Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0020440 (
hypercapnia
)
7,939
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Aortic chemoreceptor influences on vascular capacitance after changes in blood carbon dioxide and oxygen were studied in mongrel dogs anesthetized with methoxyflurane and nitrous oxide. The mean circulatory filling pressure (Pmcf), measured during transient
cardiac fibrillation
, provided a measure of capacitance vessel tone.
Hypercapnia
, hypoxia, and hypoxic
hypercapnia
significantly increased most variables, except that
hypercapnia
caused the total peripheral resistance (TPR) to decrease. Hypocapnia caused a significant decrease in mean systemic (Psa) and pulmonary (Ppa) arterial blood pressures, cardiac output (CO), and central blood volume and an increase in TPR and heart rate. The changes in Pmcf on changing blood gas tensions could be described by the equation delta Pmcf = -1.60 + 0.036 (arterial PCO2) + 50.8/arterial PO2. Thus a 10 mmHg increase in arterial PCO2 caused a 0.36 mmHg increase in Pmcf with receptors intact. Cold block (2 degrees C) of the cervical vagosympathetic trunks did not significantly influence the measured variables at control. During severe
hypercapnia
, vagal cooling caused a small but significant decrease in Pmcf, Psa, Ppa, and CO but not TPR. During hypoxia, vagal cooling caused the Pmcf, Psa, and TPR to decrease. We conclude that although
hypercapnia
or hypoxia acts reflexly to increase the capacitance vessel tone (an increase in Pmcf), the aortic and cardiopulmonary chemoreceptors with afferents in the vagi have only a small influence on the capacitance system, accounting for only approximately 25% of the total body response.
...
PMID:Effects of hypercapnia and hypoxia on the cardiovascular system: vascular capacitance and aortic chemoreceptors. 239 98
This review illustrates the importance of sleep disordered breathing in evolution and progression of atrial fibrillation. While in early years associations were mainly attributed to the impact of hypoxemia and hypertension, nowadays multiple, additional pathways have been investigated or are currently under investigation. Sleep disordered breathing has been shown to have a direct impact on mechanical and electrical remodeling. In addition
hypercapnia
and negative intrathoracic pressure seem to alter atrial electrophysiology. Finally, impacts on inflammation and metabolic dysregulation display the complex interplay between breathing disorders and evolution and progression of atrial fibrillation.
J Atr
Fibrillation
PMID:Sleep Disordered Breathing and the Pathogenesis of Atrial Fibrillation. 2849 54