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1.
Biol. Res ; 51: 57, 2018. tab, graf
Article Dans Anglais | LILACS | ID: biblio-1011401

Résumé

BACKGROUND: chronic hypoxia increases basal ventilation and pulmonary vascular resistance, with variable changes in arterial blood pressure and heart rate, but it's impact on heart rate variability and autonomic regulation have been less well examined. We studied changes in arterial blood pressure, heart rate and heart rate variability (HRV) in rabbits subjected to chronic normobaric hypoxia (CNH; PB ~ 719 mmHg; FIO2 ~ 9.2%) for 14 days and assess the effect of autonomic control by acute bilateral vagal denervation. RESULTS: exposure to CNH stalled animal weight gain and increased the hematocrit, without affecting heart rate or arterial blood pressure. Nevertheless, Poincaré plots of the electrocardiographic R-R intervals showed a reduced distribution parallel to the line of identity, which interpreted as reduced long-term HRV. In the frequency domain, CNH reduced the very-low- (< 0.2 Hz) and high-frequency components (> 0.8 Hz) of the R-R spectrograms and produced a prominent component in the low-frequency component (0.2-0.5 Hz) of the power spectrum. In control and CNH exposed rabbits, bilateral vagotomy had no apparent effect on the short- and long-term HRV in the Poincaré plots. However, bilateral vagotomy differentially affected higher-frequency components (> 0.8 Hz); reducing it in control animals without modifying it in CNH-exposed rabbits. CONCLUSIONS: These results suggest that CNH exposure shifts the autonomic balance of heart rate towards a sympathetic predominance without modifying resting heart rate or arterial blood pressure.


Sujets)
Animaux , Mâle , Lapins , Vagotomie , Pression sanguine/physiologie , Rythme cardiaque/physiologie , Hypoxie/physiopathologie , Glycémie/physiologie , Poids/physiologie , Maladie chronique , Modèles animaux de maladie humaine , Hématocrite
2.
The Korean Journal of Physiology and Pharmacology ; : 89-94, 2004.
Article Dans Anglais | WPRIM | ID: wpr-728497

Résumé

The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 (0.1, 1, 10, 20 ng/2mul) or Ang II (600 ng/10mul). A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. IL-1beta increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. IL-1beta. Both i.c.v. IL-1alpha and beta produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of IL-1beta, the magnitude of MAP fall was not different from the control. The IL-1beta group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.


Sujets)
Animaux , Rats , Potentiels d'action , Angiotensine-II , Angiotensines , Pression artérielle , Système nerveux autonome , Baroréflexe , Cathéters , Système nerveux central , Artère fémorale , Verre , Rythme cardiaque , Hémorragie , Hypertension artérielle , Injections veineuses , Interleukine-1 , Ventricules latéraux , Microélectrodes , Neurones , Nitroprussiate , Rat Sprague-Dawley , Système nerveux sympathique , Vasopressines
3.
The Korean Journal of Physiology and Pharmacology ; : 287-295, 1998.
Article Dans Anglais | WPRIM | ID: wpr-727531

Résumé

Diazepam is known to have cardiovascular depressive effects through a combined action on benzodiazepinergic receptor and the GABA receptor-chloride ion channel complex. Moreover, it is known that barbiturates also have some cardiovascular regulatory effects mediated by the central GABAergic system. Therefore, this study was undertaken to delineate the regulatory actions and interactions of these systems by measuring the responses of the cardiovascular system and renal nerve activity to muscimol, diazepam and pentobarbital, administered intracerebroventricularly in rabbits. When muscimol (0.03~-0.3 microgram/kg), diazepam (10~100 microgram/kg) and pentobarbital (1-10 microgram/kg) were injected into the lateral ventricle of the rabbit brain, there were similar dose-dependent decreases in blood pressure (BP) and renal nerve activity (RNA). The relative potency of the three drugs in decreasing BP and RNA was muscimol > pentobarbital >diazepam. Muscimol and pentobarbital also decreased the heart rate in a dose-dependent manner; however, diazepam produced a trivial, dose-independent decrease in heart rate. Diazepam (30 microgram/kg) pentobarbital (3 microgram/kg) did not. Bicuculline (0.5 microgram/kg), a GABAergic receptor blocker, significantly augmented the effect of muscimol (0.1 microgram/kg) in decreasing blood pressure and renal nerve activity, but of pentobarbital in decreasing BP and RNA, either alone or with muscimol. We inferred that the central benzodiazepinergic and barbiturate systems help regulate peripheral cardiovascular function by modulating the GABAergic system, which adjusts the output of the vasomotor center and hence controls peripheral sympathetic tone. Benzodiazepines more readily modulate the GABAergic system than barbiturates.


Sujets)
Lapins , Barbituriques , Benzodiazépines , Bicuculline , Pression sanguine , Encéphale , Système cardiovasculaire , Diazépam , Acide gamma-amino-butyrique , Rythme cardiaque , Canaux ioniques , Ventricules latéraux , Muscimol , Pentobarbital , ARN
4.
Japanese Journal of Physical Fitness and Sports Medicine ; : 114-119, 1990.
Article Dans Japonais | WPRIM | ID: wpr-371487

Résumé

Eighteen persons with both severe mental retardation and severe physical disabilities and ten normal persons participated to investigate cardiovascular response to hydrostatic pressure stress using supine and sitting positions. All of the handicapped subjects lay down on the bed during the entire day. They were classified into three groups. That is, the first group (LD) had not opportunity of sitting passively in daily living at all. Another two groups were given opportunity of sitting. In addition, the second group (ST 1) was unable to sit and stand independently in the past but the third group (ST 2) was able. The LD showed unchanged heart rate and decreased blood pressure with reduced peripheral blood flow in the sitting position. This suggested that serious lower function or dysfunction in both central and peripheral circulatory system. The cardiovascular function of the ST 1 was characterized by elevated heart rate and lowered blood pressure. This seemed to indicate lower baroreflex control to the peripheral vascular system. The ST 2 demonstrated similar function to the normal persons. The cardiovascular regulation in the severely handicapped persons may depend on opportu-unity of taking orthostatic posture in daily living in addition to motor adility in the past.

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