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PubMed1975

[Acid-base equilibrium during physiological pregnancy].

Authors applied blood-gas analysis in 30 healthy gravid women on 3,3 occassions making out 90 cases altogether by blood samples taken from the pulp of the finger capillaries. As a control 27 healthy non-gravid women were examined for comparative analysis. In 10 cases between the 16. and 28. week the results of samples taken from the arteria femoralis and the pulp were evaluated. It has been found that in the gravidity period of the 16. and 28. week respiratory alcalosis does not appear. No metabolic changes have been found during the whole period of pregnancy. The parallel examination of blood samples taken from the arteria femoralis and the pulp have proved that it is sufficient and reliable to take blood-gas analysis on the material gained from the pulp capillary only. A special importance is attached to keeping to exact methodical prescriptions.

Acid-Base Equilibrium↗
PubMed1975

The internal-alkaline pH gradient, sensitive to uncoupler and ATPase inhibitor, in growing Clostridium pasteurianum.

1. The intracellular pH was measured in growing Clostridium pasteurianum with and acid-base equilibrium distribution method. [14C]Dimethyloxazolidinedione, [14]methylamine and [14C]acetic acid were used as "deltapH-indicators". During growth the extracellular pH decreased from 7.1 to 5.1; simultaneously the intracellular pH changed from 7.5 to 5.9. Thus, the intracellular pH was more alkaline than the extracellular pH by 0.4 to 0.8 pH-units. 2. This pH gradient (interior alkaline) was abolished by the proton conductor carbonylcyanide m-chlorophenylhydrazone and the ATPase inhibitor N,N'-dicyclohexylcarbodiimide. The pH gradient could not be demonstrated in cells depleted of an energy substrate. These results suggest that the pH gradient is formed by an ATPase-driven extrusion of protons from the cells rather than by a Donnan potential. 3. Growth of the organism was inhibited by low concentrations of both carbonylcyanide m-chlorophenylhydrazone (5 muM) and dicyclohexylcarbodiimide (5 muM). This finding suggests that the pH gradient is essential for the growing cell as it may be required for substrate accumulation and other types of transport processes.

Carbodiimides↗
PubMed1975

[Past and present aspects of diarrheal disease in childhood. Clinical study and treatment (author's transl)].

The etiologic and pathophysiologic findings described in the first part of this paper have important consequences: The recognition of the specific etiology of diarrhea requires new laboratory methods: most of these, however, are technically easy to perform and do not require a large laboratory. A long-ranging consequence of this changed concept is a well-founded modification of therapy. The most important discovery was, that in a well balanced glucose electrolyte solution sodium and glucose enhance their absorption mutually and increase the absorption of water by solvent drag. Since in most acute diarrheas the mechanisms of absorption of glucose and electrolytes are retained this mechanism can be utilized for fast oral rehydration and reinstitution of normal intestinal homeostasis. Prompt institution of a diet consisting of the previously mentioned glucose-electrolyte solution usually prevents severe dehydration and the need for stationary treatment. The elimination of lactose and long chain fatty acids from the diet prevents continuation of the pathologic osmotic and chemical conditions in the intestine. Antibiotics are not indicated in acute diarrhea with the exception of diarrhea caused by enteroinvasive E. Coli or Shigella, in the case of Salmonella-gastroenteritis even contraindicated. Further research concentrates on the development of drugs for neutralisation of E. Coli enterotoxin and the prevention of diarrheas by development of effective vaccines.

Acid-Base Equilibrium↗
PubMed1975

Cardiac output response to altered acid-base status during diethyl ether anaesthesia.

The effects of acid-base changes on cardiac output during diethyl ether anaesthesia were studied in 25 mongrel dogs prepared by surgically implanting a plastic encased non-ferrous core electromagnetic probe on the ascending aorta. The findings are: (1) Metabolic acidaemia produced only slight decrease in cardiac output but a more marked fall became evident with decreasing pH(2) Respiratory acidaemia led to a slight rise in cardiac output. (3) Respiratory alkalaemia decreased cardiac output. (4) Metabolic alkalaemia also produced a decline in cardiac output.

Acid-Base Equilibrium↗
PubMed1975

Renal response to short-term hypocapnia in man.

This study examines the renal response to moderate hyperventilation in healthy man. Eight men hyperventilated for 26 hr (PaCO2 approximately 30 to 32 mm Hg) in normoxia (barometric pressure, PB approximately 740 mm Hg) and hypobaric hypoxia (PB approximately530 mm Hg). Anaerobic samples of arterial blood and urine were studied at two-hour intervals. Plasma [HCO3-] fell with time during sustained hypocapnia and after 26 hr was reduced 2.5 mEq/liter, with plasma pH compensated approximately 60%. Statistically significant changes in renal H+ handling were observed within the initial 2 hr of hyperventilation and were evident over the first 12 hr. Over 26 hr, mean total HCO3-excretion in hypocapnia was 10.2 mEq above control and mean total acid excretion (UVTA + UVNH4+) was 17.5 mEq below control. An increased urinary excretion of cations, especially sodium, accompanied the decrease in acid excretion. Plasma lactic acid accumulation was negligible. We conclude that renal mechanisms contribute significantly and relatively quickly to plasma pH compensation during the early phase of adaptation to hypocapnia in man.

Acid-Base Equilibrium↗
PubMed1976

The intracellular pH of human leucocytes in response to acid-base changes in vitro.

1. Viable human leucocytes were isolated from venous blood and suspended in artificial media. Intracellular pH measurements were made by the dimethyloxazolidinedione technique in conditions simulating "respiratory" or "metabolic" acid-base disturbances. 2. Normal intracellular pH was 7-11 +/- 0-02 (mean +/- 2 SD) at an extracellular PCO2 of 5-8 kPa and a bicarbonate concentration of 25 mmol/l. 3. "Respiratory" and "metabolic" acidosis caused little change in pHi although increases in PCO2 led to relatively greater falls in pHi than did reduction in external bicarbonate concentration. 4. "Respiratory" and "metabolic" alkalosis caused similar and relatively greater increases in the pHi when compared with the response to an external acidosis.

Acid-Base Equilibrium↗
PubMed1976

The effects of narcotics on fetal acid base status.

This paper reports two randomized control trials on the effects of nalorphine, pethidine, morphine and heroin on fetal and maternal acid base status. The drugs decreased pH and increased pCO2 in the mother, and decreased pH and base excess in the fetus. The changes in the fetus were independent of the changes in the mother. In equivalent dosages, nalorphine increased maternal pCO2 more than pethidine and morphine. The effects of heroin were found to be greater than that of other drugs, and we suggest that heroin should be avoided where the fetus is already at risk.

Acid-Base Equilibrium↗
PubMed1975

Changes in the acid base status of sheep anaesthetised with a combination of atropine sulphate acepromazine and ketamine hydrochloride.

pH, PaCO2, PaO2, standard bicarbonate, base excess and reduced pH were measured in sheep before and at regular intervals after administration of ketamine with and without atropine and acepromazine premedication. A decrease in pH and PaO2 and a rise in PaCO2 was observed 15 minutes after administration of ketamine. Administration of atropine with and without acepromazine had no significant effect on pH, PaCO2 and PaO2. The values for standard bicarbonate, base excess and reduced pH were not significantly affected. This indicates that minor changes observed in pH, PaCO2 after ketamine administration are compensated for by the healthy animal's blood buffer system.

Acepromazine↗
PubMed1975

Renal response to acid loading in the developing lamb fetus, intact in utero.

Response of the fetal kidney to metabolic acidosis was studied in five fetal lambs, 115-125 days gestation, in order to evaluate the renal contribution to elimination of hydrogen ion during intra-uterine development. Experiments were conducted on healthy unanesthetized fetuses, intact in utero, with catheters implanted at hysterotomy into a fetal femoral artery and vein and into the bladder via the urachus, four or more days prior to the study. A metabolic acidosis was induced by infusion of isotonic lactic acid, 15 m mole/kg, intravenously over a period of 90 minutes. Serial arterial samples were taken and urine collected in fractions before, during and for three hours following the infusion, for measurements of pH, bicarbonate, lactate and electrolytes as well as urine output. During the infusion, urine pH fell from 6.65 to 6.25 and was 6.34 three hours later (Figs. 1 to 4, Tabs. III to IV). Lactic acid infusion caused a prompt increase in urine output from a mean rate of 0.12 to a maximum of 0.28 ml/kg/min at the end of the infusion, returning to control rates three hours later. Lactate excretion increased from 0.05 to a maximum of 4.6 mumole/kg/min at the end of infusion; titratable acid increased from 0.22 to a maximum of 4 muEq/kg/min; the rates of excretion of lactate and titratable acid were still higher than control at the end of three hours. Ammonia excretion increased from 0.21 to a maximum of 0.56 muEq/kg/min three hours after the end of infusion. The acid infusion caused a small but significant fall in excretion of bicarbonate. During the 90 minutes of infusion and over the following three hours, about 800 mumole lactate was excreted while net acid excretion over the same period was no more than half that amount. The diuresis was also accompanied by a net loss of sodium and chloride, the excretion of these ions increasing more than threefold following acid infusion; excretion of potassium decreased to one-third its rate prior to the infusion. During the 90 minutes of infusion, blood pH fell from 7.36 to 7.13, base deficit rose from 3.8 to 16.4 mEq/L and lactate rose from 2.2 to 14.8 mM/L; there was also a small but significant rise in both blood PCO2 and PO2 (Figs. 1 to 2, Tabs. I to II). During the following three hours of recovery, pH rose gradually to 7.29, base deficit and lactate fell to 7.4 mEq/L and 8.7 mM/L respectively. Since renal excretion of net acid and lactate was small, the decrease in blood base deficit and lactate levels during the recovery must therefore be mainly due to equilibration in various fetal compartments as well as placental transfer. These experiments indicate that, in the lamb fetus, intact in utero, the kidney although limited by immaturity of several mechanisms, is capable of responding to an acid load and thus can make a small contribution to fetal homeostasis. The increase in excretion of net acid is accompanied by loss of sodium and chloride in the urine.

Acid-Base Equilibrium↗
PubMed1975

Recognition and significance of maternogenic fetal acidosis during intensive monitoring of labor.

FHR monitoring and microanalysis of fetal blood are mutually complementary procedures, and optimal knowledge of the fetal state is achieved by making use of both, the former for the preliminary screening of all cases at risk and the latter for the purpose of deciding on obstetric management where pathological changes are evident in the FHR. The major difficulty in obtaining a precise value for the fetal acid-base balance lies in the occurence of "falsely abnormal" cases, i.e. cases in which the fetal pH falls during labor but the clinical condition at birth is good (APGAR greater than or equal to 7). In our own series the incidence of such cases among fetuses at risk was 11.2% (Tab. I). In the majority of these cases the fetal acidosis is thought to be a result of increased metabolic acidosis in the mother (maternogenic fetal metabolic acidosis). The importance of the maternogenic fetal acidosis during labor lies in the fact that unless it is recognised, rapid extraction of the fetus will appear necessary on clinical grounds, although it is in fact unnecessary, since this form of acidosis has no adverse effect on the fetus. Various parameters have been proposed for the differential diagnosis of the maternogenic fetal acidosis. These include the feto-maternal difference in base deficit (F/M deltaBD), the materno-fetal differences in pHqu 40 (M/F deltapHqu 40) the materno-fetal difference actual pH (M/F actual deltapH), and the materno-fetal difference in base deficit of the extra-cellular fluid (M/F deltaBDHb5). A critical analysis of these parameters has been carried out on the results of microtests performed during a 5 year period (1968-1972) at the First Clinic of Obstetrics and Gynecology of Milan University. The cases comprised 59 regarded as normal (normal course of pregnancy, spontaneous commencement of labor at term, clear amniotic fluid, regular FHR, spontaneous birth, APGAR at 90 sec between 8 and 10, weight at birth greater than 2500 g), and 335 considered to be at risk (maternal disease, presence of meconium stained amniotic fluid and/or abnormal changes in FHR). In all of these cases the FHR was recorded by cardiotokography, and the tracings were interpreted according to HON. Microsamples of blood were taken from both mother and fetus during labor and the following determinations were carried out: actual pH, pHqu 40, Hb concentration, hemoglobin oxygen saturation, base deficit Hb5 (BDHb5). The maternofetal differences were then calculated. The same determinations were carried out on samples of maternal blood and of arterial and venous cord blood taken immediately after delivery. The clinical condition of the infant was evaluated by the APGAR score at 90 seconds after birth.

Acid-Base Equilibrium↗
PubMed1975

[Peroperative resuscitation in abdominal reoperations].

Resuscitation of these patients during operation is the only the logical continuation of their preparation. The authors therefore take up the preceding points while emphasizing: - checking vascular filling, by central venous pressure and hourly diuresis; - the necessity for a supply of carbohydrates, which is even more indispensable when the subjects were submitted to parenteral hyperalimentation previously; - the advantages of performing arterial blood gases in order to check artificial ventilation.

Abdomen↗
PubMed1977

[Determination of acid-base parameters by means of programmable pocket calculators (author's transl)].

The possibility to calculate parameters of acid-base status derived by common laboratory devices without built-in computers is described. The calculation is carried out faster and more exactly than it is possible by nomograms, which is especially suitable when a great quantity of dates occurs. The number of programmable steps in some inexpensive pocket calculators is sufficient for this purpose; this type of "microcomputers" offers advantages of economy and small size so that calculations can be carried out immediately at the site where measurements are taken.

Acid-Base Equilibrium↗
PubMed1975

Hydrogen ion changes and contractile behavior in the perfused rat heart.

The effect of acid-base alterations was analyzed using isolated rat hearts perfused at constant coronary perfusion pressure, and stimulated to contract at constant rat. The amount of shortening in the major axis and its derivative were measured to assess myocardial contractility. Both the 'respiratory' and 'metabolic' alterations affected the contractile behavior to the same extent. In the physiological range studied by us, acidosis depresses and alkalosis increases myocardial contraction. However acidosis seems to depress contractility more than the enhancement produced by the same change in pH towards the alkalotic side. When either amount of shortening or max dl/dt was plotted as a function of hydrogen ion acitvity (aH+) a linear correlation was obtained, either with pure 'metabolic' or 'respiratory' acid-base induced alterations (correlation coefficients higher than -.95; P less than .01). Our findings suggest that in the range studied by us, contraction of the perfused rat heart following acid-base alterations, is a linear function of hydrogen ion activity.

Acid-Base Equilibrium↗
PubMed1975

[Studies on low volume priming heart lung bypass (author's transl)].

This report concerns the feasibility of low volume priming extracorporeal circulation. Through this study, the bubble oxygenator with Zuhdi's heat exchange was used. Moderate hypothermia with surface cooling and hemodilution perfusion with 5 per cent D/W was evaluated in 32 mongrel dogs and 16 clinical open heart cases. The results obtained here were as follow: 1) Body temperature reduction by surface cooling before bypass provided more even cooling than did core cooling by low flow partial bypass alone. 2) In regard to cardiac loading on returning the whole perfusate of the circuit to patient, approximately 20 ml/kg of 5 per cent D/W was feasible as a priming solution. 3) To reduce the blood visicosity, hemodilution technique with 5 per cent D/W was superior, and hemodilution effect during postoperative periods was temporaly. 4) The excess lactate volume postulated by Huckabee was a available index to evaluate metabolic acidosis during the extracorporeal circulation. 5) With aid of surface cooling, the acid-base balance during perfusion was kept to lesser extent than that of core cooling only. 6) This study indicated that the low priming perfusion in conjunction with surface cooling hypothermia was a reliable technique for the open heart operation and may be applied in more prolonged perfusion.

Acid-Base Equilibrium↗