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Biomedical subjects

C Prys-Roberts

Publications and source records attributed to C Prys-Roberts.

At least 127 records · Page 7Linked to original sources
PubMed1979

Cardiovascular studies during induction with minaxolone.

The cardiovascular effects of induction of anesthesia with minaxolone, a new water soluble steroid agent, have been studied in 12 normotensive patients and 5 patients with treated hypertension. The arterial pressure, heart rate and ECG were continuously recorded before and during induction of anesthesia with Minaxolone 0.5 mg kg-1. Cardiac output measurements were made in the awake patient, at 3 minutes after the induction of anesthesia and 2 minutes after an increment of the drug. In both groups of patients, induction of anesthesia led to a decrease in systolic arterial pressure and a smaller decrease in diastolic arterial pressures. This was coupled with an increase in the heart rate. The decrease in cardiac output was similar in both the normal and treated hypertensive patients. Administration of an increment of minaxolone (0.1 mg kg-1) did not produce further significant changes in the cardiovascular variables. The results of this study show that the changes in hemodynamic variables with minaxolone are comparable with those seen following induction of anesthesia with other intravenous agents, with the one difference in that there was only minimal change in the diastolic arterial pressure.

Anesthesia, Intravenous↗
PubMed1977

Haemodynamic responses to isoflurane anaesthesia and hypovolaemia in the dog, and their modification by propranolol.

In six dogs chronically implanted with flow and pressure transducers, equipotent inspired concentrations of halothane and isoflurane were determined as the minimum inspried concentration of each agent which would abolish an individual dog's response to paw clamping. In equipotent concentration, isoflurane (1.2%, SD 0.2%) caused less myocardial depression than halothane (1.0%, SD 0.1%). Dose-response studies were possible up to a mean inspired isoflurane concentration of 3.0%, both before and after propranolol 0.3 mg kg-1, i.v. After propranolol, sensitive indices of myocardial contractility were depressed at all concentrations of isoflurane, indicating a moderate degree of beta-receptor activation by isoflurane. The haemodynamic response to hypovolaemia during isoflurane anaesthesia was not modified by propranolol.

Anesthesia, Inhalation↗
PubMed1977

Haemodynamic responses to enflurane anaesthesia and hypovolaemia in the dog, and their modification by propranolol.

The haemodynamic responses to minimum equipotent concentrations of halothane and enflurane were compared in seven dogs. The haemodynamic responses to increasing concentrations of enflurane, and to induced hypovolaemia during enflurane anaesthesia, were studied in the same dogs, both before and after administration of propranolol 0.3 mg kg-1 i.v. In equipotent concentrations, enflurane caused marginally greater impairment of left ventricular function than halothane, and caused a dose-dependent reduction of arterial pressure, cardiac output and myocardial contractility. Following administration of propranolol, these haemodynamic effects of enflurane were marked, and withdrawal of 20% of estimated blood volume was tolerated poorly.

Anesthesia, Inhalation↗
PubMed1976

Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. II: The effects of acute arterial hypoxaemia at increasing depths of halothane anaesthesia.

Beta-adrenergic blockade may impair the normal cardiovascular response to hypoxia occurring during general anaesthesia. The haemodynamic effects of acute hypoxia, induced by a 90-s period of ventilation with nitrogen, were studied during increasing depths of halothane anaesthesia up to a maximum of 2.5% inspired halothane in dogs chronically implanted with intracardiac catheters, a left-ventricular pressure transducer and an aortic blood flow transducer. An untreated group of dogs and a group which had been treated for 3 weeks with propranolol 20 mg/kg/day were compared. The beta-blocked group had lesser cardiac output values, left-ventricular contractility indices, external left-ventricular work and peak left-ventricular power at all depths of anaesthesia except 2.5% halothane, but both groups responded to hypoxia similarly at each depth of anaesthesia. Cardiac performance was enhanced in both groups during acute hypoxia. No adverse haemodynamic effect of the combination of propranolol, halothane and hypoxia was demonstrated.

Anesthesia, General↗
PubMed1976

Interaction of anesthesia, beta-receptor blockade, and blood loss in dogs with induced myocardial infarction.

The cardiovascular effects of halothane-nitrous oxide anesthesia, and beta-receptor blockade with either propranolol or practolol, were studied in 15 dogs in which severe myocardial infarction had been induced ten days earlier. The hemodynamic responses to blood loss amounting to 25 per cent of estimated blood volume, and its subsequent replacement, were studied before and after induction of beta-receptor blockade. In terms of cardiac output and aortic blood flow acceleration, cardiac performance in the absence of beta-blockade was markedly impaired during steady-state anesthesia, compared with corresponding values in normal dogs. Practolol (2.0 mg/kg) administered during anesthesia induced no significant circulatory change other than a 14 per cent decrease in heart rate and a 25 per cent increase in strode volum. Propranolol (0.3 mg/kg) caused a comparable reduction of heart rate, but significantly reduced cardiac output (-27 per cent), aortic blood flow acceleration (-26 per cent), and peak LV power (-19 per cent), and increased systemic vascular resistance (+49 per cent). The two drugs caused comparable shifts of the isoproterenol dose-response curve during anesthesia. Graduated blood loss during anesthesia, to a total of 25 per cent of blood volume, caused consistent circulatory changes (decreased mean arterial pressure cardiac output, peak LV power, LV minute work) that were essentially similar before and after beta-receptor blockade with either propranolol or practolol. The positive inotropic effect of calcium gluconate during halothane anesthesia was significantly reduced following either propranolol or practolol, but the hemodynamic responses to changes of systemic vascular resistance induced with acetylcholine or phenylephrine were not modified by beta-receptor blockade.

Acetylcholine↗
PubMed1976

The Penlon Oxford ventilator. A new ventilator for adult or paediatric use.

A pneumatically powered lung ventilator for anaesthesia and intensive care of both adult and paediatric patients is described. The design criteria were selected to produce a small machine with high power, simple to control, sterilise and service. Laboratory and clinical results are presented andprocedure for clinical use of the controls suggested.

Adult↗
PubMed1976

Cardiac responsiveness to beta-adrenergic stimulation in experimental anemia.

Cardiac reactivity of beta-adrenergic stimulation was assessed by isoproterenol dose-reponse curves (dose range 0.025-0.4 mug/kg) before and 1 h after the rapid induction of anemia in dogs anesthetized with halothane:N2O:O2. Anemai (hematocrit = 16 +/- 4%) was induced by an isovolumic exchange transfusion with Dextran 70, and was followed by significant increments in cardiac output (+57 +/- 9%), max dP/dt of the left ventricle (+37 +/- 7%), and in peak acceleration of blood flow in the ascending aorta (+46 +/- 13%). Anemia was associated with a significant reduction of the chronotropic responses to all but the lowest dose of isoproterenol. The simultaneously determined inotropic responses (max dP/dt) where the same before and after the induction of anemia. The responses in terms of peak acceleration of aortic blood flow tended to be greater in the anemic than in the control phase, at all dose levels used. These findings indicate that in rapidly induced experimental anemia the heart is capable of responding to marked degrees of beta-adrenergic stimulation, representing a more than two-fold increase in the dP/dt.

Adrenergic beta-Agonists↗
PubMed1976

Medical problems of surgical patients. Hypertension and ischaemic heart disease.

Pre-existing disease in the form of hypertension or ischaemic heart disease may increase morbidity and mortality in patients presenting for anaesthesia and surgery. The interaction of these two cardiovascular conditions in relation to anaesthesia has been studied in a series of 115 patients. The results did not support the view that antihypertensive drugs and beta-receptor blocking agents should be withdrawn before anaesthesia and surgery. The main cause for concern in providing anaesthesia for these patients is that sympathetic nervous activation induced either by anaesthetic manoeuvres or by surgical stimulation may lead to reflex cardiovascular responses which, by increasing myocardial oxygen demand, lead to episodes of myocardial ischaemia. In this respect beta-receptor blocking drugs appear to have a protective effect on the ischaemic myocardium.

Adrenergic beta-Antagonists↗
PubMed1975

Effect of CO2 on myocardial contractility and aortic input impedance during anaesthesia.

The haemodynamic responses to hypocapnia and hypercapnia have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia (1% halothane in oxygen) and under nitrous oxide anaesthesia (30% oxygen in nitrous oxide). In the absence of significant variations of either myocardial contractility or left ventricular end-diastolic pressure, the changes of stroke volume and cardiac output (diminution because of hypocapnia, augmentation because of hypercapnia) were determined by alterations of systemic vascular resistance (augmentation because of hypocapnia, diminution because of hypercapnia).

Anesthesia, Inhalation↗
PubMed1975

Effects of changes in PaCO2 on pulmonary input impedance.

Pulmonary arterial input impedance spectra were computed in goats in whom the appropriate pressure and flow transducers had been chronically implanted. In response to either hypocapnia or hypercapnia, under anesthesia (1% halothane in a 70% nitrous oxide--30% oxygen mixture) there were no significant modifications of impedance at zero frequency; no consistent or significant changes in the impedance moduli at frequencies between 2 and 14 Hz were observed; the position of the first impedance minimum or the subsequent maximum was not modified; however, pulmonary vascular resistance increased significantly with hypercapnia. Although the load opposing right ventricular ejection was not modified by variation of Paco2, right ventricular work was reduced in response to hypocapnia and augmented in response to hypercapnia.

Animals↗