Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Guinea pigs were sensitized and boostered with i.p. injections of ovalbumin (OA) 10 micrograms + Al(OH)3 100 mg. Thirteen days after the last injection animals (800-1100 g) were placed in bias flow ventilated whole body plethysmographs and allowed to stabilize for 2 h. Lung function was recorded for up to 2 h before and 5 h after aeroallergen challenge (OA 20 mg/ml, 60 s, 20 psi) by a noninvasive pulmonary analyzer for unrestrained rodents. Aeroallergen challenge produced immediate dyspnea and gasping (peaking between 8 and 17 min). Gasping was associated with an increase in amplitude in the box pressure fluctuations (93%), and in the slope of the fluctuations (391%). Respiratory rate increased (103 to 175 breaths/min, 78%), the product of breathing rate times box pressure amplitude increased (161 to 432, 180%). Relaxation time (the time it takes the box pressure signal to drop from its peak to 1/3 of its peak value) declined (0.16 to 0.05 s, 72%). All of these lung dysfunction changes were highly significant (p < 0.001). Lung dysfunction persisted for 60 to 120 min after challenge. One of 8 animals tested died within 10 min. None of the animals exhibited late asthmatic responses during the 5 h post-challenge period. Based on these data we conclude that this technique allows quantitative analysis of dyspnea, gasping, and an abnormal pattern (waveform) of breathing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aeroallergen-induced dyspnea in freely moving guinea pigs: quantitative measurement by bias flow ventilated whole body plethysmography. 832 57

Hypoxic gasping emerges under severe hypoxia/ischemia in various species, exerting a life-protective role by assuring minimum ventilation even in loss of consciousness. However, the molecular basis of its generation and maintenance is not well understood. Here we found that mice lacking Kir6.2- but not Kir6.1-containing ATP-sensitive potassium (K(ATP)) channels [knockout (KO) mice] exhibited few gaSPS when subjected to abrupt ischemia by decapitation, whereas wild-type mice all exhibited more than 10 gaSPS. Under anesthesia, wild-type mice initially responded to severe hypoxic insult with augmented breathing (tachypnea) accompanied by sighs and subsequent depression of respiratory frequency. Gasping then emerged and persisted stably (persistent gasping); if the hypoxia continued, several gaSPS with distinct patterns appeared (terminal gasping) before cessation of breathing. KO mice showed similar hypoxic responses but both depression and the two types of gasping were of much shorter duration than in wild-type mice. Moreover, in the unanesthetized condition, the onset of terminal gasping in KO mice, which was always earlier than in wild-type mice, was unaltered by decreasing O(2) concentrations within the severe range (4.5-7.0%), whereas onset in wild-type mice became earlier in response to lowered O(2) concentrations. Thus, the mechanism responsible for regulating the hypoxic response in accordance with the severity of the hypoxia was dysfunctional in these KO mice, suggesting that Kir6.2-containing K(ATP) channels are critically involved in the maintenance rather than the generation of hypoxic gasping and depression of respiratory frequency.
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PMID:Disruption of Kir6.2-containing ATP-sensitive potassium channels impairs maintenance of hypoxic gasping in mice. 1744 33