Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent hypoxia is encountered in life more often than sustained hypoxia. The purpose of this article is to summarize the long-term effects of intermittent hypoxia on control of breathing. Emphasis is given to intermittent hypoxia associated with recurrent apneas and with brief repeated ascents to high altitude. Reported responses to chronic recurrent apneas include both depressed and enhanced hypoxic ventilatory responses (HVR). In addition, recurrent apneas are often associated with depression of the hypercapnic ventilatory response (HCVR). On the other hand, intermittent hypoxia associated with repeated ascents to high altitude augments HVR with little or no influence on the HCVR. In a rat model, prolonged exposure to intermittent hypoxia simulating recurrent apneas selectively enhances carotid body sensitivity to acute hypoxia and induces long-lasting activation of baseline activity, whereas intermittent hypoxia simulating repeated ascents to high altitude has little or no effect on peripheral chemoreceptor activity. Thus the mechanisms by which episodic hypoxia alter HVR appear to differ and seem to depend on the paradigm of intermittent hypoxia. Prolonged episodic hypoxia also leads to long-term facilitation (LTF) of respiratory motor output in humans and in experimental animals. Recent studies on experimental animals suggest the involvement of HIF-1 transcription factor in inducing enhanced HVR in response to chronic recurrent apnea pattern. Future studies are needed to identify the molecular and cellular signaling pathways associated with intermittent hypoxia and their impact on ventilatory control during hypoxia and hypercapnia.
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PMID:Ventilatory changes during intermittent hypoxia: importance of pattern and duration. 1216 63

Increasing water CO2, aquatic hypercapnia, leads to higher physiological pCO2 levels in fish, resulting in an acidosis and compensatory acid-base regulatory response. Senegalese sole is currently farmed in super-intensive recirculating water systems where significant accumulation of CO2 in the water may occur. Moreover, anthropogenic releases of CO2 into the atmosphere are linked to ocean acidification. The present study was designed to assess the effects of acute (4 and 24 h) and prolonged exposure (4 weeks) to CO2 driven acidification (i.e., pH 7.9, 7.6, and 7.3) from normocapnic seawater (pH 8.1) on the innate immune status, gill acid-base ion transporter expression and metabolic rate of juvenile Senegalese sole. The acute exposure to severe hypercapnia clearly affected gill physiology as observed by an increase of NHE3b positive ionocytes and a decrease of cell shape factor. Nonetheless only small physiological adjustments were observed at the systemic level with (1) a modulation of both plasma and skin humoral parameters and (2) an increased expression of HIF-1 expression pointing to an adjustment to the acidic environment even after a short period (i.e., hours). On the other hand, upon prolonged exposure, the expression of several pro-inflammatory and stress related genes was amplified and gill cell shape factor was aggravated with the continued increase of NHE3b positive ionocytes, ultimately impacting fish growth. While these findings indicate limited effects on energy use, deteriorating immune system conditions suggest that Senegalese sole is vulnerable to changes in CO2 and may be affected in aquaculture where a pH drop is more prominent. Further studies are required to investigate how larval and adult Senegalese sole are affected by changes in CO2.
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PMID:Effects of Water Acidification on Senegalese Sole Solea senegalensis Health Status and Metabolic Rate: Implications for Immune Responses and Energy Use. 3208 90