WITH increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusion injury to respiratory distress syndromes, blistering skin disorders, and ulcerative colitis.1 , 2 In each of these diseases, as well as a variety of other acute inflammatory disorders, important components of these pathologic processes are being linked to the neutrophil's ability to release a complex assortment of agents that can destroy normal cells and dissolve connective tissues. Although these toxins normally defend the host against invading microbes, the neutrophil has little intrinsic ability to differentiate between foreign . . .

Tissue Destruction by Neutrophils

Psychological Assessment Resources

DILL, D. B., AND I>. L. &STILL. Calculation of pcrccntage changes in volumes of blood, plasma, and red cells in dehydration. J. Appl. Physiol. 37(2): 247-248. 1974.-Observations on hematocrit (Hct) and hemoglobin (Hb) were Inade in six men before and after running long enough to cause a 4y0 decrease in body weight. Subscripts B and A were used to denote before dehydration and after dehydration, respectively. Relations were derived between BVn, BVA, Hbn, HbA, Hctg, and HctA with which one can calculate the percentage decreases in BV, CV, and PV, as well as the concentration of hemoglobin in red cells, g. 100 ml-l (MCHC). When subjects reach the same level of dehydration the water loss from the various body compartments may vary reflecting difference in salt losses in sweat. Changes in PV calculated from the increase in plasma protein concentration averaged 7.5(z compared with 12.2 y0 calculated from changes in Hb and Hct. The difference could be accounted for by a loss of 6v10 plasma protein from the circulation.

Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration.

WASSERMAN, KARLMAN, BRIAN J. WHIPP, SANKAR IX KOYAL, AND WILLIAM L. BEAVER. Anaerobic threshold and respiratory gas exchange during exercise. J. Appl. Physiol. 35(Z): 236-243. 1973.-Alterations in gas exchange were studied in man during exercise increasing in increments of 15 w each minute, to determine the noninvasive indicators of the onset of metabolic acidosis (anaerobic metabolism). Expired airflow and CO 2 and 0 2 tensions at the mouth during the breath were continuously monitored with rapid1 y responding gas analyzers. These measurements were recorded directly as well as processed by a minicomputer, on-line, to give minute ventilation (VE), COP production #co& 02 consumption (voz), and the gas exchange ratio (R), breath-by-breath. The anaerobic threshold (AT) could be identified by the point of I) nonlinear increase in VE, 2) nonlinear increase in Vco2, 3) an increase in end-tidal 02 without a corresponding decrease in endtidal COz, and 4) an increase in R, as work rate was increased during an incremental exercise test. Of these measurements, R was found least sensitive. The AT was determined in 85 normal subjects between 17 and 91 years of age, by these techniques. The lower limit of normal was 45 w (KTo 2 = 1 liter/min), while values for very fit normal adults were as high as 180 w. The patients studied with cardiac disease above functional class I have lower anaerobic thresholds than the least fit normal subjects. The I-min incremental work rate test is associated with changes in gas exchange which can be used as sensitive on-line indicators of the AT, thus bypassing the need for measuring arterial lactate or acid-base parameters to indicate anaerobiosis.

Anaerobic threshold and respiratory gas exchange during exercise.

The determination of ascorbic acid in whole blood and urine through the 2,4-dinitrophenylhydrazine derivative of dehydroascorbic acid

Although direct evidence of a quantitative relationship between oxygen debt and lactic acid production in man has never been given, there is general agreement with A. V. Hill’s hypothesis that the oxygen debt is due to the delayed oxidation of a fraction of the lactic acid produced during the anaerobi .c processes of muscular activity. After the “revolution” produced in muscle physiology by the discoveries of the last few years, m ainiy after Lundsgaard’s work, and the further observations on men, it seemed to us that the lactic acid mechanism alone is inadequate to explain all the processes which occur in the payment of the oxygen debt, particularly for the following reasons: a. It has been observed in isolated muscle that most of the lactic acid is produced after the contraction is over, during the first minute of recovery; this does not seem to agree with the fact that the payment of the oxygen debt at the beginning shows no lag even if the exercise is of very short duration. b. In moderate exercise of long duration in man, involving an oxygen debt of 3 to 4 liters, the changes in lactic acid concentration or in pH of blood are negligible in comparison with the values implied by the assumption of an increment of lactic acid in the body corresponding to the amount of oxygen debt. (See, for the lactic acid concentration in blood following muscular exercise, Owles, 1930; Dill, Edwards, Foiling, Oberg, Pappenheimer and Talbott, 1931; for data on pH, Margaria and Talenti, 1933.) c. There exist oxidative recovery processes following muscular contraction other than the glycogen resynthesis from lactic acid ; Lundsgaard (1931) has demonstrated in muscles poisoned with iodoacetic acid the partial resynthesis of the phosphocreatine in the presence of oxygen and in the absence of any lactic acid formation or remo val; Clark, Eggleton and

D. B. Dill

Papers

Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration.

The possible mechanisms of contracting and paying the oxygen debt and the rôle of lactic acid in muscular contraction

Experimental Human Scurvy.

Blood as a physicochemical system xi. man at rest

Respiratory and metabolic effects of hypothermia