Biomedical subjects
C Borland
Publications and source records attributed to C Borland.
Elevated exhaled nitric oxide in patients with hepatopulmonary syndrome.
The hypoxaemia of hepatopulmonary syndrome, seen in severe chronic liver dysfunction, occurs as a result of precapillary pulmonary arterial dilatation and arteriovenous communications. These abnormalities contribute to the mismatch between ventilation and perfusion, and the right to left blood flow shunting. Nitric oxide (NO) is a powerful vasodilator concerned with the regulation of pulmonary vascular tone in man. Using a chemiluminescence analyser, we have measured endogenously produced NO in the exhaled air of three patients with the hepatopulmonary syndrome, six normoxaemic cirrhotic patients and six healthy volunteers. The subjects breathed NO-free air throughout the measurements. The molar rate of production of exhaled NO was raised almost threefold in the patients with hepatopulmonary syndrome compared with normal volunteers and with normoxaemic cirrhotic patients. Hypoxia per se, achieved in the normal volunteers by breathing a hypoxic gas mixture, reduced rather than increased the exhaled NO. One hepatopulmonary syndrome patient received an orthotopic liver transplant and achieved normoxaemia after 3 months. The exhaled NO also returned to normal. Increased pulmonary production of NO could contribute to the development of the hepatopulmonary syndrome.
Case report: perinephric-splenic fistula--a complication of percutaneous perinephric abscess drainage.
A case of acute perinephric abscess due to chronic parenchymal disease and calculi is presented. During percutaneous drainage a reno-splenic vein communication developed acutely. The aetiology and treatment complications of perinephric abscesses are reviewed.
Mixed expired nitric oxide in primary pulmonary hypertension in relation to lung diffusion capacity.
The mixed expired nitric oxide (NO) production of the lungs of patients with primary pulmonary hypertension (PPH) and normal subjects was measured to determine the relationship between NO production and the diffusion capacity of the lung (KCO). Expired air was collected from eight patients with PPH and 20 healthy volunteers for analysis by a chemiluminescent analyser. Mean pulmonary artery pressure in the PPH patients was 59.5 +/- 6.45 mmHg and their mean cardiac output was 2.95 +/- 0.35 l/min. All patients and subjects underwent measurements of FEV1, VC and KCO. The rate of production of NO in mixed exhaled air was lower in the PPH group compared to the controls (2.85 +/- 0.7 vs. 4.69 +/- 0.35 nM/min; p < 0.05). There was a good correlation of expired NO with the KCO (r = 0.7; n = 30; p < 0.001). When corrected, KCO differences in exhaled NO were not significant (p = 0.09). We conclude that the low exhaled NO observed in PPH patients is a reflection of the reduced blood capillary volume in these patients rather than a decreased basal production of NO.
Measurement of exhaled nitric oxide in man.
BACKGROUND: Nitric oxide is released from pulmonary endothelial cells and contributes to the low pulmonary vascular resistance. The resistance pulmonary arteries are in close anatomical proximity to membranous airways, so it is likely that some pulmonary endothelial nitric oxide will enter the airspace to allow its measurement in the exhaled breath. METHODS: Exhaled air was collected from a single full exhalation and during tidal breathing. This was analysed for concentrations of nitric oxide, nitrogen dioxide, and carbon dioxide to give alveolar (FA) and mixed expired (FE) concentrations. Eight normal subjects were studied and laboratory air was similarly analysed using, respectively, chemiluminescent and infrared analysers. RESULTS: There was no relation between FA concentrations and the laboratory air concentrations. From the single breath, the ratio of (Fano/Faco2) x (Feco2/Feno) had a mean value of 0.92 (95% confidence interval 0.7 to 1.14). As this does not differ from unity, nitric oxide is likely to be derived from the same regions of the lungs as carbon dioxide. During tidal breathing the Feno ranged from 8.3 to 20.3 parts per billion. CONCLUSIONS: It is possible to measure endogenous pulmonary nitric oxide production in the exhaled air in man.
Safety guidelines for use of nitric oxide.
Explore the source record for details and available documents.
Acute angle closure glaucoma occurring after nebulized bronchodilator treatment with ipratropium bromide and salbutamol.
Explore the source record for details and available documents.
Endothelium in control.
Explore the source record for details and available documents.
Nitric oxide yields of contemporary UK, US and French cigarettes.
To determine what governs nitric oxide (NO) yields of cigarettes and to obtain a range of yields for contemporary cigarettes 17 UK, 14 US, 8 French and 1 Turkish brand were analysed using a chemiluminescent analyser and standard smoking machine. The country of origin appeared to be the major factor affecting NO yield. US and French brands exceeded UK values by 3-5 fold. Apart from a reduced NO yield in UK ventilated filtered brands, the design of a cigarette and its tar, nicotine and carbon monoxide (CO) yield had little effect on NO yield. It is argued that these international differences in NO yields reflect differences in the nitrate content of tobaccos traditionally used in manufacture in those countries over many years. Despite their probable increased lifetime exposure to NO (and by implication nitrosamine exposure) there appears to be little evidence that US and French smokers are at greater risk of lung disease than their UK counterparts.
Chemical specificity of coughing in man.
The purpose of this study was to test whether cough response to inhaled ultrasonically nebulized fluid is dependent on the ionic content of the fluid. Coughing was recorded in human volunteers during inhalation of aqueous solutions in a series of double blind randomized experiments. The occurrence of cough was found to be dependent on the concentration of chloride ions in the inhaled fluid, cough frequency progressively increasing as chloride ion concentration was reduced. It is proposed that the ion composition of the surface lining fluid of the airway may moderate the cough response by means of a chemo-receptor, although tonicity may also be important.
Biochemical and clinical correlates of diuretic therapy in the elderly.
To estimate the frequency of diuretic-related electrolyte disorders in the elderly, 561 consecutive admissions to three acute geriatric units were studied. For the 287 admissions to one unit, discharge/death diagnoses were also examined in relation to admission diuretic therapy. Sodium concentrations were significantly lower, and urea and creatinine significantly higher, in patients on diuretics, though the size of the differences was small. Comparing different preparations sodium concentrations were significantly lower on Moduretic than on Dyazide or Navidrex K and on frusemide when combined with a potassium-retaining diuretic rather than a potassium supplement. Potassium concentrations were significantly lower on Bendrofluazide alone compared to Navidrex K or Moduretic. Diuretics were positively associated with cardiac failure, ischaemic heart disease, airflow obstruction and obstructive large bowel disorders but negatively with Parkinson's disease. No significant association was found with falls, immobility or confusion. Major electrolyte disorders on diuretics appear to be unusual but important differences exist between preparations. Similarly major illness resulting from diuretic therapy is rare but minor morbidity may be more common.
Pulmonary epithelial permeability after inhaling saline, distilled water "fog" and cold air.
It is recognized that hyperventilation of cold air and the inhalation of fine mists of distilled water provoke significant bronchoconstriction in the asthmatic individual, yet little is known as to how these provocations affect the structural integrity of the alveolar epithelial membrane. In 11 normal subjects, the following effects have been studied: cold air hyperventilation for three minutes, inhalation of 80 L of ultrasonically nebulized distilled water "fog," and 80 L of isotonic saline "fog" on the half time clearance (T1/2) from the alveoli of technetium 99m diethylene triamine penta acetate (DTPA), inhaled as an aerosol. The DTPA T1/2 provided a measurement of pulmonary epithelial permeability.
Do the oxides of nitrogen in cigarette smoke cause emphysema in smokers?
Explore the source record for details and available documents.
Hyponatraemia and Moduretic (amiloride plus hydrochlorothiazide)
Explore the source record for details and available documents.
Carbon monoxide yield of cigarettes and its relation to cardiorespiratory disease.
Estimates of the carbon monoxide yield of their cigarettes have been obtained for 4910 smokers (68% of all smokers) in the Whitehall study of men aged 40 to 64. In the 10 years after examination 635 men died. When men smoking cigarettes with high carbon monoxide yield were compared with those smoking cigarettes with a low yield, and after adjusting for age, employment grade, amount smoked, and tar yield, the risk of death was 32% lower for coronary heart disease, 49% higher for lung cancer, and 10% lower for total mortality; these differences were not statistically significant. Among men who said that they inhaled the risk of fatal coronary heart disease was 51% lower in the high carbon monoxide group (p less than 0.01), while the risk of lung cancer was 75% higher. These results provide no evidence that a smoker can reduce his risk of death by smoking a brand with a low carbon monoxide yield; he might even increase it. The complex interactions between characteristics of the smoker, smoking behaviour, constituents of tobacco smoke, and health are again demonstrated.
Methemoglobin levels in smokers and non-smokers.
The authors analyzed the blood of a group of 336 smokers and 336 non-smokers to determine if tobacco smoke, potentially the major source of nitrogen oxide pollution for 40% of the adult population, significantly reduces oxygen carrying capacity as a result of methemoglobin formation. Each blood sample was analyzed for carboxyhemoglobin, methemoglobin, and hemoglobin using an automated spectrophotometer. The mean value of methemoglobin in the smokers did not exceed that in the non-smokers; in fact, the level in the non-smokers was significantly greater. As expected, carboxyhemoglobin levels in smokers substantially exceeded those in non-smokers. The authors conclude that methemoglobin arising from cigarette smoke exposure does not interfere with the oxygen carrying capacity of the blood in smokers.