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Titolo:
REFLEX STIMULATION OF RENAL SYMPATHETIC-NERVE ACTIVITY AND BLOOD-PRESSURE IN RESPONSE TO APNEA
Autore:
ODONNELL C; SCHWARTZ AR; SMITH PL; ROBOTHAM JL; FITZGERALD RS; SHIRAHATA M;
Indirizzi:
JOHNS HOPKINS ASTHMA & ALLERGY CTR,ROOM 4B63,5501 HOPKINS BAYVIEW CIRCLE BALTIMORE MD 21224 JOHNS HOPKINS UNIV,DEPT ANESTHESIOL & CRIT CARE MED,PULM ANESTHESIA LAB BALTIMORE MD 00000 JOHNS HOPKINS UNIV,DEPT MED,DIV PULM & CRIT CARE MED BALTIMORE MD 00000 JOHNS HOPKINS UNIV,DEPT ENVIRONM HLTH SCI,DIV PHYSIOL BALTIMORE MD 00000
Titolo Testata:
American journal of respiratory and critical care medicine
fascicolo: 6, volume: 154, anno: 1996,
pagine: 1763 - 1770
SICI:
1073-449X(1996)154:6<1763:RSORSA>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
OBSTRUCTIVE SLEEP-APNEA; STROKE VOLUME; VOLUNTARY APNEA; HYPOXEMIA; OXYGEN; CONSEQUENCES; HEMODYNAMICS; TERMINATION; DECREASE; HYPOXIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
21
Recensione:
Indirizzi per estratti:
Citazione:
C. Odonnell et al., "REFLEX STIMULATION OF RENAL SYMPATHETIC-NERVE ACTIVITY AND BLOOD-PRESSURE IN RESPONSE TO APNEA", American journal of respiratory and critical care medicine, 154(6), 1996, pp. 1763-1770

Abstract

The purpose of this study was to examine the role of afferent input in the reflex modulation of renal sympathetic nerve activity (SNA) in response to apnea. Apneas of 20-, 40-, and 60-s duration were induced in the anesthetized, paralyzed cat (n = 7) ventilated with either room air or 100% oxygen. While receiving room air, there were increases (p < 0.005) in renal SNA of 34.5 +/- 4.2%, 53.3 +/- 6.4%, and 59.9 +/- 7.2% of maximum during the 20-, 40-, and 60-s apneas, respectively. There were corresponding increases (p < 0.025) in mean arterial pressure (Pal of 9 +/- 3, 30 +/- 9, and 45 +/- 12 man Hg during the 20-, 40-, and 60-s apneas while receiving room air, respectively. The effect of 100% oxygen was to reduce (p < 0.0001) the renal SNA response to apnea, at a matched level of Pa-co2, by at least 80%, and to eliminate any increase in Pa. During the first breath of the postapneic period, there was a partial inhibition of renal SNA. During the second and third breaths of the postapneic period, there was a marked fall in renal SNA that was associated with a precipitous decline in directly recorded carotid chemoreceptor activity (n = 2). The magnitude of the fall in renalSNA after apnea was related to the degree of postapneic hypertension. We conclude that hypoxic chemoreceptor stimulation is the predominantfactor generating the renal SNA response to apnea, with modulating inputs from thoracic afferents and arterial baroreceptors likely contributing to the marked inhibition of renal SNA immediately after the apnea.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 09:57:18