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

10 patients with juvenile hypertension were investigated during normoxia, hypoxia and hyperoxia in comparison to 10 healthy volunteers. The results of heart rate, stroke volume, cardiac output and blood pressure in supine position as well as in passive orthostasis are significantly different in both groups. It seems that in the initial phase of hypertension the arterial chemoreceptors might be on an enhanced functional state.
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PMID:Orthostatic cardiovascular regulation during hypoxia and hyperoxia in patients with juvenile hypertension. 345 76

The study was carried out in 30 subjects with mild primary hypertension and in 82 normotensive age-matched volunteers, 18-20 years of age. Hyperoxia test was used to withdraw the tonic chemoreceptor reflex drive. The following circulatory and respiratory effects of short lasting hyperoxia were observed in the hypertensive group and in most of the normotensive subjects yet with a family background of hypertension: a decrease in the mean arterial pressure, in total peripheral vascular resistance, and in forearm vascular resistance, and a significantly greater reduction of the resting ventilation as compared to the normotensive group. Our results suggest that the augmented arterial chemoreceptor drive is one of the mechanisms responsible for the elevated arterial blood pressure and total peripheral resistance in early human hypertension. The positive response to hyperoxia test in healthy subjects with a family background of hypertension suggests a familial occurrence of the hyperactivity of the arterial chemoreceptors.
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PMID:Augmented chemoreceptor reflex tonic drive in early human hypertension and in normotensive subjects with family background of hypertension. 383 54

We tested the hypothesis that in renal hypertension the increased peripheral vascular resistance of neurogenic origin might be due to a reflex through resetting of the carotid body chemoreceptors. The reflex respiratory and cardiovascular functions of the carotid bodies were studied in a one-kidney wrapped hypertension model in conscious rabbits, and compared with a control group of animals, by breathing 100% oxygen, three hypoxic gas mixtures to which were added sufficient CO2 to maintain the PaCO2 constant, and 2 and 4% CO2 in 21% O2 and N2. In the control state (breathing room air) the renal hypertensive animals had a slightly higher respiratory minute volume, a higher level of arterial blood pressure and increased calculated systemic vascular resistance, compared with the normal group, but there was no difference in cardiac output. Hyperoxia had no consistent effect on respiration, heart rate or arterial blood pressure. Increasing degrees of isocapnic hypoxia caused the same degree of hyperventilation and bradycardia in both groups of animals. The arterial blood pressure did not change in either group but there was a transient increase in systemic vascular resistance in the renal hypertensives breathing 9 and 7.5% O2. The respiratory responses to 2 and 4% CO2 were similar in the two groups of animals. In the renal hypertensive animals, serial sections of the carotid bodies showed pathological changes, including subendothelial proliferation in vessels supplying the carotid bodies with narrowing of their lumens, fragmentation of the elastic laminae of the media, hypertrophy of the smooth muscle and extensive fibrosis with occasional haemorrhages. The capillaries, however, were normal. The rostral-caudal lengths of the carotid bodies were similar in the two groups. In view of our findings we conclude that the relatively normal carotid chemoreceptor responses in renal hypertensive rabbits may, in part at least, be the result of the carotid body blood flow through the partially occluded vessels being maintained at near normal levels by the elevated blood pressure.
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PMID:Respiratory and cardiovascular responses to hyperoxia, hypoxia and hypercapnia in the renal hypertensive rabbit: role of carotid body chemoreceptors. 402 Jan 28

In rats anesthetized by pentobarbital, hyperoxia, induced by inhalation of 100% O2 for 5 minutes, provokes transient bradycardia and long lasting systemic arterial hypertension. Pure oxygen initially depresses ventilation for 3 minutes. Blockade of alpha 1 adrenergic receptors does not suppress arterial hypertension, which appears to be due to a direct vasoconstriction.
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PMID:[Effects of ventilatory hyperoxia in the rat]. 646 3

In normotensive Wistar rats of a random-bred strain and in spontaneously hypertensive rats (SHR) of the Okamoto-Aoki-strain, the mean systemic arterial blood pressure, the pO2, pCO2, pH-values and the base excess of the arterial blood were measured during ventilating normal air as well as hypoxic (12.6% O2 in N2) and hyperoxic (100% O2) gas mixtures. The animals were anaesthetized and breathed spontaneously; they aged 5-6, 15-20, 30-40, and 50-70 weeks. The volume of their carotid bodies was determined morphometrically. When compared with the age-matched normotensive controls at an age of 5-6 weeks the SHR already exhibited slightly but significantly elevated blood pressures but had equal carotid body size and arterial carbon dioxide tension. In contrast, hypertensive animals in the established phase of hypertension (older than 15 weeks) showed greater carotid bodies and a highly significant respiratory alkalosis when compared with the corresponding age-group of the normotensive rats. The reactions of the mean systemic arterial blood pressure and the arterial pCO2 provoked by hypoxia and hyperoxia proved to be age-dependent in both the normotensive and hypertensive animals but this influence of age was different in the two strains of rats. The data support the concept that alterations of arterial chemoreceptor structures and reflex effects found in the established phase of hypertension are the result of this disease. Furthermore they indicate that, when interpreting arterial chemoreceptor reflex effects in hypertensive humans and animals, the stage of hypertension must be taken into account.
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PMID:Influence of age on carotid body size and arterial chemoreceptor reflex effects in spontaneously hypertensive (SHR) and normotensive rats. 673 56

Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
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PMID:Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury. 677 23

Bilateral carotid occlusion (BCO) was performed in pentobarbital anesthetized adult rats neonatally treated with capsaicin (50 mg/kg, sc, CNT rats). Pressor and ventilatory responses to BCO in CNT rats were compared with those of littermate controls injected with a same volume of solvent (olive oil, 0.1 ml). Capsaicin was used in order to produce partial degeneration of unmyelinated C fibres related to baroreflexes and peripheral chemoreflexes. In control rats, BCO provoked in less than 5 s, hyperventilation, hypocapnia and hyperoxia. Systemic arterial hypertension and tachycardia developed more slowly. They were maximum at 65 s. At this time, ventilation was returned to control values. Hyperventilation results from the stimulation of the carotid chemoreceptors by stagnant asphyxia generated by the blood flow stop. Hypertension and tachycardia are provoked by an increase in the orthosympathetic outflow when carotid baroreceptors are unloaded. In a first time, chemoreceptors stimulation tends to oppose to the increase of heart rate in normal rats. In a second one, development of hypertension is autolimited by the stimulation of the aortic baroreceptors particularly effective in rats. Simultaneously the hyperoxic inhibition from aortic chemoreceptors, the central hypocapnia and the reperfusion of the carotid bodies lead to the suppression of hyperventilation. As hyperventilation decreases when hypertension develops, even in rats with vago-sympathetic section at low cervical level, the part of aortic baroreceptors effects is probably reduced except for the fibres travelling through superior laryngeal nerves. Carotid bodies reperfusion seems to predominate. Before any manipulations, CNT rats had lower heart rate and systemic blood pressure than controls. During BCO, initial hyperventilation was moderately prolonged as hypertension slowly developed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral carotid occlusion in the rat neonatally treated with capsaicin]. 800 42

We analyzed the spatial structure of contact radiographs of barium-filled pulmonary arteries of rats raised in room air and in two environments that induce pulmonary arterial hypertension (PAH)--hypoxia and hyperoxia. We found that the spatial structure of the pulmonary arteries was fractal in both the control and the hypertensive lungs. The fractal dimension of the pulmonary arteries of the control lungs was 1.62 +/- 0.01 (mean +/- SEM), which is greater than that of both the hypoxic lungs 1.50 +/- 0.03 (p < 0.01) and the hyperoxic lungs 1.44 +/- 0.01 (p < 0.01). There was no significant difference between the hypoxic and hyperoxic lungs. The fractal dimension may be a useful clinical index to quantify pathologic changes in the pulmonary arterial tree.
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PMID:Fractal analysis of pulmonary arteries: the fractal dimension is lower in pulmonary hypertension. 811 70

After it was reported in 1981 that phenobarbital reduced the incidence of intraventricular hemorrhage from 46.7% in control infants to 13.3% in treated premature infants, routine phenobarbital prophylaxis (loading dose, 20 mg/kg; maintenance, 5 mg/kg per day for 5 days) was introduced at the hospital of the original trial for all premature infants with birth weights of < or = 1800 gm. To assess continued efficacy, we reviewed all records of these infants from 1985 through 1989. The overall incidence of intraventricular hemorrhage was 27.5% (168/612); the proportion of severe intraventricular hemorrhage (grade 3 and 4) was 41.1% (69/168). The incidence of intraventricular hemorrhage was lower when loading occurred at < 4 hours: 25.9% (124/478) versus 32.8% (44/134). Outborn infants had a higher incidence of intraventricular hemorrhage than inborn infants (45.3% vs 23.0%). In addition to already known risk factors (gestational age, vaginal delivery, outborn status, pneumothorax, birth asphyxia, patent ductus arteriosus), intraventricular hemorrhage occurred more often in infants with hyperoxia (PO2 > 180 mmHg), hypocarbia (PcO2 > 28 mmHg), hypercarbia (PcO2 > 55 mmHg), and hypotension and hypertension (blood pressure > norm +/- 15 mmHg). These results support the hypothesis that phenobarbital has a role in the prophylaxis against intraventricular hemorrhage. Differences in the efficacy of phenobarbital prophylaxis between various studies may be caused by variations of age at loading and differences in the proportion of very low birth weight infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Routine administration of phenobarbital for the prevention of intraventricular hemorrhage in premature infants: five years' experience. 816 72

These studies were undertaken to determine the relationship of early changes in the synthesis rates and contents of collagen, elastin, and soluble tissue protein of pulmonary arteries in rats exposed chronically to normobaric hyperoxia. The growth response of pulmonary arteries was characterized by proportionate increases in the contents of the three protein fractions after 7 days (130% of control) and 21 days (194% of control) of exposure. Fractional rates of protein synthesis were assessed both in vivo and in vitro with the use of several radiolabeled amino acids as tracers to minimize uncertainties of the relationships of the specific radioactivities of measured amino acid pools and the precursors for the proteins fractions. Values for fractional synthesis rates of collagen, elastin, and soluble protein in vitro in pulmonary arteries isolated from control rats were 2.2, 1.6, and 19%/day, respectively. Rates of synthesis of collagen and soluble protein in vitro were approximately 20% lower than that determined in control rats in vivo. The fractional synthesis rates of the three protein fractions in isolated arteries from experimental rats were unchanged after 1 day of hyperoxic exposure, decreased marginally after 3 days, and markedly increased after 7 days. At this time the absolute increments in the fractional synthesis rates of collagen (+4.7%/day) and elastin (+5.0%/day) were less than that of soluble tissue protein (+16%/day) and were more comparable to the accumulation rate of proteins in the tissue. The disproportionate increment in the fractional rate of soluble protein synthesis suggests that the fractional rate of degradation of soluble protein was also increased during the growth response in this model of hypertension.
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PMID:Protein synthesis in pulmonary arteries from rats exposed to hyperoxia. 843 Aug 19


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