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At least 145 records · Page 8Linked to original sources
PubMed1978

The effect of beta adrenergic receptor blockade on the renin response to respiratory acidosis.

The effect of beta adrenergic blockade on the increase in plasma renin activity produced by acute respiratory acidosis was studied in chloralose anesthetized dogs. Sixteen mongrel dogs were given 4%, 8% and 12% CO2 in room air, successively. Propranolol (2 mg/Kg) was given to 8 dogs prior to CO2 inhalation. The other 8 dogs served as the control group. The response of elevated plasma renin activity during 4% and 8% CO2 inhalation was not different between the control and propranolol groups. However, the increase of plasma renin activity in the control group was greater than that of the propranolol treated group during 12% CO2 inhalation. It is suggested that activation of beta adrenergic receptors is not the sole factor in renin control during acute respiratory acidosis, although these receptors do mediate a significant fraction of the renin response to CO2 inhalation.

Acidosis, Respiratory↗
PubMed1977

Effect of respiratory acidosis and activity on airway smooth muscle intracellular pH.

Previous work in our laboratory has shown that respiratory acidosis (RA) impaired mechanical function in canine tracheal smooth muscle (TSM). Since an intracellular acidosis could be brought on by the increased CO2 content of the bathing medium and alter the Km's of rate-limiting glycolytic enzymes in the pathway of energy production for contractile function, we have investigated the effects of RA on the intracellular pH (pHi) of TSM. Using the DMO method, paired unstimulated or resting TSM strips were incubated under normocapnic conditions (PO2 600 Torr, PCO2 40 Torr, pH 7.40) and RA (PO2 550 Torr, PCO2 110 Torr, pH 6.95) with 14C-labeled DMO and 3H-labeled inulin or PEG-4000. In another set of paired experiments, TSM strips were tetanized electrically every 5 min or pharmacologically throughout the incubation period ("active" muscle strips). The tissue and an aliquot of bathing medium were counted for 3H and 14C content and the values entered into the Wadell and Butler equation. The pHi's of "resting" normocapnic and acidotic strips were 7.041 +/- 0.017 (SE) and 6.752 +/- 0.012, respectively. However, the pHi's of "active" normocapnic and acidotic strips were 7.275 +/- 0.017 and 7.017 +/- 0.015, respectively. We conclude that respiratory acidosis lowers intracellular pH in both resting and mechanically active TSM's; however, "active" preparations whether exposed to normocapnia or acidosis were unexpectedly more alkaline than their "resting" counterparts.

Acidosis, Respiratory↗
PubMed1984

Effects of acetazolamide on ionic composition of cisternal fluid during acute respiratory acidosis.

We studied the effects of intravenous acetazolamide (50-200 mg/kg) on cerebrospinal fluid (CSF) electrolytes and pH regulation in 10 anesthetized and nephrectomized dogs (group II): acetazolamide was injected at -1 h, and respiratory acidosis was induced at zero time for 6 h. A control group of 10 animals (group I) was treated similarly except that an equal volume of 0.45% saline was injected intravenously instead of acetazolamide. The mean CSF PCO2 values in group I were 49.7 +/- 3.4 (SD), 50.2 +/- 3.6, 92.3 +/- 7.0, 100.3 +/- 8.1, and 97.8 +/- 7.3 Torr, respectively, at -1, 0, 3, 4.5, and 6 h; respective values in group II were 49.8 +/- 2.0, 55.2 +/- 5.2, 95.8 +/- 6.4, 103.1 +/- 16.7, and 104.9 +/- 14.1 Torr. During acute respiratory acidosis CSF [HCO3-] rose progressively with time in group I, and the mean values were 28.1 +/- 1.4 (SD), 29.2 +/- 1.7 and 30.1 +/- 1.9 mmol/l, respectively, 3, 4.5, and 6 h after induction of acidosis; respective values in group II were 28.2 +/- 1.1, 28.3 +/- 0.9, and 28.5 +/- 1.4 mmol/l. Acetazolamide at various doses administered inhibited any further rise in CSF [HCO3-] beyond the 3rd h of acidosis. The lower rise in CSF [HCO3-] in group II could not be ascribed to differences in CSF lactate concentration which changed similarly in both groups. Increments in CSF K+ and phosphate concentrations were significantly higher in the acetazolamide group than in the control group, the former presumably reflecting efflux of K+ from intracellular to extracellular fluid compartment. We conclude that in nephrectomized dogs during acute respiratory acidosis intravenously administered acetazolamide diminishes the rise in CSF [HCO3-], impairs CSF H+ regulation, and increases CSF K+ and phosphate concentrations.

Acetazolamide↗
PubMed1984

Acetazolamide teratogenesis: association of maternal respiratory acidosis and ectrodactyly in C57BL/6J mice.

Exposure of C57BL/6J mice to CO2 during a critical period of gestation results in predominantly right-sided, postaxial, forelimb ectrodactyly in the offspring. The incidence and severity of CO2-induced limb malformations has been shown to be dependent on the concentration of inspired CO2, the developmental age of the embryo at exposure and the duration of CO2 exposure. Offspring of acetazolamide-treated C57BL/6J mice also display this highly specific form of ectrodactyly (Green et al., '73). Since the drug has been shown to elevate tissue CO2 tension (Mithoefer and Davis, '58), the teratogenic effect of acetazolamide may be related to induction of a hypercapnic embryonic environment.

Abnormalities, Drug-Induced↗
PubMed1984

Acetazolamide teratogenesis: interaction of maternal metabolic and respiratory acidosis in the induction of ectrodactyly in C57BL/6J mice.

Exposure of C57BL/6J mice to 20% CO2 for 8 hours on day 10 of gestation has been shown to produce right-sided postaxial forelimb ectrodactyly in 23% of the offspring. Carbon dioxide exposure produces a dramatic increase in maternal plasma CO2 accompanied by an inevitable decrease in plasma pH, both of which appear to be involved in the induction of ectrodactyly. However, the low incidence of ectrodactyly associated with NH4Cl-induced metabolic acidosis suggests that the primary teratogenic factor in respiratory acidosis is elevated CO2 tension. This conclusion is supported by the observation that moderation of maternal plasma pH in the face of sustained elevated PCO2 fails to reduce the incidence of ectrodactyly; moreover, there is a strong correlation between maternal serum CO2 content and the incidence of ectrodactyly.

Abnormalities, Drug-Induced↗