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

Reversal of saxitoxin (STX; 10 micrograms/kg, ip) induced cardiorespiratory effects by oxygen ventilation and burro-raised alpha-STX antitoxin (60 mg/kg, i.v.) was studied in urethane-anesthetized guinea pigs acutely instrumented for concurrent monitoring of medullary respiratory-related single units, diaphragm EMG, Lead II electrocardiogram, arterial blood pressure (BP), arterial pH, and O2/CO2 tensions, electrocorticogram (ECoG), and end-tidal CO2. STX-induced cardiorespiratory effects included (1) a state of progressive bradypnea and hypercapnia; (2) a functional blockade of the diaphragm; (3) a prolongation of respiratory cycle duration; (4) an aberrant bulbar respiratory-related neuronal activity pattern; and (5) a decline in BP and heart rate. The therapeutic effect of artificial ventilation following STX-induced apnea was equivocal in that the cardiorespiratory activities, be they of central or peripheral nature, remained dysfunctional despite continued oxygen ventilation. Spontaneous breathing and cardiovascular performance following STX-induced apnea could all be promptly restored (typically in less than a minute) by combined oxygen/antitoxin therapy. Notable also was a state of uncompensated acidemia (as revealed by changes in arterial pH and CO2 tension) which persisted throughout the course of therapeutic intervention. Notwithstanding, the ventilatory frequency continued to be low, the central respiratory activity pattern remained aberrant, and the ECoG amplitudes were still depressed. In consideration of these findings, and of the large molecular weight of alpha-STX antitoxin (> 150,000 Da) which limits its entry into the CNS, we are of the opinion that the therapeutic effects of antitoxin are probably confined primarily to the periphery.
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PMID:Reversal of saxitoxin-induced cardiorespiratory failure by a burro-raised alpha-STX antibody and oxygen therapy. 829 Oct 60

Effects of saxitoxin (STX; 10 micrograms/kg; i.p.) on cardio-respiratory activities were evaluated in urethane-anesthetized guinea-pigs. Concurrent recordings were made of electrocorticogram (ECoG), bulbar respiratory-related unit activities, diaphragmatic electromyogram (DEMG), electrocardiogram (Lead II ECG), blood pressure, heart rate, end-tidal CO2, arterial O2/CO2 tensions, and arterial pH. The average time to STX-induced respiratory failure was about 10 min. The most striking effect prior to apnea was a state of progressive bradypnea which emerged 5-7 min after the toxin administration. Other noteworthy responses included (i) a time-dependent decrease in ECoG amplitudes which typically began before the development of a bradypneic profile; (ii) an increasing degree of diaphragm neuromuscular blockade; (iii) a state of combined hypercapnia and uncompensated acidemia; (iv) a declining blood pressure; (v) an incrementally dysfunctional myocardial performance; and (vi) an increasingly degenerative central respiratory activity profile which ultimately culminated in a complete loss of central respiratory drive. The therapeutic effect of intratracheally administered oxygen was equivocal in that the cardio-respiratory activities, be they of central of peripheral nature, remained conspicuously dysfunctional and precarious despite 100% oxygen ventilation. What can be inferred from this study is two-fold. First, STX-induced ventilatory insufficiency can be attributed to a loss of functional integrity of both central and peripheral respiratory system components. That is, although diaphragm blockade contributes significantly to STX-induced respiratory failure, analyses of single respiratory unit activity data revealed that the central respiratory rhythmogenic mechanism also appeared to play a pivotal role in the development of a bradypneic profile which promotes, and directly causes, a complete loss of respiratory drive. Second, a state of unabating depression of central respiratory activities, which seemed to be refractory to the effect of O2, suggests STX has a direct and persistent action on medullary rhythmogenic mechanisms. In conclusion, these findings indicate that both central and peripheral cardio-respiratory components are critically involved in STX-induced apnea, dysfunctional cardiovascular performance, and lethality.
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PMID:Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs. 833 95