Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of respiratory and metabolic acidosis (pH approximately 6.8) on myocardial function were studied in the newborn and adult rabbits. Mechanical function was studied in the isolated arterially perfused heart preparation. Acidosis was induced either by increase of the perfusate PCO2 or by decrease of the bicarbonate content. During respiratory acidosis, developed tension (DT) decreased to 43 +/- 3% of control (n = 18) in the adult and this depression was significantly greater than in the newborn (DT = 92 +/- 4%, n = 6). Depression of DT by respiratory acidosis was observed even at high extracellular Ca. During metabolic acidosis, mechanical function decreased gradually and DT at 30 min into acidosis in the adult was 78 +/- 3% of control (n = 6). This depression of DT in the adult was significantly greater than in the newborn (DT at 30 min = 96 +/- 1% of control, n = 6). Statistical analysis using paired t test showed that respiratory acidosis, but not metabolic acidosis, caused significant negative inotropism in the newborn. Myofibrils were isolated and the ATPase was measured at 10(-8) to 10(-4) M Ca and at pH of 7.1 (control), 6.5, and 6.0. Reducing pH depressed the ATPase activity similarly in the newborn and adult. Intracellular buffer capacity was determined by titrating muscle homogenate with HCI. Although the initial pH was not different, addition of HCl to the homogenate caused less decrease in pH in the newborn. These data indicate that contractile function in the newborn heart is more resistant to acidosis and this may be due partly to the greater intracellular buffer capacity.
 ...
PMID:Effect of acidosis on contractile function in the newborn rabbit heart. 315 69

The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCI infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone).
 ...
PMID:The plasma potassium concentration in metabolic acidosis: a re-evaluation. 334 45

The role of smooth muscle [Ca2+]i and membrane potential for the relaxation to hypercapnic (increased CO2) and normocapnic (unchanged CO2) acidosis is not complete understood. It is often stated that membrane hyperpolarization plays an important role but this has not been vigorously tested. In this study we investigated isolated rat cerebral small arteries under isobaric conditions. Lumen diameter was measured simultaneously with either [Ca2+]i or membrane potential, and acidosis was induced by increasing PCO2 or reducing HCO3- of the bathing solution or by adding HCI to a nominally bicarbonate-free solution. Confocal microscopy verified loading of smooth muscle cells with fluorescent dyes. Acidosis always reduced myogenic tone at transmural pressures between 20 and 120 mmHg. Acidification at a transmural pressure of 40 mmHg caused an increase in diameter and a decrease in [Ca2+]i. This was also seen in the presence of L-NNA and after depolarization with 50 mM K+. The response to hypercapnic and normocapnic acidosis was similar. However, while hypercapnic acidosis caused hyperpolarization, normocapnic acidosis caused depolarization. Dilatation, decrease of [Ca2+]i and depolarization, was also seen with reduction of pH in bicarbonate-free solution. We conclude that the isobaric relaxation to both hypercapnic and normocapnic acidosis is most likely mediated by a reduction of [Ca2+]i. Membrane potential may on the other hand not play a major role for this reduction of [Ca2+]i and it is possible that molecular CO2 has an effect on the membrane potential.
 ...
PMID:On the cellular mechanism for the effect of acidosis on vascular tone. 988 74