA and ventilatory CO2 response curves. Increasing the inspired PN2 to 4.8 bar caused, on the average, a 40% increase of P0.1 at PCO2 = 50 Torr, whereas the slope of the ventilatory CO2 response curve was reduced by 39%. It was concluded that, at raised air and nitrogen pressures, CIA is increased, although not sufficiently to prevent a reduction of ventilation brought about by the increased gas density and consequent increase in airway resistance. The increased airway resistance is thought to be responsible for the increase in CIA by causing a reflex stimulation of the respiratory centers.
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PMID:Dissociated ventilatory and central respiratory responses to CO2 at raised N2 pressure. 73 May 72

Understanding the mismatching of ventilation and perfusion (VA/Q) is of special interest in the intensive care setting because - given a stable cardiac output and a given inspiratory oxygen fraction - it allows one to explain certain essential respiratory problems in critically ill patients, namely hypoxemia and hypercarbia. Several different methods are available today for the evaluation VA/Q mismatching. Analysis of the PCO2 and PO2 in arterial and mixed venous blood and mixed expired gas yields information about the quality and the degree of the mismatching present. Calculation of the physiologic dead space (VD/VT) and venous admixture (QVA/QT) from the PCO2 and PO2 data allow the VA/Q mismatching to be quantified according to a three-compartment model of the lung. Determination of the arterial-alveolar nitrogen partial-pressure difference permits a more precise estimation of the true right-to-left shunt as a cause of arterial hypoxemia, but the measurement of the arterial PN2 remains a delicate procedure. The multiple inert gas elimination technique permits virtually continuous ventilation-perfusion distributions to be described over the whole range of VA/Q ratios and has contributed to explaining the pathophysiological mechanisms in various pulmonary diseases. This method, however, is technically very complex and hence will remain a sophisticated investigational tool. Scintigraphic approaches allow the description of regional topographic VA/Q distributions, but their application is still difficult in the intensive care setting.
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PMID:[Foundation for the understanding of ventilation-perfusion ratio abnormalities]. 312 40

Transgenic mice overexpressing the amyloid precursor protein (APP) have a profound impairment in endothelium-dependent cerebrovascular responses that is counteracted by the superoxide scavenger superoxide dismutase (SOD). The authors investigated whether the amyloid-beta peptide (A beta) is responsible for the cerebrovascular effects of APP overexpression. Cerebral blood flow (CBF) was monitored by a laser-Doppler flowmeter in anesthetized-ventilated mice equipped with a cranial window. Superfusion of A beta1-40 on the neocortex reduced resting CBF in a dose-dependent fashion (-29% +/- 7% at 5 micromol/L) and attenuated the increase in CBF produced by the endothelium-dependent vasodilators acetylcholine (-41% +/- 8%), bradykinin (-39% +/- 9%), and the calcium ionophore A23187 (-37% +/- 5%). A beta1-40 did not influence the CBF increases produced by the endothelium-independent vasodilators S-nitroso-N-acetylpenicillamine and hypercapnia. In contrast, A beta1-42 did not attenuate resting CBF or the CBF increases produced by endothelium-dependent vasodilators. Cerebrovascular effects of A beta1-40 were reversed by the superoxide scavengers SOD or MnTBAP. Furthermore, substitution of methionine 35 with norleucine, a mutation that blocks the ability of A beta to generate reactive oxygen species, abolished A beta1-40 vasoactivity. The authors conclude that A beta1-40, but not A beta1-42, reproduces the cerebrovascular alterations observed in APP transgenics. Thus, A beta1-40 could play a role in the cerebrovascular alterations observed in Alzheimer's dementia.
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PMID:Exogenous A beta1-40 reproduces cerebrovascular alterations resulting from amyloid precursor protein overexpression in mice. 1112 82