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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiovascular responses to breath-holding (BH) during short-lasting supramaximal exercise (415 W) on a cycle ergometer were investigated in 15 healthy male subjects. The arterial oxygen saturation, heart rate (HR), endtidal PO2 and PCO2 were continuously monitored. Firstly, 15 subjects performed exercise during BH, preceded by air breathing (air-BH test), and secondly, exercise without BH. Then 9 of the subjects performed the same procedure as in the air-BH test, except that all subjects breathed 100% O2 for 1 min before apnoea (O2-BH test). In 2 of these subjects, the systemic arterial blood pressure was continuously measured via a catheter in the radial artery and plasma catecholamine concentration [CA] was also measured both during the air-BH and the O2-BH tests. In the later period of the air-BH test, the high HR level became progressively depressed. This response, however, was absent in the O2-BH test. There was a late increase in the arterial blood pressure in both tests, and both tests produced hypercapnia. Only the air-BH test resulted in hypoxia, substantial hypertension and HR-depression. The increase in plasma CA was similar in both tests. The marked HR-depression demonstrated here is ascribed mainly to activation of the peripheral arterial chemoreceptors by asphyxia, and partially to baroreceptor activity due to elevated blood pressure.
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PMID:Heart rate response to breath-holding during supramaximal exercise. 258 43

During the last years, medical interest has focused on sleep related diseases, especially the sleep apnea syndrome (SAS) and the nocturnal breathing abnormalities associated with broncho-pulmonary diseases. It now appears that SAS is far more prevalent than previously believed. In this review article we present the clinical features, the investigations and the current therapeutic methods. We also discuss the recent developments in our understanding of the SAS pathophysiology and their implications in the disease's management. Clinical importance of sleep related disorders of breathing is appreciated when one looks at some of the secondary effects including hypertension, angina pectoris, cardiac insufficiency and worsening of a broncho-pulmonary disease (hypoxemia, hypercapnia); these are associated with a high degree of morbidity. The recent advent of ambulatory screening systems allows an easier evaluation of patients at risk, such as obese or hypertensive snorers and patients with hypersomnolence; then the diagnostic polysomnographic studies can be reserved for subjects in whom home recording is abnormal. A precise and early diagnosis is important to allow the initiation of treatment such as Continuous Positive Airway Pressure (CPAP) or naso-pharyngeal surgery.
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PMID:[The sleep apnea syndrome. A general review]. 265 45

The cerebral blood flow is maintained at a constant level in spite of blood pressure variations, because of a very performing auto-regulation phenomenon: vasoconstriction in case of elevated blood pressure, vasodilatation in case of blood pressure drop. The upper limit of the mean blood pressure beyond which nothing can prevent the cerebral blood flow from increasing, ranges between 150 and 170 mmHg. The lower limit, from which the dilatation of the cerebral blood vessels is not able to prevent the decreased cerebral blood flow, has been set between 50 and 70 mmHg. The auto-regulation of the cerebral blood flow is influenced by numerous factors: hypercapnia, hypoxia and ischemia complete inhibit it, making the cerebral blood flow directly related to the blood pressure; the sympathetic stimulation shifts the entire curve toward the right, because of the constriction of the pia-mater arteries, followed with a reactional vasodilatation of the small cerebral vessels. In the course of chronic arterial hypertension, the same shift of the auto-regulation curve toward high pressures is observed, related to structural alterations of the vascular wall; this make them more prone to constriction than dilatation: when these alterations are reversible, antihypertensive treatment may sometimes bring the auto-regulation curve in its initial position.
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PMID:[The brain and arterial hypertension. 1. Physiologic and physiopathologic aspects]. 266 Jul 35

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
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PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

Calcium channel blockers such as nicardipine act as arterial vasodilators and are effective in the treatment of hypertension. Although they are also effective tocolytic agents, fetal effects have not been fully studied. Fifteen chronically catheterized near-term ewes were studied. Maternal and fetal cardiorespiratory parameters were measured in the control period and again 15 minutes after maternal venous infusion of angiotensin II. Nicardipine 20 micrograms/kg/min was given over 2 minutes and maternal and fetal cardiorespiratory parameters and fetal blood flow were measured 5.30 and 60 minutes later. Nicardipine reversed maternal hypertension and produced transient tachycardia. Fetuses responded initially with transient bradycardia and then developed hypercapnia and acidemia (p less than 0.03) by 60 minutes after nicardipine. Fetal placental blood flow decreased and vascular resistance increased by 5 minutes after nicardipine but returned toward control values after 30 minutes. Unexpectedly we observed the death of five fetuses by 65 minutes after nicardipine. We conclude that the administration of nicardipine in the hypertensive ewe results in significant alterations of fetal cardiorespiratory status and placental function that may lead to acidemia.
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PMID:Fetal vascular responses to maternal nicardipine administration in the hypertensive ewe. 280 19

When a patient with chronic obstructive pulmonary disease (COPD) requires medical therapy for systemic hypertension, a number of special considerations may affect the choice of antihypertensive drug and subsequent management. Thiazide diuretics have no adverse effect on airway function and are the agents of choice for initial therapy. beta-Antagonists are usually considered first-line agents in antihypertensive therapy, but even relatively cardioselective ones may increase airway resistance in patients with obstructive lung diseases, and they should be used with caution, if at all, in such patients. Although potassium-wasting diuretics are the preferred agents for treating hypertension in patients with COPD, they may worsen carbon dioxide retention in hypoventilating patients and potentiate hypokalemia in those receiving corticosteroids. In addition, beta-agonists may substantially lower serum potassium levels in patients already rendered hypokalemic by diuretics. Patients with COPD receiving potassium-wasting diuretics who have chronic respiratory acidosis or are receiving corticosteroids or beta-agonists should undergo close monitoring of electrolyte levels and be considered for therapy with potassium supplements or, preferably, potassium-sparing agents.
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PMID:Fluid and electrolyte considerations in diuretic therapy for hypertensive patients with chronic obstructive pulmonary disease. 286 47

Arterial hypertension developed in a horse anesthetized for arthroscopy and lavage of an inflamed right carpal joint. Anesthesia was induced with xylazine HCl, butorphanol, guaifenesin, and thiamylal Na and was maintained with halothane in oxygen. Arterial hypertension and tachycardia developed within 15 minutes after a pneumatic tourniquet was placed 8 to 10 cm proximal to the right carpus and inflated to 800 mm of Hg. The surgical procedure was expedited, halothane was discontinued and anesthesia was maintained with guaifenesin to facilitate bandaging. Heart rate decreased from 72 to 42 beats/min after the tourniquet cuff was deflated. Mean arterial pressure decreased from 260 mm of Hg to 128 mm of Hg. Differential diagnosis for a rapidly increasing arterial pressure during halothane anesthesia include inadequate plane of anesthesia, signs of pain, hypercapnia, hypoxemia, and/or hyperthermia.
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PMID:Tourniquet-induced hypertension in a horse. 291 9

Cerebral blood flow was measured and compared in 10 symmetrical brain regions following unilateral trigeminal ganglionectomy (n = 13), sham operation (n = 6), or trigeminal root section (rhizotomy) (n = 8) in cats. Multiple determinations were obtained in anesthetized and paralyzed animals using radiolabeled microspheres during (i) normocapnia-normotension, (ii) hypercapnia (5% CO2/95% room air), (iii) angiotensin-induced acute severe hypertension (190 greater than mean arterial blood pressure less than 210 mmHg), or (iv) bicuculline-induced seizures. Flow was symmetrical in all brain regions at rest and during increases induced by hypercapnia in the three groups. During severe hypertension or seizures, marked elevations developed bilaterally (approximately 93% and approximately 130%, respectively). In ganglionectomized animals, increases due to hypertension or seizures were attenuated by 28-32% on the denervated side within cortical gray matter regions corresponding to the anterior, middle, and posterior cerebral arteries. Flow was symmetrical within all brain regions in sham-operated animals and in the rhizotomy group, despite comparable increases in regional cerebral blood flow induced by angiotensin. Hence, the trigeminal nerve mediates blood flow adaptations during severe hypertension and seizures. Furthermore, since trigeminal cell bodies and peripheral axons are destroyed or degenerate following ganglionectomy but not following rhizotomy, local "axon reflex-like" mechanisms mediate these increases in cerebral blood flow.
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PMID:Trigeminovascular fibers increase blood flow in cortical gray matter by axon reflex-like mechanisms during acute severe hypertension or seizures. 291 86

The histories and the results of the postmortem examinations of 507 patients with chronic pulmonary heart disease were studied. In 62.6% of them left ventricular hypertrophy was found. As probable causes for this left ventricular hypertrophy are suggested: arterial hypertension, ischemic heart disease, hypoxemia, hypercapnia, heart failure, diabetes mellitus. The weight measurement correlations between the left and the right heart ventricles were studied in: "normal hearts", hearts with right ventricular, hypertrophy only, hypertrophy of both ventricles, left ventricular hypertrophy only. A correlation between the mass increase and the wall thickness of the ventricles was established. In the patients with chronic pulmonary heart disease and hypertrophy of both ventricles the mass and the wall thickness of the ventricles increase simultaneously. The possible pathogenetic mechanisms of the left ventricular involvement in patients with chronic pulmonary heart disease are discussed.
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PMID:[Left heart ventricle in chronic cor pulmonale patients. Etiological, pathomorphological and organ weight measurement studies]. 296 38

Blood flow in the feline thoracic spinal cord was measured, using a laser-Doppler flowmetry. Rhythmic changes in the spinal cord blood flow were repeatedly observed with a frequency of about three to eight cycles per minute, unrelated to the respiratory or cardiac cycles. These changes were unaffected by hypertension induced by angiotensin II, but disappeared when systemic blood pressure was lowered by trimethaphan or when hypercapnia was induced. CO2 responsiveness of the blood flow and postocclusive reactive hyperemia were also examined, in both the normal and injured spinal cord. CO2 responsiveness was lost 1 h after a 500 gm/cm injury without rhythmic changes, but was partially regained 2 days later, at which time rhythmic changes were frequently observed. Postocclusive hyperemia apparently diminished 1 h after a 500 gm/cm injury, but reappeared 2 days later. Vasomotion in the normal and injured spinal cord is discussed.
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PMID:Vasomotion in normal and injured spinal cord. 296 40


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