Leukokinetic Studies. Iii. The Distribution of Granulocytes in the Blood of Normal Subjects*

Abstract

In a previous publication (1) it was noted that when granulocytes were labeled in vitro with radioactive diisopropylfluorophosphate (DFP32 ) and then returned to the circulation of the donor, about half of the labeled cells could not be found in the circulation at the completion of the infusion (T0). Thereafter the remaining labeled cells left the circulation in a random fashion with a mean halftime disappearance (T.) of 6.6 hours.Since cell damage and significant elution of the label could not be demonstrated tinder the conditions of the study, it was suggested that the immediate disappearance of half the infused cells was due to their rapid dilution in a larger pool than that calculated from the blood volume and the venous granulocyte count.The concept that the circulating granulocyte pool (CGP) does not constitute all of the intravascular leukocytes is not new. Vejlenis (2)

Acute pro‐inflammatory actions of endothelin‐1 in the guinea‐pig lung: involvement of ETA and ETB receptors

“…The marked decline in the percentage of neutrophil granulocytes with a concomitant increase in the percentage of monocytes and lymphocytes indicates that ET-1-induced leukopenia can primarily be attributed to a decrease in the number of circulating neutrophil granulocytes. The ability of adrenaline, which causes neutrophilia by demargination of the substantial pool of marginated intravascular neutrophils (Athens et al, 1961;Joyce et al, 1976), to prevent ET-1-induced neutropenia would suggest that the underlying mechanism is increased intravascular sequestration rather than egress of neutrophil granulocytes from the circulation into tissues. The findings that ET-1 had no significant effect on pulmonary myeloperoxidase activity, a sensitive marker of neutrophil infiltration (Krawisz et al, 1984;Mullane et al, 1985), and on the number and composition of bronchoalveolar lavage cells lend further support to this notion.…”

Haematological alterations in protein malnutrition

“…37,44 As should the action of the different growth factors and cytokines, hormonal action -especially that of the estrogens, androgens, thyroid hormones, corticosteroids and epinephrine, plasmatic and cellular mediators of the inflammatory response and, obviously, the nutritional state of the individual. 45,46,47 One can see that haemopoiesis is a complex and highly regulated phenomenon which depends on (i) the existence of primitive cells with a proliferative capability; (ii) the regulatory action of growth factors; (iii) the components of the microenvironment and (iv) the architectural structure of this microenvironment. 48,49,50 Concepts acquired on the effect of human protein privation have largely been based on information obtained from severely malnourished individuals, suffering multiple nutritional deficiencies, or from patients with chronic systemic diseases in which the effects of the disease and its therapy are difficult to distinguish from those of nutritional deficiency.…”

“…Endotoxins alter cell mobilisation not only dislocating "marginal" granulocyets, but also modifying the influx into the maturation compartment. 45,69 The apparent difficulty in leukocyte response in bacterial infections in PCM is, according to Suda et al (1976) due to a reduction in the reserve compartment of the bone marrow, and not due to the primary impairment of leukocyte mobilisation from blood to tissue. 70 However, data regarding cell mobilisation are also divergent.…”

Studies of leukocyte kinetics by liquid scintillation counting in normal individuals and in patients with chronic myelocytic leukemia.

“…Leukocyte kinetics have been investigated with the use of a number of different radioisotopic labels including 32p as disodium acid phosphate and as diisopropylfluorophosphate (DFP32), adenine-14C, and guanine (1)(2)(3)(4). All of these have disadvantages that limit their usefulness.…”