Systemic arterial pressure wave reflections during acute hemorrhage*

In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N–REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks. On a étudié avec des méthodes polygrafiques trois sujets (1 homme et deux femmes) souffrant d'hémicranie chronique avec des crises nocturnes. Chez deux malades les crises étaient précédées d'augmentation et d'irrégularité de la tension artérielle. Ces modifications commençaient pendant le sommeil N-REM et contineaient pendant le sommeil REM qui précédait le réveil avec hémicranie. La fréquence cardiaque n'a pas subi de modification avant les crises. Les résultats obtenus ne confirment l'hypothèse selon laquelle le facteur causant les crises est l'instabilité anticronique à la fase REM. Sono stati studiati con metodiche poligrafiche 3 soggetti (1 maschio e 2 femmine) affetti da emicrania cronica con attacchi notturni. In 2 di essi gli attacchi erano preceduti da incrementi ed irregolarità della pressione arteriosa. Tali modificazioni iniziavano durante il sonno N-REM e perduravano nel corso del sonno REM che precedeva il risveglio con cefalea. La frequenza cardiaca non si modificava prima dell'attacco. I risultati ottenuti non confermano l'ipotesi che il fattore precipitante gli attacchi emicranici sia l'instabilità anticronica della fase REM.

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Chronic EDRF inhibition and hypoxia: effects on pulmonary circulation and systemic blood pressure

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.4.1748 ◽

1993 ◽

Vol 75 (4) ◽

pp. 1748-1757 ◽

Cited By ~ 77

Author(s):

V. Hampl ◽

S. L. Archer ◽

D. P. Nelson ◽

E. K. Weir

Keyword(s):

Pulmonary Hypertension ◽

Arterial Pressure ◽

Chronic Hypoxia ◽

Acute Hypoxia ◽

Systemic Blood Pressure ◽

Systemic Circulation ◽

Systemic Arterial Pressure ◽

Hypoxic Pulmonary Hypertension ◽

Basal Tone ◽

Isolated Lungs

It has been suggested that chronic hypoxic pulmonary hypertension results from chronic hypoxic inhibition of endothelium-derived relaxing factor (EDRF) synthesis. We tested this hypothesis by studying whether chronic EDRF inhibition by N omega-nitro-L-arginine methyl ester (L-NAME) would induce pulmonary hypertension similar to that found in chronic hypoxia. L-NAME (1.85 mM) was given for 3 wk in drinking water to rats living in normoxia or hypoxia. Unlike chronic hypoxia, chronic L-NAME treatment did not increase pulmonary arterial pressure. Cardiac output was reduced and mean systemic arterial pressure was increased by chronic L-NAME treatment. The vascular pressure-flow relationship in isolated lungs was shifted toward higher pressures by chronic hypoxia and, to a lesser degree, by L-NAME intake. In isolated lungs, vasoconstriction in response to angiotensin II and acute hypoxia and vasodilation in response to sodium nitroprusside were increased by chronic L-NAME treatment in normoxia and chronic hypoxia. Chronic hypoxia, but not L-NAME, induced hypertensive pulmonary vascular remodeling. Chronic supplementation with the EDRF precursor L-arginine did not have any significant effect on chronic hypoxic pulmonary hypertension. We conclude that the chronic EDRF deficiency state, induced by L-NAME, does not mimic chronic hypoxic pulmonary hypertension in our model. In addition, EDRF proved to be less important for basal tone regulation in the pulmonary than in the systemic circulation.

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