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PubMed1990

Interaction of hypoxia and hypercapnia on respiratory drive in patients with COPD.

The objective of this study was to compare the response of respiratory drive to progressive hypoxia under eucapnic and hypercapnic conditions in patients with severe COPD. Twenty-five patients with severe COPD and 13 nonsmoking young men were studied. The pressure in the occluded airway measured 0.1 second after the onset of inspiration was used as an index of respiratory drive. The occlusion pressure was measured at levels of SaO2 between 97 and 85 percent while eucapnic. The PETCO2 was then increased 10 mm Hg and the study repeated. The response of respiratory drive to hypoxia as measured by the slope of the regression line relating occlusion pressure to SaO2 was weak and variable in eucapnic hypoxia, and some subjects had no demonstrable response. When mild respiratory acidosis was created by increasing the PETCO2, the response to hypoxia was much greater and occurred in all subjects studied. Respiratory acidosis resulting from acute elevation of the PaCO2 greatly potentiates the increase in respiratory drive in response to hypoxia in normal subjects and in patients with severe COPD. Increase in occlusion pressure may occur with slight degrees of hypoxia when acute hypercapnia is present. These observations suggest that patients with acute respiratory failure complicating COPD, treated with controlled oxygen administration with only partial correction of hypoxia and continued respiratory acidosis, will have high respiratory drive.

Aged↗

PubMed2006

Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule.

The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P < 0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P < 0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P < 0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.

Acidosis, Respiratory↗

PubMed1991

Expression of rat renal Na/H antiporter mRNA levels in response to respiratory and metabolic acidosis.

The mammalian proximal tubule is an important mediator of the renal adaptive response to systemic acidosis. In chronic metabolic and respiratory acidosis the bicarbonate reabsorptive (or proton secretory) capacity is increased. This increase is mediated, at least in part, by an increase in Vmax of the luminal Na/H antiporter. To determine whether this adaptation involves increased mRNA expression, Na/H antiporter mRNA levels were measured by Northern analysis in renal cortex of rats with metabolic (6 mmol/kg body wt NH4Cl for 2 or 5 d) and respiratory (10% CO2/air balanced for 2 or 5 d) acidosis and of normal, pair-fed rats. Na/H antiporter mRNA levels were unchanged after 2 d of both metabolic and respiratory acidosis. After 5 d, however, Na/H antiporter mRNA expression was increased 1.76 +/- 0.12-fold in response to metabolic acidosis (P less than 0.005, n = 8), but was not different from normal in response to respiratory acidosis: 1.1 +/- 0.2 (NS, n = 8). Thus, the renal adaptive response to metabolic acidosis involves increased cortical Na/H antiporter mRNA levels. In contrast, the enhanced proximal tubule Na/H antiporter activity and bicarbonate reabsorption in respiratory acidosis seem to involve mechanisms other than increased Na/H antiporter gene expression.

Acidosis↗

PubMed2006

Hormonal regulation of alveolarization: structure-function correlation.

BACKGROUND: Dexamethasone (Dex) limits and all-trans-retinoic acid (RA) promotes alveolarization. While structural changes resulting from such hormonal exposures are known, their functional consequences are unclear. METHODS: Neonatal rats were treated with Dex and/or RA during the first two weeks of life or were given RA after previous exposure to Dex. Morphology was assessed by light microscopy and radial alveolar counts. Function was evaluated by plethysmography at d13, pressure volume curves at d30, and exercise swim testing and arterial blood gases at both d15 and d30. RESULTS: Dex-treated animals had simplified lung architecture without secondary septation. Animals given RA alone had smaller, more numerous alveoli. Concomitant treatment with Dex + RA prevented the Dex-induced changes in septation. While the results of exposure to Dex + RA were sustained, the effects of RA alone were reversed two weeks after treatment was stopped. At d13, Dex-treated animals had increased lung volume, respiratory rate, tidal volume, and minute ventilation. On d15, both RA- and Dex-treated animals had hypercarbia and low arterial pH. By d30, the RA-treated animals resolved this respiratory acidosis, but Dex-treated animals continued to demonstrate blood gas and lung volume abnormalities. Concomitant RA treatment improved respiratory acidosis, but failed to normalize Dex-induced changes in pulmonary function and lung volumes. No differences in exercise tolerance were noted at either d15 or d30. RA treatment after the period of alveolarization also corrected the effects of earlier Dex exposure, but the structural changes due to RA alone were again lost two weeks after treatment. CONCLUSION: We conclude that both RA- and corticosteroid-treatments are associated with respiratory acidosis at d15. While RA alone-induced changes in structure andrespiratory function are reversed, Dex-treated animals continue to demonstrate increased respiratory rate, minute ventilation, tidal and total lung volumes at d30. Concomitant treatment with Dex + RA prevents decreased septation induced by Dex alone and results in correction of hypercarbia. However, these animals continue to have abnormal pulmonary function and lung volumes. Increased septation as a result of RA treatment alone is reversed upon discontinuation of treatment. These data suggest that Dex + RA treatment results in improved gas exchange likely secondary to normalized septation.

Acidosis, Respiratory↗

PubMed1999

Effect of high arterial carbon dioxide tension on efficiency of immunoglobulin G absorption in calves.

OBJECTIVES: To determine whether high PaCO2 reduced apparent efficiency of IgG absorption (AEA) in calves and whether assisted ventilation of calves with high PaCO2 increased AEA. ANIMALS: 48 Holstein calves. PROCEDURES: Arterial and venous blood samples were collected 1, 13, and 25 hours after birth; an additional venous sample was collected at 37 hours after birth. Arterial samples were analyzed for PaCO2, PaO2, pH, and bicarbonate and base excess concentrations; venous samples were analyzed for plasma IgG concentrations. On the basis of 1-hour PaCO2, calves were assigned to nonrespiratory acidosis (PaCO2 < 50 mm Hg; n = 19) or respiratory acidosis (PaCO2 > or = 50 mm Hg; 29) groups. Calves in the respiratory acidosis group were assigned randomly to receive no further treatment (n = 17) or to be given 5 minutes of assisted ventilation (12). All calves received between 1.8 and 2 L of colostrum 2, 14, 26, and 38 hours after birth. Plasma volume and AEA were determined 25 hours after birth. RESULTS: 1-hour PaCO2 had no effect on AEA or on plasma IgG concentrations determined 13, 25, or 37 hours after birth. Artificial ventilation had no effect on plasma IgG concentration or AEA. CONCLUSIONS AND CLINICAL RELEVANCE: Lack of effect of 1-hour PaCO2 on AEA and IgG concentration indicated that calves compensated for moderate acid-base imbalances associated with birth. Calves born with high PaCO2 achieved adequate plasma IgG concentrations if fed an adequate amount of high-quality colostrum early in life. The effect of artificial ventilation on PaCO2 was temporary and did not increase AEA.

Acidosis, Respiratory↗

PubMed1975

CO2 retention as a basis for increased toxicity of salicylate with acetazolamide: avoidance of increased toxicity with benzolamide.

Two carbonic anhydrase inhibitors, acetazolamide and benzolamide, are capable of increasing the toxicity of sodium salicylate in mice. Beginning at about 2 mg/kg, each of the inhibitors, in combination with a fixed (400 mg/kg) dose of salicylate, generates a dose-mortality curve that reaches a plateau at about 60% deaths at 6 to 8 mg/kg. This effect can be duplicated by 8 to 10% inspired CO2. It appears that the respiratory acidosis secondary to the inhibition of red cell carbonic anhydrase is responsible for the increased toxicity; earlier work by others shows that acidosis increases the concentration of salicylate in the brain. In the treatment of salicylate poisoning by carbonic anhydrase inhibitors, the goal is to alkalinize the urine and increase the excretion of salicylate. With the newer inhibitor, benzolamide, it is possible to dissociate the respiratory acidosis from the renal effect. Maximal alkalinization of the urine is possible with a dose (about 1 mg/kg) below that which generates a respiratory acidosis. With this dose, there is no increase in the early toxicity of salicylate.

Acetazolamide↗

PubMed2006

The impact of PCO2 and H+ on the release of acetylcholine from the cat carotid body.

The carotid body (CB) is a sensor of oxygen, carbon dioxide, hydrogen ion, and glucose in the arterial blood. Many studies of the CB's responses to low oxygen (hypoxia) have been reported. Recently attention has been increasingly focused on its responses to elevated CO2 (hypercapnia). An increase in ventilation or carotid body neural output (CBNO) can result from stimulating the CB with blood or perfusion fluids having an elevated CO2 or H+. The increase in ventilation seen with a hypoxic stimulus is accompanied with an increase in CBNO and an increased release of both acetylcholine (ACh) and ATP from the CB. The present in vitro study using both CBs harvested from six cats was undertaken to determine if hypercapnia also provoked an increased release of ACh from the incubated CBs. The anesthetizing, handling, and euthanizing of the animals were according to the guidelines of the Johns Hopkins Animal Care and Use Committee which are totally consonant with those of the NIH. CBs, once harvested and prepared for the experimental protocol, were subjected to the following steps each lasting 10 min: (1) control; (2) stress; (3) recovery. The stresses were respiratory acidosis (RAC; acidic hypercapnia), compensated respiratory acidosis (CRAC; isohydric hypercapnia), and metabolic acidosis (MtAC). The first and last forms of acidosis generated small but significant increases in the release of ACh from the CBs; the second generated a very small and insignificant increase in ACh release. Since it is generally accepted that ACh is a key excitatory neurotransmitter in the CB along with ATP, these data are consistent with other studies measuring the increase in ventilation in response to a small increase in CO2 and those studies recording CBNO in response to hypercapnia. In five of the six animals the responses to RAC and MtAC were compared to the responses to hypoxia. The latter were statistically indistinguishable from the former two.

Acetylcholine↗

PubMed2001

Protective effects of hypercapnic acidosis on ventilator-induced lung injury.

To investigate whether respiratory acidosis modulates ventilator-induced lung injury (VILI), we perfused (constant flow) 21 isolated sets of normal rabbit lungs, ventilated them for 20 min (pressure controlled ventilation [PCV] = 15 cm H(2)O) (Baseline) with an inspired CO(2) fraction adjusted for the partial pressure of CO(2) in the perfusate (PCO(2) approximately equal to 40 mm Hg), and then randomized them into three groups. Group A (control: n = 7) was ventilated with PCV = 15 cm H(2)O for three consecutive 20-min periods (T1, T2, T3). In Group B (high PCV/normocapnia; n = 7), PCV was given at 20 (T1), 25 (T2), and 30 (T3) cm H(2)O. The targeted PCO(2) was 40 mm Hg in Groups A and B. Group C (high PCV/hypercapnia; n = 7) was ventilated in the same way as Group B, but the targeted PCO(2) was approximately equal to 70 to 100 mm Hg. The changes (from Baseline to T3) in weight gain (Delta WG: g) and in the ultrafiltration coefficient (Delta K(f) = gr/min/ cm H(2)O/100g) and the protein and hemoglobin concentrations in bronchoalveolar lavage fluid (BALF) were used to assess injury. Group B experienced a significantly greater Delta WG (14.85 +/- 5.49 [mean +/- SEM] g) and Delta K(f) (1.40 +/- 0.49 g/min/cm H(2)O/100 g) than did either Group A (Delta WG = 0.70 +/- 0.43; Delta K(f) = 0.01 +/- 0.03) or Group C (Delta WG = 5.27 +/- 2.03 g; Delta K(f) = 0.25 +/- 0.12 g/min/cm H(2)O/ 100 g). BALF protein and hemoglobin concentrations (g/L) were higher in Group B (11.98 +/- 3.78 g/L and 1.82 +/- 0.40 g/L, respectively) than in Group A (2.92 +/- 0.75 g/L and 0.38 +/- 0.15 g/L) or Group C (5.71 +/- 1.88 g/L and 1.19 +/- 0.32 g/L). We conclude that respiratory acidosis decreases the severity of VILI in this model.

Acidosis, Respiratory↗

PubMed1975

Glycoside inotropy in the absence of an increase in potassium efflux in the rabbit heart.

The inotropic effect of 1.25 times 10(-6)M acetylstrophanthidin (ACS) and the influx and efflux of labeled potassium (42K+) were studied in the arterially perfused rabbit interventricular septum under control conditions and during respiratory acidosis. An increase in the CO2 content of the gas mixture with which the modified Ringer's solution was equilibrated from 5 to 30% reduced the perfusate pH from 7.37 to 6.66. The increment in developed tension in the presence of ACS was 3.0 +/- 0.2 g (n equals 10) under control conditions, but it was greater, 7.1 +/- 0.9 g (N equals 9) during acidosis (P less than less than 0.001). The net K+ loss due to an increase in K+ efflux was 1.8 +/- 0.2 mmoles/kg wet weight in control experiments but only 0.1 +/- 0.1 mmoles/kg net weight under acidotic conitions (P less than less than 0.001); in seven of nine experiments in respiratory acidosis, no increase in K+ efflux occurred despite a marked positive inotropy. In three septums, K+ influx was reduced by ACS during respiratory acidosis. These results demonstrate that during acidosis ACS inhibits sodium-potassium adenosinetriphosphatase (Na+-K+ ATPase) and causes an inotropic effect but does not increase K+ efflux. K+ efflux cannot be linked to calcium (Ca2+) influx or regarded as the controlling factor of glycoside-induced inotropy. The results give further support to the proposal that digitalis-induced inotropy is secondary to an enhancement of a Na+-Ca2+ exchange system.

Acidosis, Respiratory↗

PubMed1976

Effects of respiratory alkalosis and acidosis on myocardial excitation.

In anesthetized dogs electrocardiogram and monophasic action potentials (MAPs) were recorded from the right atrium and the right ventricle by intracardiac suction electrode technique. The animals were subjected, by means of ventilation with CO2 and hyperventilation, to periods of respiratory acidosis and respiratory alkalosis, respectively. Pronounced respiratory acidosis induced an increased sympathetic activity followed by a decrease in heart rate and prolongation of the A-V conduction time whereas the shape and duration of the atrial and ventricular MAPs remained unaltered. Arterial hypoxia in combination with pronounced respiratory acidosis did not influence the MAP durations. Respiratory alkalosis resulted in an increased sympathetic influence on the heart activity whereas the shape and duration of the atrial and the ventricular MAPs remained unaffected. During pronounced hyperventilation with increasing central venous pressure an increased parasympathetic influence on the heart activity with decrease in the heart rate, prolongation of the A-V conduction time and shortening of the atrial MAP duration was recorded.

Acidosis, Respiratory↗

PubMedDate not supplied

Respiratory influence on the total and regional cerebral blood flow responses to intracranial hypertension.

The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.

Acidosis, Respiratory↗

PubMed1995

Heliox therapy in acute severe asthma.

STUDY OBJECTIVE: To assess how patients with respiratory acidosis from acute severe asthma respond to helium-oxygen (heliox) mixtures. DESIGN: Consecutive case series. SETTING: Urban community teaching hospital. PATIENTS: Over a 2-year period, 12 asthmatics (mean age, 33.8 +/- 11.3 years) presented to the emergency department with acute respiratory acidosis (pH < 7.35 and PaCO2 > or = 45 mm Hg). All 12 patients were treated with heliox (60 to 70% helium/30 to 40% oxygen). Five patients received heliox through a ventilator and seven received heliox via face mask. RESULTS: Arterial blood gases (ABGs) were drawn immediately before and at a mean of 49.2 +/- 25.2 min after beginning heliox therapy. No therapeutic interventions were made between ABGs. For the entire group, the mean PaCO2 decreased from 57.9 to 47.5 mm Hg (p < 0.005) and the arterial pH increased from 7.23 to 7.32 (p < 0.001). In an attempt to find characteristics that might predict the response to heliox, a clinically significant response to heliox was defined as a drop in PaCO2 (to normal or by > or = 15%) coupled with a rise in pH by > or = 0.05. Using this definition, there were eight responders (67%) and four nonresponders (33%). The responders had a shorter duration of symptoms (17.8 vs 78.0 h, p < 0.05) and a lower preheliox pH (7.20 vs 7.30, p < 0.05). All of the responders presented within 24 h of symptom onset. Three of the four nonresponders reported prolonged (> or = 96 h) duration of symptoms, and two eventually required intubation. CONCLUSION: Heliox can rapidly improve ventilation in patients presenting to an emergency department with acute severe asthma with respiratory acidosis and a short duration of symptoms.

Acidosis, Respiratory↗

PubMed1995

Noninvasive nasal mask ventilation beyond the ICU for an exacerbation of chronic respiratory insufficiency.

STUDY OBJECTIVE: To assess the usefulness of noninvasive nasal mask ventilation (NMV) in the treatment of an exacerbation of chronic respiratory insufficiency in patients stable enough to be admitted to a non-ICU ward. DESIGN: A prospective study in which the beneficial effect of NMV was compared with conservative treatment. SETTING: A ward of respiratory medicine of a tertiary-referral teaching hospital. PATIENTS: The study group included 15 patients with acute respiratory acidosis. These patients had pH less than 7.35 and PaCO2 more than 60 mm Hg, respiratory rate of 30 breaths or less per minute, hemodynamic stability, and alertness and willingness of cooperation with the NMV treatment. The control group consisted of 16 patients who fulfilled the same arterial blood gas requirements, retrospectively selected from the discharge forms of the ward of respiratory medicine for the year 1993. INTERVENTIONS: Patients underwent NMV for two sessions per day (one in the morning and one in the afternoon), each session lasting 4 h. A volumetric respirator (Monnal D; Taema; Paris, France) was used in four patients with restrictive disease. A positive-pressure ventilator (DP90; Taema; Paris, France) was used in 11 patients with obstructive disease. Control patients received standard medical, oxygen, and chest physical therapy. RESULTS: As compared with pre-NMV values, mean pH was significantly higher at 4 h of NMV after the patient's ventilatory adaptation (t = 8.814, p < 0.001) and at the end of NMV (t = 12.06, p < 0.001). Ventilatory support also produced a significant improvement in hypercapnia (pre-NMV vs NMV after the patient's ventilatory adaptation, t = 6.675, p < 0.001; pre-NMV vs post-NMV, t = 6.976, p < 0.001). Posttreatment pH and PaCO2 values were significantly higher and lower, respectively, in NMV-treated patients than in controls. At the end of treatment, a significantly higher PaO2/FIO2 ratio was documented in the study group than in controls (post-NMV vs posttreatment, t = 2.846, p < 0.01). CONCLUSIONS: NMV associated with standard treatment may be more beneficial than conservative treatment alone for improving blood gas exchange in patients with chronic respiratory insufficiency admitted to the hospital (but not the ICU) for an episode of acute decompensation and respiratory acidosis.

Acidosis, Respiratory↗

PubMed1999

[Noninvasive intermittent positive pressure ventilation in treatment of chronic respiratory disease exacerbation].

Noninvasive intermittent positive pressure ventilation (NIPPV) via nasal mask became a routine method of treatment of severe exacerbations of chronic respiratory failure. The aim of the study was to apply NIPPV in patients with COPD admitted to hospital due to exacerbation of the disease who on standard treatment developed progressing respiratory acidosis (pH < 7.30). Fourteen COPD patients were treated with NIPPV. Arterial blood gases at the beginning of treatment were: PaO2 41 +/- 9 mmHg, PaCO2 = 87 +/- 17 mmHg, pH = 7.30 +/- 0.05. In 10 patients NIPPV applied quasi continuously resulted in clinical improvement and an amelioration of arterial blood gases. PaO2 rose from 41 +/- 9 mmHg to 56 +/- 12 mmHg, PaCO2 fell from 85 +/- 17 to 57 +/- 9 mmHg and pH rose from 7.30 +/- 0.05 to 7.41 +/- 0.04. In 4 patients NIPPV did not prevent further progression of respiratory acidosis. They were intubated and mechanically ventilated. Three patients survived and were discharged home. One patient died from septic shock. We conclude that NIPPV is an effective method to treat respiratory acidosis developing during exacerbation of severe COPD.

Acidosis, Respiratory↗

PubMed1990

Acid-base-electrolyte balance responses to catecholamine antagonists in Ambystoma tigrinum.

Neotenic larval Ambystoma tigrinum were subjected to hypercapnia (3% CO2, 22 Torr) for 24 h under different conditions: alpha-adrenergic blockade using phentolamine, beta-adrenergic blockade using propranolol, and sham treatments. The sham animals were able to carry out a partial extracellular pH compensation that consisted of an increase in extracellular [HCO3-]. Animals treated with catecholamine antagonists did not compensate to the same extent. Analysis of plasma samples by high-performance liquid chromatography with electrochemical detection revealed a significant increase in circulating norepinephrine, but not epinephrine, during the high-CO2 exposure. Measurements of cutaneous ion transport showed that beta-antagonists block the increased Na+ influx associated with hypercapnia, whereas alpha-antagonists inhibited the decrease in cutaneous Cl- influx that is also associated with respiratory acidosis. Additionally, both alpha- and beta-blockers inhibited the increase in transcutaneous potential difference that accompanied the respiratory acidosis. The results are consistent with a role for circulating catecholamines in compensatory ion transport responses to respiratory acidosis in this species.

Acid-Base Equilibrium↗

PubMed1997

Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acidbase status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acidbase compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.

Journal Article↗

PubMed1984

Chronic mountain sickness at an elevation of 2,000 meters.

A resident living at Lake Tahoe, Calif, at an elevation of 2,000 meters, had fatigue, edema, and erythrocythemia. Hematocrit was 63 percent, and arterial blood gas values revealed hypoxemia and respiratory acidosis. Results of pulmonary function tests, sleep study, and thyroid function all were normal. Erythrocytosis, cor pulmonale, and respiratory acidosis resolved after the patient moved to sea level. This patient suffered from chronic mountain sickness. Her symptoms resolved with relief of hypoxia.

Acidosis, Respiratory↗

PubMed1993

Inhaled nitric oxide reverses pulmonary vasoconstriction in the hypoxic and acidotic newborn lamb.

We determined whether inhaling low levels of nitric oxide (NO) gas could selectively reverse hypoxic pulmonary vasoconstriction in the near-term newborn lamb and whether vasodilation would be attenuated by respiratory acidosis. To examine the mechanism of air and NO-induced pulmonary vasodilation soon after birth, we measured plasma and lung cGMP levels in the newly ventilated fetal lamb. Breathing at FIO2 0.10 nearly doubled the pulmonary vascular resistance index in newborn lambs and decreased pulmonary blood flow primarily by reducing left-to-right blood flow through the ductus arteriosus. Inhaling 20 ppm NO at FIO2 0.10 completely reversed hypoxic pulmonary vasoconstriction within minutes. Maximum pulmonary vasodilation occurred during inhalation of > or = 80 ppm NO. Breathing 8% CO2 at FIO2 0.10 elevated the pulmonary vascular resistance index to a level similar to breathing at FIO2 0.10 without added CO2. Respiratory acidosis did not attenuate pulmonary vasodilation by inhaled NO. In none of our studies did inhaling NO produce systemic hypotension or elevate methemoglobin levels. Four minutes after initiating ventilation with air in the fetal lamb lung, cGMP concentration nearly doubled without changing preductal plasma cGMP concentration. Ventilation with 80 ppm NO at FIO2 0.21 increased both lung and preductal plasma cGMP concentration threefold. Our data suggest that inhaled NO gas is a rapid and potent selective vasodilator of the newborn pulmonary circulation with an elevated vascular tone due to hypoxia and respiratory acidosis that acts by increasing lung cGMP concentration.

Acidosis, Respiratory↗