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Biomedical subjects

R Wakusawa

Publications and source records attributed to R Wakusawa.

At least 37 records · Page 2Linked to original sources
PubMed1989

Prolonged nitrous oxide exposure inhibits settlement of transplanted hemopoietic stem cells in murine spleen.

In order to clarify the mechanism of hemopoietic depression induced by nitrous oxide inhalation, effects of prolonged nitrous oxide exposure on the settlement of transplanted bone marrow cells were investigated. Mice were continuously exposed to mixed gas containing 50% nitrous oxide, 21% oxygen and 29% nitrogen for 7 days and then they were irradiated with 850 rads. By the irradiation, endogenous pluripotent hemopoietic stem cells (CFU-S) almost disappeared in the mice. Normal syngenic murine bone marrow cells were injected intravenously and the numbers of CFU-S, which settled in the bone marrow and spleen 2 hr after injection, were measured. There was no difference of the numbers of CFU-S settled in the bone marrow between nitrous oxide and control gas exposed mice. In contrast, the numbers of CFU-S in the spleen of nitrous oxide exposed mice were approximately 60% of the control. These results and our previous data suggest that hemopoietic inhibitory effects of nitrous oxide in mice are due to a damage of splenic hemopoietic microenvironment, that supports the settlement of hemopoietic stem cells.

Journal Article↗
PubMed1988

Increased lethality and delay in the recovery of hemopoietic stem cells after irradiation in mice exposed to nitrous oxide.

Effects of N2O-exposure on the survival rate and growth kinetics of hemopoietic stem cells after irradiation were investigated. LD 50, 30 days after irradiation, was 300 rad for N2O exposed mice and over 550 rad for control mice. Recovery of the pluripotent hemopoietic stem cells (CFU-S) and granulocyte-macrophage progenitor cells (GM-CFC) was significantly delayed in the spleen of N2O-exposed mice after 150 rad irradiation, compared to that of control mice. However, in bone marrow, there was a significant but slight difference in the recovery of GM-CFC and no significant difference in the recovery of CFU-S between the two groups. These results suggest that N2O augments the damage of splenic hemopoiesis in irradiated mice, and this may be responsible for the increased hemopoietic death.

Animals↗
PubMed1987

Effects of prolonged nitrous oxide exposure on hemopoietic stem cells in mice.

The effects of prolonged exposure to nitrous oxide on the hemopoietic progenitor cells in bone marrow and spleen in mice were investigated. Fifty percent nitrous oxide caused a marked decrease in the number of pluripotent stem cells (CFU-S) and granulocyte-macro-phage progenitor cells (GM-CFC) in the spleen, whereas it caused only a slight decrease in these cells in the bone marrow. These results suggest that prolonged exposure to nitrous oxide induces damage in the splenic hemopoiesis in mice.

Journal Article↗
PubMed1987

Management of acid-base balance with red blood cell carbonic anhydrase (RCA). II. Control of acid-base balance with acetazolamide.

Acetazolamide, a carbonic anhydrase (CA) inhibitor, was used to normalize metabolic alkalemia. A dosage of acetazolamide for normalizing metabolic alkalemia has not yet been experimentally determined. The dosage of acetazolamide for this purpose is experimentally calculated in this paper. The correlation between various concentration of acetazolamide mixed with blood and the base excess (BE) levels in blood at the start of normalizing metabolic alkalosis was studied in vitro. The change rate of the BE level was calculated from BE levels noted before and after tonometry of the blood with and without acetazolamide. A dosage of acetazolamide which can cause the change rate of the BE level to decrease is considered to be an effective dosage. Metabolic alkalosis in vitro was produced by adding bicarbonate into the blood. An effective dosage of acetazolamide for metabolic alkalemia of which the BE range was from 0 to + 30 mEq/liter was calculated. CA activities in the kidney and the blood of dogs administered acetazolamide were examined. The effective dosage of acetazolamide obtained from in vitro experiments inhibited the CA activities not only in the blood but also in the kidneys. An effective dosage of acetazolamide to normalize a BE of + 10 mEq/liter in vitro was converted into about 7-12 mg/kg in vivo. This dosage inhibited the red blood cell carbonic anhydrase (RCA) activity to 20-40%, whereas the normal physiological variation range is 25%. An effective dosage of acetazolamide in the blood did not proportionally increase with an increase of HCO3- during severe alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1986

Disturbance of CO2 elimination in the lungs by carbonic anhydrase inhibition.

Carbonic anhydrase in the red blood cell and in the pulmonary endothelium facilitates the elimination of CO2 in the lungs. Although a carbonic anhydrase inhibitor, such as acetazolamide which is frequently used in patients with glaucoma or with metabolic alkalosis, is known to impair the CO2 elimination in the lungs, the dose-response curve of CO2 elimination with acetazolamide has not been well documented in CO2 homeostasis. In the present study, the effects of inhibited carbonic anhydrase were tested in 8 anesthetized dogs; various dosages of acetazolamide were used. When the administered clinical dosage of acetazolamide increased from 5 to 20 mg/kg, PaCO2, PVCO2, arterial-alveolar PCO2 difference (a-ADCO2), and physiological VD/VT ratio increased progressively to 52.0 +/- 2.1 Torr, 58.0 +/- 3.0 Torr, 23.4 +/- 1.2 Torr, and by 19.2 +/- 1.8% (S.E.) respectively, whereas inhibition rate of red blood cell carbonic anhydrase (RCA) activity increased progressively to 73.1 +/- 2.1% (S.E.). On the other hand, PACO2 decreased to 27.1 +/- 1.8 Torr (S.E.) upon the first injection of 5 mg/kg of acetazolamide, but PACO2 did not change further upon 3 additional 5 mg/kg injections. Mixed venous-arterial PCO2 difference [V-a)PCO2), VCO2, and anatomical VD/VT ratio were unchanged by the administration of any doses of acetazolamide.

Acetazolamide↗
PubMed1983

Management of the acid-base balance by the red blood cell carbonic anhydrase (RCA). I. Correlation of the RCA activity and acid-base balance in the in vitro and in vivo experiments.

Changes in RCA activity are known to affect the acid-base balance, but a clear relationship between RCA activity and acid-base balance has not yet been established. The relationship between RCA activity and acid-base balance was studied in tonometry with 4 mixed gases for 6-9 hr, in healthy adults at rest, in halothane anesthesia and in hypothermia. RCA activity increases when pH and HCO3-/PCO2 ratio increase and PCO2 decreases in vitro. It also increases when pH and HCO3-/PCO2 ratio decrease and the range of PCO2 broadens in vivo. The relationship between RCA activity and the HCO3-/PCO2 ratio is a fan shape, because a change of the HCO3-/PCO2 ratio precedes the change of RCA activity. Some factor which increases the RCA activity may be produced secondarily in the body under the influence of high PCO2. Probably the acid-base balance is corrected by reduction of the RCA activity in the case of alkalosis, and the acid-base balance may be corrected by an increase in RCA activity in the case of acidosis.

Acid-Base Equilibrium↗