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Biomedical subjects

W Ponsold

Publications and source records attributed to W Ponsold.

At least 37 records · Page 2Linked to original sources
PubMed1979

Effect of repeated carbon monoxide intoxications on the myoglobin concentration in heart and skeletal muscle of rats.

A study was made to determine whether or not myoglobin plays a role in the adaptation response of an organism to chronic carbon monoxide exposure. Rats were injected subcutaneously with carbon monoxide (2.4 and 7.2 mmol CO/kg body weight, once daily on 5 days a week) 30times, 60times, or 107times. These exposure conditions resulted in carboxyhemoglobin concentrations of about 45 and 60%, respectively, as well as in an increase in both the hemoglobin concentration and the hematocrit. In skeletal muscle the myoglobin concentrations were not changed significantly, whereas the heart muscle showed an increase mean myoglobin concentration after the prolonged CO hypoxia (7.2 mmol CO/kg, 107times) by 54%.

Animals↗
PubMed1978

Urinary catecholamine excretion and blood sugar response during acute poisonings with dinitrobenzenes.

Rats were injected intraperitoneally with 0.015 mmol of p-dinitrobenzene/kg, 0.15 mmol of m-dinitrobenzene/kg and 0.45 mmol of o-dinitrobenzene/kg body wt. The dinitrobenzenes induced methaemoglobin concentrations of 86%, 60% and 49%, respectively, as well as increases of urinary catecholamine excretion and blood sugar concentration. Due to hyperglycaemia the glycolysis may be stimulated as mechanism for energy production in methaemoglobin-induced oxygen deficiency and as mechanism for reduction of methaemoglobin, that means as responses favouring survival after poisoning.

Animals↗
PubMed1978

Effect of single and repeated carbon monoxide intoxications on urinary catecholamine excretion in rats.

In preliminary experiments it had been shown that the total catecholamines in the urine of rats collected during 5 hrs after stimulation of diuresis with 50 ml tap water/kg body weight per os were not changed significantly following a 3-week training in individual metabolic cages, a short pressing of the animals against the laboratory table, a single i. p. injection of 2 ml sodium chloride solution (145 mmol/l)/kg body weight, or a single s. c. injection of 40 ml air per animal. The excretion was increased after puncture of the retroorbital plexus and after exposure to cold (+5 degrees C) during the 5 hrs. Carbon monoxide poisoning produces an inhibition of diuresis. Therefore, to study the effect of carbon monoxide intoxications on urinary catecholamine excretion we administered 25 ml tap water/kg additionally. Single s. c. injection of 7.2 mmol CO/kg body weight (53% COHb) induced a significant increase of urinary catecholamines. Due to repeated injections of the same CO dose a gradual disappearance of this effect was seen. After 4 weeks the differences to controls are negligible.

Animals↗
PubMed1977

[Hypothermia and carbon monoxide poisoning].

The lethality of 187 patients with severe carbon monoxide intoxication was investigated in relation to body temperature. 22 per cent of the normothermic, but 36 per cent of hypothermic or hyperthermic patients did not survive the carbon monoxide poisoning. The lethality increases following enhancement of degree and duration of hypothermia. Pretreatment of rats with chlorpromazine producing a decrease of body temperature of 4 degree C induces a small reduction of toxicity after subcutaneous carbon monoxide injection. However, the CO-DL50 decreases from 17 to 11,5 mmol/kg following administration of the same dose of chlorpromazine after carbon monoxide injection. Changes in carboxyhemoglobin levels are consistent with alterations of CO toxicity. On the basis of these results, it appears that it is not advisable to maintain a spontaneous hypothermia during carbon monoxide intoxication.

Animals↗
PubMed1976

[Loss of blood and carbon tetrachloride poisoning].

In rats the induced enhancement of glutamic-pyruvic transaminase and leucine aminopeptidase activity in plasma to 5.2 mMol CC14/kg (per 05) is potentiated after repeated drawing of blood. The DL50 of CC14 following oral application in rats after loss of blood is reduced significant comparatively to controls and to animals with increased content of haemoglobin in blood.

Alanine Transaminase↗
PubMed1975

Motor nerve conduction velocity after carbon monoxide or m-dinitrobenzene poisoning following elimination of the poisons.

24 hrs after acute carbon monoxide or m-dinitrobenzene poisoning (about 60% CO-Hb or Met-Hb) the sciatic motor conduction velocity of rats is significantly reduced by 33% and 16% respectively. Whereas 48 hrs after methemoglobinemia the nerve conduction is normal, a retardation is detectable even 4 weeks following carboxyhemoglobinemia. Also, 4 weeks after single carbon monoxide intoxication producing a mean CO-Hb content of 19%, the motor conduction velocity is significantly decreased. This effect may be useful for detection of carbon monoxide intoxication after elimination of the poison. The results show that there are carbon monoxide effects independent of blockade of hemoglobin.

Animals↗
PubMed1975

[Adaptation of rats following sodium-nitrite-induced methemoglobinemia].

Adaptation of rats following sodium nitrite induced methemoglobinemia. The effect of repeated intraperitoneal injections of sodium nitrite on methemoglobin, hemoglobin and blood sugar level, on leucine aminopeptidase activity in plasma and methemoglobin reductase activity in red blood cells was investigated in rats. Repeated methemoglobinemia produced gradual disappearance of hyperglycemia, changes of hemoglobin content in blood and increase of methemoglobin reductase activity in red blood cells.

Adaptation, Physiological↗