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Biomedical subjects

J G Roberts

Publications and source records attributed to J G Roberts.

At least 55 records · Page 3Linked to original sources
PubMed1980

Cancer of the oesophagus--how should tumour biology affect treatment?

An analysis of the biology of cancer of the oesophagus suggests that significant dissemination may not have taken place at the time of diagnosis in approximately one-third of cases. Positive nodal histology in the mediastinum or abdomen is the best available evidence of disseminated disease. Patients without such nodal involvement therefore represent a group in whom the disease is most likely to be localized. It is suggested that only these patients be subjected to aggressive local therapy. The effects of no treatment, orth- and megavoltage radiotherapy, surgery and combinations of surgery and radiotherapy are reviewed. The need for cooperative randomized clinical trials to test the biological hypothesis outlined is discussed. Megavoltage radiotherapy as a primary treatment for oesophageal cancer followed by radical surgery in those patients without evidence of dissemination from nodal histology is proposed as a basis for such clinical trials.

Abdomen↗
PubMed1980

Circulatory responses of the dog to acute isovolumic anaemia in the presence of high-grade adrenergic beta-receptor blockade.

The haemodynamic responses to isovolumic anaemia (dextran-for-blood exchange) were studied in seven dogs pretreated with propranolol 20 mg/kg body weight for 3 weeks. Adrenergic beta-receptor blockade did not prevent significant increases in heart rate (up to 19%). Cardiac output increased by about 20% while systemic vascular resistance decreased by the same proportion. Oxygen extraction increased from 24% to 35% and this was reflected by a decrease in mixed venous PO2 by 1.2 kPa. The modest hyperdynamic response of the circulation to haemodilution in the presence of high-grade adrenergic beta-receptor blockade is in sharp contrast with the large hyperdynamic response that has been reported in its absence and indicates that normal compensatory mechanisms are considerably impaired.

Acute Disease↗
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

Evaluation of radiography and isotopic scintigraphy for detecting skeletal metastases in breast cancer.

Experience with technetium-phosphate compounds for skeletal scintigraphy in patients with breast cancer was analysed. When tumours were 5 cm or less in diameter (T1-2N0-1M0) metastases were demonstrated by radiographs in 1-7% (2/114). However, when radiography did not demonstrate metastases, lesions were found by scintigraphy in 41-3% (19/46). When lesions demonstrated by scintigraphy at the same site as abnormalities regarded as "benign" by radiography were excluded, 23% (11/46) had scintigraphs strongly suggestive of metastases. It is proposed that routine radiographic skeletal survey for patients presenting with breast cancer be abandoned, and replaced by skeletal scintigraphy, chest radiography, and specific localised radiographs of lesions demonstrated by scintigraphy. It is suggested that with this policy the development of expertise in interpreting scintigraphs will be accelerated, the cost of pre-treatment assessment will be reduced, and clinical management rationalised.

Bone Neoplasms↗
PubMed1976

Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. I: Halothane dose-response studies.

The effect of pretreatment for 3 weeks with propranolol 20 mg/kg/day on cardiovascular function during increasing depths of halothane anaesthesia (range 1.0-2.5% inspired halothane with IPPV and normocapnia) were studied in a group of seven closed-chest dogs which had been implanted previously with cardiovascular flow- and pressure-measuring instruments. The results were compared with those observed in a similar group of five untreated dogs. Propranolol pretreatment resulted in a small degree of additional cardiac depression at any inspired halothane concentration. The cardiac depressant effects of propranolol and halothane were found to be simply additive and therefore predictable. The presence of propranolol did not result in morbidity or mortality at any depth of halothane anaesthesia.

Animals↗
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

Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. III: The effects of haemorrhage during halothane and trichloroethylene anaesthesia.

We have examined the haemodynamic effects of 0.8% trichloroethylene and 1% halothane anaesthesia in a control group of five dogs, chronically implanted with cardiovascular flow- and pressure-measuring apparatus and compared them with a similar group of six dogs pretreated for 3 weeks with oral propranolol (20 mg/kg/day). The effects of graded haemorrhage of 25% of the estimated blood volume and re-transfusion were studied. Cardiovascular function was satisfactory at all stages of the study except during trichloroethylene anaesthesia in the beta-blocked dogs when the response to blood loss was impaired severely. Therefore the use of trichloroethylene in the presence of propranolol may not be advisable in clinical practice.

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

Prediction of human spleen size by computer analysis of splenic scintigrams.

A method of assessing spleen size from splenic scintigraphs obtained using autologous heat damaged 99Tcm labelled red cells is described. The method depends on a "computed volume" estimate. The method has a correlation coefficient of 989 with the exsanguinated weight ofthe spleen after splenectomy and has been shown to have an accuracysuperior to methods previously described.

Computers↗