Publications by authors named "Angell-James J"

The antihypertensive effects and safety profiles of lisinopril (10 to 40 mg) and atenolol (50 to 100 mg) were compared in a randomized, double-blind, parallel group trial in 144 patients with essential hypertension. After 8 weeks of therapy, seated blood pressure (BP) decreased by 26/15 mm Hg with lisinopril and by 19/14 mm Hg with atenolol. Lisinopril produced a greater reduction (p less than 0.

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We tested the following hypothesis: if carotid body blood flow, and hence the relationship of the frequency of discharge in chemoreceptor afferent fibres to arterial PO2, were affected by atherosclerotic change, then a modification of the control of the respiratory and cardiovascular systems might result. Carotid body reflexes were therefore studied in conscious atherosclerotic rabbits and a control group of normal animals breathing 100% O2, three hypoxic gas mixtures to which was added sufficient CO2 to maintain the arterial PCO2 constant, and 2% and 4% CO2 in 21% O2 and N2. When breathing room air, the atherosclerotic rabbits breathed at a higher respiratory frequency and lower tidal volume than the normal animals, although there was no difference in the respiratory minute volume.

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In order to assess whether carotid endarterectomy had any long-term hypotensive effect, by altering the function of the carotid sinus baroreceptors, blood pressure and carotid sinus baroreceptor function were recorded in 25 patients undergoing carotid endarterectomy. No overall change in blood pressure was recorded 6 months after surgery. Sinus function was shown to decrease in 2 (8 per cent), to remain unchanged in 15 (60 per cent) and to increase in 8 (32 per cent) patients 6 months postoperatively.

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The neonatal death of calves and lambs is responsible for a heavy financial loss to the farming industry; respiratory failure accounts for 6 per cent of the post parturient deaths in lambs. A simple method of pulmonary resuscitation with expired air is described employing a device portable and simple enough for emergency use by herdsmen and shepherds. The rationale of the use of the equipment is explained.

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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.

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In the anesthetized harbor seal, Phoca vitulina, the Hering-Breuer inflation reflex was weak and comparable to that in humans. Single inflations of the lungs from a syringe during the expiratory phase of normal breathing caused temporary inhibition of breathing and an immediate tachycardia dependent on the integrity of the cervical vagosympathetic nerves. A similar cardiac response occurred when the lungs were artificially inflated during an experimental dive and under conditions in which apnea and bradycardia were reflexly induced by a combination of stimulation of the carotid body chemoreceptors and of the trigeminal or laryngeal input.

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We studied the reflex control of blood pressure, heart rate, and hindlimb vascular resistance by the carotid sinus baroreceptors in normal (N), experimental renal hypertensive (RH, one kidney renal wrap model), and medial sclerotic (MS) rabbits under urethane anaesthesia using an isolated perfused carotid sinus preparation and auto-perfused hindlimb. The contralateral carotid sinus was denervated. Compared to N rabbits, the blood pressure and hindlimb vascular resistance of RH and MS rabbits were significantly elevated at all carotid sinus pressures 15 weeks after inducing the disease process.

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Baroreflex sensitivity was assessed in 9 normotensive (N), 8 renal wrap (one kidney model, RH) and 16 medial sclerotic rabbits (MS, fed on calciferol 50,000 i.u. and calcium lactate 1g for 10 days) before (mean BP;N, 79 +/- 3.

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Stimulation of the carotid-body chemo-receptors by asphyxia during an apnoeic episode may contribute to the vagally mediated cardiac arrest and sudden death that sometimes occurs in man. Apnoeic asphyxia may be induced centrally or reflexly by stimulation of upper airways receptors. Conditions associated with apnoeic asphyxia and in which the risk is likely to be greatest include intubation, laryngoscopy and bronchoscopy; accidents involving underwater swimming; inhalation of sympathomimetic amines in aerosols by asthmatic patients; and chronic hypoventilation syndromes.

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1. The carotid bodies were stimulated in the anaesthetized pig-tailed macaque monkey (M. nemestrina) using (i) brief injections of cyanide or CO2-equilibrated bicarbonate solution into a common carotid artery, and (ii) longer perfusion with hypoxic hypercapnic blood in vascularly isolated chemoreceptor preparations.

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The carotid bodies were stimulated in the anesthetized pig-tailed macaque monkey (Macaca nemestrina) using i) brief injections of cyanide or CO2-equilibrated bicarbonate solution into a common carotid artery, and ii) longer perfusion with hypoxic hypercapnic blood in vascularly isolated chemoreceptor preparations. In spontaneously breathing animals, brief stimulations of the chemoreceptors consistently caused an increase in pulmonary ventilation, bradycardia, and an increase in femoral vascular resistance. When the same chemoreceptor stimulus was superimposed during the apneic period, reflexly evoked by stimulating either the central ends of the superior laryngeal nerves or the nasopharynx, the respiratory stimulation was absent or minimal, but the bradycardia and vasconstriction were greatly enhanced and exceeded the summed responses of separate stimulation of the chemoreceptors and one or the other of the upper-airways inputs.

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1. The cardiac effects of artificial inflation of the lungs were studied during reflexly induced apnoea and bradycardia in anaesthetized dogs.2.

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In the anesthetized spontaneously breathing harbor seal Phoca vitulina stimulation of the carotid body chemoreceptors by intracarotid injections of sodium cyanide or by hypoxic hypercapnic blood causes an increase in tidal volume, respiratory frequency, and respiratory minute volume. The heart rate invariably decreased. Experimental dives caused apnea and bradycardia.

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The diving responses of apnea and bradycardia, produced experimentally by immersing the face in water, were successfully elicited in the harbor seal Phoca vitulina anesthetized with urethan. The role of the carotid body chemoreceptors in the production of the diving bradycardia was studied in isolated carotid sinus-body preparations autoperfused with blood from the arterial circulation. When asphyxia was well developed during a dive the chemoreceptor drive was withdrawn by temporarily perfusing the chemoreceptors with blood of high PO2 (greater than 400 mmHg) and normal PCO2 from a disk oxygenator.

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1. Hypertension was produced experimentally in three groups of rabbits by atherosclerosis, meical sclerosis and renal encapsulation. 2.

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