One of the original objects, which Hartridge & Roughton (1923) had in mind in developing their method of measuring the velocity of rapid chemical reactions, was to estimate the extents to which the rates of the reactions of haemoglobin, in the intact red cell, with oxygen and/or carbon monoxide limit the rate of uptake of these gases in the human lung. For these purposes, measurements are necessary of the rates of these reactions in human blood solutions and suspensions at physiological pH and temperature. Such determinations are so far almost wholly lacking, the only exceptions being the data obtained by Roughton (1945 a) on the rate at which carbon monoxide displaces oxygen from combination with oxygenated human haemoglobin, in solution and in red cell suspensions. These data were used by him (1945b) in estimating, by a theoretical method, the average time spent by the blood in traversing the capillaries of the lung. It is the aim of the present paper to fill some of the many existing gaps in knowledge as to the kinetics, in vitro, of human haemoglobin in solution and in the red cell, not only for the intrinsic interest of such studies, but also to provide the necessary basis for the solution of further problems of physiological interest in human subjects in vivo.The present paper contains measurements of:(i) The rate of combination of (a) oxygen, (b) carbon monoxide, at 370 C, with human haemoglobin, both in dilute solution and in suspensions of intact red cells.(ii) The effect of temperature on (a) the rate of combination of carbon monoxide with dilute human haemoglobin solutions, (b) the rate of dissociaton of the first oxygen molecule from fully saturated human oxyhaemoglobin solutions.

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Background: Chronic Obstructive Pulmonary Disease (COPD) is a common respiratory disease among elderly with its prognosis greatly determined by the presence of comorbidities including cognitive impairment. We hypothesized that baseline airway obstruction and cognitive impairment are independent predictors of survival in persons aged 60 years and over, and further that there is no positive interaction between these risk factors. Methods: We utilized the Third National Health and Nutrition Examination Survey (NHANES III), from 1988-1994 with mortality follow-up data through December 31, 2011. The ratio of the forced expiratory volume in the first second (FEV1) to the forced vital capacity (FVC) <0.7 was used to define airway obstruction. Cognitive function was assessed using a short index of cognitive function (SICF). SICF score <12 (range 0-17) indicated impairment in cognitive function. The number interviewed was 33,994 and 5,302 of these were aged 60 years. Of these 4,488 had mortality follow-up data, reliable spirometry data and no missing data. Results: 1930 (43%) were men and 2,558 (57%) were women. SICF <12 occurred in 2,761. 2152 had neither FEV1/FVC<0.7 nor SICF<12, 1131 had FEV1/FVC<0.7 only, 758 had SICF <12 only and 447 had both FEV1/FVC<0.7 and SICF<12. Over the follow-up period (min¼0, median¼ 200 months, maximum¼ 276 months) there were a total 3,335 deaths in the analysis sample. There were 1413 deaths among those with neither SICF <12 nor FEV1/FVC < 0.7, 902 with FEV1/FVC < 0.7 only, 615 with SICF <12 only and 405 with both SICF <12 and FEV1/FVC < 70%. Weighted Cox proportional hazards regression revealed increasing hazard ratio in persons with FEV1/FVC <0.7, SICF <12, and both FEV1/ FVC <0.7and SICF <12 respectively compared with persons with neither (reference group). After adjusting for multiple confounders, adjusted hazards ratios (95%CI) were 1.39(1.25-1.56)), 1.33 (1.15-1.53), 1.55(1.18-2.04), respectively. Further analysis assessing for interaction between FEV1/FVC ratio and SICF revealed a negative interaction (p ¼0.006) after adjusting for multiple confounders. Conclusions: Elderly persons with airway obstruction or cognitive impairment or both had increased all-cause mortality over the follow-up period when compared to those having neither. A negative interaction was significant. Further prospective studies are needed to replicate these findings.Background: Few data exist on cognitive and depressive symptoms and vascular factors in American Indian (AI) elders. Since vascular factors increase risk for cognitive impairments, depression and dementia, and since AI elders are at high vascular risk, it is timely

The intravenous infusion of platelet activating factor (PAF) (0.8 micrograms/kg b.w.) induced ECG and hemodynamic alterations characterized by the following sequential three phases. Phase I (15 sec) consisted of a transient bradycardia with reduction in left ventricular pressure (LVPs), mean arterial pressure (MAP) and cardiac output (CO). Phase II developed within 30 sec and consisted of a rise in cardiac frequency, increase in LVPs, MAP and total peripheral resistances (TPR), which were associated with a decrease in CO. Finally, phase III, that occurred about 90 sec after PAF infusion, was characterized by marked ECG changes (ST segment depression and conduction arrhythmias), a decrease in LVPs and MAP, as well as a rise in TPR and in right atrial pressure (RAP). All these alterations were reversible within 30-60 min. Pretreatment with promethazine and cimetidine, as H1 and H2 histamine receptor antagonists, markedly prevented the development of phase II, namely the rise in cardiac frequency, LVPs, MAP and TPR, but did not significantly modify phase I and III. In contrast, pretreatment with indomethacin, an inhibitor of cyclooxygenase, moderatively attenuated, but did not abolish, the three phases of cardiovascular changes induced by PAF infusion.

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