Management of hypertension. Patients from ethnic minorities are at greater risk.
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Biomedical subjects
Publications and source records attributed to G Drummond.
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A patient with cerebral infarction was certified clinically brainstem dead. However, 4 h after the diagnosis of death, while the patient was being ventilated using the biphasic positive airway pressure mode, the 'assist' indicator light on the Drager Evita 2 ventilator illuminated intermittently. There was no evidence of spontaneous breathing. 'Triggering' was probably caused by a decrease in airway pressure in time with cardiac contraction. The trigger flow rate is crucial as factors other than the patient's inspiratory effort can initiate flow from the ventilator with very sensitive settings.
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This study examined the role of heme oxygenase (HO) in the acquisition of resistance to hydrogen peroxide (H2O2) and hemin toxicity by renal epithelial cells (BSC-1). BSC-1 cells adapted by long-term exposure to H2O2 exhibited a twofold increase in basal HO activity and expression of HO-1 mRNA as compared with their wild-type counterparts. Exposure of both adapted and wild-type BSC-1 cells to H2O2 induced HO-1 mRNA. When cells were exposed to H202 for 24 hours, cell viability was reduced; however, an inhibitor of HO activity, Zn 2,4-bis-glycol protoporphyrin IX, improved cell viability. In a similar manner, ZnDBG completely overcame the reduction in cell viability brought about by 1 hour of hemin treatment. In addition, cells preexposed to hemin for 24 hours maintained a high level of HO mRNA and acquired resistance to further challenge with H2O2. Hemin treatment per se was associated with a detectable reduction in BSC-1 cell viability; however, the effect of hemin was not additive to the cytotoxicity of hydrogen peroxide, suggesting a common pathway of cell injury. In conclusion, two interrelated stressors, H2O2 and hemin, produced a stimulation of HO-1, and this was associated with a reduction in the viability of BSC-1 cells. Long-term exposure (24 hours) to both stressors resulted in the acquisition of some resistance to a further acute challenge of oxidant stress in BSC-1 cells.
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A case of craniopagus twins is presented. Large contralateral flaps were used to cover the bony defect and exposed brain. Details of the planning and problems are discussed.
Acoustic pulse reflectometry is a relatively recent technique which allows the non-invasive measurement of human airways. The technique consists of guiding an acoustic impulse through the subject's mouth and into the airway. Suitable analysis of the resulting reflection (the 'echo') allows a reconstruction of the area-distance function. The non-invasive nature of the technique offers significant advantages over the established methods of x-ray cephalometry and CT scanning, and makes it very attractive for the investigation of ENT problems and sleep apnoea, and in the anaesthetic management of patients. This paper describes the theory and limitations of acoustic reflectometry, discusses previous work, and suggests some modifications: it is currently being implemented clinically.
We describe two children with corneal epithelial defects resistant to healing in whom protective temporary ptosis was induced with type A botulinum toxin injected to the levator palpebrae superioris. Epithelial healing was rapid, and no complications were noted. With further study this procedure may become useful in the treatment of corneal epithelial defects resistant to healing.
Sn(tin4+)-protoporphyrin, a potent competitive inhibitor of haeme oxygenase, the rate limiting enzyme in the degradation of haeme to bile pigments, was given intravenously to six patients with primary biliary cirrhosis and to four patients with idiopathic haemochromatosis. Serum bilirubin concentrations decreased in all patients after administration of 1-2 mumol/kg body weight of the metalloporphyrin, given in two doses eight to 24 hours apart. This reduction lasted approximately four to five days after injection of the compound. Excretion of endogenous haeme in bile increased (mean increase approximately two to threefold) in parallel with the decrease in serum bilirubin concentrations in both patient groups, and the highest biliary haeme concentrations were found during the first 48 hours after treatment. Sn-protoporphyrin was cleared rapidly from plasma with a half-life of 3.4 hours. Biliary bilirubin concentrations decreased (mean decrease, 49%) in the haemochromatosis patients after Sn-protoporphyrin administration. No decrease in biliary bilirubin concentrations could be detected in the primary biliary cirrhosis patients under the same conditions. Thus, Sn-protoporphyrin treatment resulted in a decrease in serum bilirubin concentrations and an increase in biliary haeme excretion in patients with haemochromatosis and primary biliary cirrhosis, as has previously been shown in normal subjects. The results indicate that the synthetic haeme analogue inhibits haeme oxidation activity in the two patient groups studied, as it does in normal people and in experimental animals. The lack of effect of Sn-protoporphyrin on biliary bilirubin excretion in primary biliary cirrhosis may be related to a differently affected hepatic clearance system or to a different distribution of tissue bilirubin pools in this condition.
Chest physiotherapy using a manual ventilation technique was carried out on 9 intubated patients. One patient was studied on two occasions. The maximum expiratory flow rate (MEFR) was recorded during: (A) manual ventilation without physiotherapy, (B) manual ventilation with chest compression, (C) manual ventilation and chest compression, after application of the abdominal binder. Statistical analysis was carried out to allow for differences in tidal volume (Vt). Chest physiotherapy increased the mean MEFR and application of an abdominal binder (together with physiotherapy) caused a further increase in MEFR. The mean MEFR (assuming a common Vt of 1360 ml) in each group was; (A) = 73.3 l min-1, (B) = 103.9 l min-1, (C) = 113.93 l min-1.
The measurement of plasma glutathione S-transferase (GST) concentrations have been used to assess the changes in hepatocellular integrity which occur following general anaesthesia. Of 20 selected patients, who received halothane for minor urological procedures, 16 showed a small transient rise in GST between 1 h and 3 h after anaesthesia. Similar changes were also observed in 8 consecutive patients who received halothane for various operative procedures. In 3 of these 28 patients a marked secondary rise in plasma GST was observed 24 h after anaesthesia. No significant changes in ALT were observed in either of the groups of patients. These data indicate two possible phases of hepatotoxicity following halothane administration which results in a transient impairment in hepatocellular integrity in the majority of patients who undergo anaesthesia with this agent.
The effects of fentanyl and sufentanil with and without N2O on left ventricular myocardium supplied by a critically narrowed and a normal coronary artery were studied in 16 dogs. Regional ventricular function was measured by recording ventricular segment length with the use of ultrasonic length detectors in the left anterior descending (LAD) and the left circumflex (LC) coronary artery territories before and during critical stenosis of the LAD. Critical stenosis was documented by the absence of a hyperemic response following a 10-s total occlusion of the LAD. Hemodynamic variables (aortic flow and pressure, left ventricular pressure, heart rate, and coronary blood flow) were measured and the first derivative of left ventricular pressure (LVdP/dt) and coronary perfusion pressure derived. Eight dogs received fentanyl 100 micrograms X kg-1 followed by an infusion of 1 microgram X kg-1 X min-1 while ventilated with O2:N2 (1:2), and eight dogs received sufentanil 30 micrograms X kg-1 with an infusion of 0.3 micrograms X kg-1 X min-1. Replacement of N2 with N2O produced evidence of mild systolic myocardial depression but no dysfunction in either group. After application of the critical constriction, the addition of N2O rapidly produced evidence of dysfunction with significant postsystolic shortening only in the LAD territory. This was not accompanied by hypotension or a decrease in coronary flow and was not always reversible. Higher infusion rates of either narcotic (fentanyl 2 micrograms X kg-1 X min-1, 4 micrograms X kg-1 X min-1; sufentanil 0.6 micrograms X kg-1 X min-1, 1.2 micrograms X kg-1 X min-1) in the absence of N2O did not produce dysfunction but had no protective effect when N2O was added.(ABSTRACT TRUNCATED AT 250 WORDS)
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