Ventilation is stimulated by small reductions in arterial pressure in the awake dog

1992 ◽  
Vol 73 (4) ◽  
pp. 1549-1557 ◽  
Author(s):  
P. J. Ohtake ◽  
D. B. Jennings

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.

2001 ◽  
Vol 79 (9) ◽  
pp. 825-830
Author(s):  
Donald B Jennings

Intravenous (iv) infusion of the angiotensin II (ANG II) receptor blocker saralasin in resting conscious dogs during physiological pertubations, such as hypotension and prolonged hypoxia, indicates the presence of an ANG II drive to increase respiration and decrease the arterial partial pressure of CO2 (PaCO2). In contrast, in eupneic resting dogs on a regular chow diet, iv infusion of saralasin for short periods (up to 30 min) provides no evidence of a tonic effect of circulating levels of ANG II on acid-base balance, respiration, metabolism, or circulation. However, ANG II influences physiological processes involving salt, water, and acid-base balances, which are potentially expressed beyond a 30 min time period, and could secondarily affect respiration. Therefore, we tested the hypothesis that blocking ANG II with iv saralasin would affect respiration and circulation over a 4-h period. Contrary to the hypothesis, iv infusion of saralasin in resting conscious eupneic dogs on a regular chow diet over a 4-h period had no effects on plasma strong ions, osmolality, acid-base balance, respiration, metabolism, or circulation when compared with similar control studies in the same animals. Thus, ANG II does not play a tonic modulatory role in respiratory control under "normal" physiological conditions.Key words: acid-base balance, arginine vasopressin, saralasin, strong ions, strong ion difference.


1994 ◽  
Vol 76 (3) ◽  
pp. 1211-1219 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones

The interaction between systems regulating acid-base balance (i.e., CO2, strong ions, week acids) was studied in six subjects for 10 min after 30 s of maximal isokinetic cycling during control conditions (CON) and after 3 days of chronic acetazolamide (ChACZ) administration (500 mg/8 h po) to inhibit carbonic anhydrase (CA). Gas exchange was measured; arterial and venous forearm blood was sampled for acid-base variables. Muscle power output was similar in ChACZ and CON, but peak O2 intake was lower in ChACZ; peak CO2 output was also lower in ChACZ (2,207 +/- 220 ml/min) than in CON (3,238 +/- 87 ml/min). Arterial PCO2 was lower at rest, and its fall after exercise was delayed in ChACZ. In ChACZ there was a higher arterial [Na+] and lower arterial [lactate-] ([La-]) accompanied by lower arterial [K+] and higher arterial [Cl-] during the first part of recovery, resulting in a higher arterial plasma strong ion difference (sigma [cations] - sigma [anions]). Venoarterial (v-a) differences across the forearm showed a similar uptake of Na+, K+, Cl-, and La- in ChACZ and CON. Arterial [H+] was higher and [HCO3-] was lower in ChACZ. Compared with CON, v-a [H+] was similar and v-a [HCO3-] was lower in ChACZ. Chronic CA inhibition impaired the efflux of CO2 from inactive muscle and its excretion by the lungs and also influenced the equilibration of strong ions.(ABSTRACT TRUNCATED AT 250 WORDS)


1976 ◽  
Vol 231 (2) ◽  
pp. 579-587 ◽  
Author(s):  
EE Nattie ◽  
SM Tenney

We have examined the effect of K depletion on CSF [HCO3-] homeostasis in awake rats. The relationship of CSF [HCO3-] to arterial [HCO3-] in metabolic acid-base disturbances is displaced is an upward direction and has a significantly increased slope in K-depleted vs. control rats (0.51 +/- 0.02 vs. 0.42 +/- 0.02). Results of partial K-repletion experiments, with peripheral acid-base balance held constant, suggest that the effect is K specific. The K-depleted animals also exhibit a wider (CSF-arterial) PCO2 difference than controls (11.1 vs. 8.4 mmHg). When CSF [HCO3-] is shown as a function of CSF PCO2 the data of K-depleted rats are no longer displaced when compared to controls but still have a significantly greater slope (1.21 +/- 0.23 vs. 0.89 +/- 0.08). This increased slope is interpreted to reflect enhanced HCO3- movement from blood to CSF at high arterial [HCO3-]. Analysis of our data and observations from the literature in conditions of mixed acid-base disturbances suggest that CSF [HCO3-] is determined by a) CSF PCO2 and b) the level of arterial [HCO3-] when the latter is greater than the normal CSF [HCO3-].


1981 ◽  
Vol 240 (1) ◽  
pp. R29-R37 ◽  
Author(s):  
G. S. Mitchell ◽  
T. T. Gleeson ◽  
A. F. Bennett

Arterial PCO2, hydrogen ion ([H+]a), and lactate ([L]a) concentrations, rates of metabolic CO2 production (VCO2) and O2 consumption (VO2), and effective alveolar ventilation (Veff) were determined in the lizards Varanus exanthematicus and Iguana iguana at rest and during steady-state treadmill exercise at 35 degrees C. In Varanus, VCO2 increased ninefold and VO2 sixfold without detectable rise in [L]a at running speeds below 1.0 to 1.5 km x h-1. In this range, Veff increased 12-fold resulting in decreased levels of PaCO2 and [H+]a. At higher speeds [L]a rose. Increments of 5 mM [L]a were accompanied by hyperventilation, reducing PaCO2 and thus maintaining [H+]a near its resting level. When [L]a increased further, [H+]a increased. Sustainable running speeds (0.3-0.5 km x h-1 and below) were often associated with increased VO2, VCO2, and [L]a in Iguana. Sixfold increases in VCO2 and 9-mM increments in [L]a were accompanied by sufficient increase in Veff (9-fold) to maintain [H+]a at or below its control level. When [L]a increased further, [H+]a increased. These results indicate that both lizard species maintain blood acid-base homeostasis rather effectively via ventilatory adjustments at moderate exercise intensities.


2003 ◽  
Vol 95 (6) ◽  
pp. 2333-2344 ◽  
Author(s):  
E. Wrenn Wooten

A general formalism for calculating parameters describing physiological acid-base balance in single compartments is extended to multicompartment systems and demonstrated for the multicompartment example of human whole blood. Expressions for total titratable base, strong ion difference, change in total titratable base, change in strong ion difference, and change in Van Slyke standard bicarbonate are derived, giving calculated values in agreement with experimental data. The equations for multicompartment systems are found to have the same mathematical interrelationships as those for single compartments, and the relationship of the present formalism to the traditional form of the Van Slyke equation is also demonstrated. The multicompartment model brings the strong ion difference theory to the same quantitative level as the base excess method.


2007 ◽  
Vol 197 (6) ◽  
pp. S182
Author(s):  
Yoni Cohen ◽  
Jessica Ascher Landsberg ◽  
Michael Kupferminc ◽  
Joseph B. Lessing ◽  
Adi Nimrod ◽  
...  

1982 ◽  
Vol 101 (1) ◽  
pp. 255-264 ◽  
Author(s):  
RAYMOND P. HENRY ◽  
JAMES N. CAMERON

When transferred from 865 to 250 m-osmol salinity, the blue crab C. sapidus maintains its blood Na+ and Cl− concentrations significantly above those in the medium. When branchial carbonic anhydrase is inhibited by acetazolamide, ion regulation fails and the animals do not survive the transfer. An alkalosis occurs in the blood at low salinity, indicated by an increase in HCO3− and pH at constant PCO2. The alkalosis is closely correlated with an increase in the Na+-Cl− difference, a convenient indicator of the overall strong ion difference. The contribution of changes in PCO2 to acid-base changes was negligible, but the change in the total weak acid (proteins) may be important. It is suggested that the change in blood acidbase status with salinity is related to an increase in the strong ion difference, which changes during the transition from osmoconformity to osmoregulation in the blue crab, and which is related to both carbonic anhydrase and ionactivated ATPases. Note:


1982 ◽  
Vol 52 (1) ◽  
pp. 114-118 ◽  
Author(s):  
D. G. Davies ◽  
J. L. Thomas ◽  
E. N. Smith

Pulmonary ventilation and arterial blood acid-base balance were measured in six unanesthetized alligators, Alligator mississipiensis, at 15, 25, and 35 degree C. The animals exhibited pronounced ventilatory responses to hypercapnia at all temperatures studied. Arterial PCO2 increased and pH decreased with increases in body temperature during both normocapnia and hypercapnia. The fractional dissociation of imidazole (alpha Pr) remained constant with changes in body temperature during normocapnia, but increased with temperature during hypercapnia. Ventilatory sensitivity, defined as delta (VE/VO2/delta (alpha Pr), was independent of body temperature. We conclude that the control of breathing in the alligator is a physiological defense of alpha Pr and that ventilatory responses occur following nontemperature-induced changes in blood acid-base balance, which tend to return alpha Pr to a normal value.


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