Anomalous hypoxic acidification of medullary ventral surface

1991 ◽  
Vol 71 (6) ◽  
pp. 2211-2217 ◽  
Author(s):  
F. D. Xu ◽  
M. J. Spellman ◽  
M. Sato ◽  
J. E. Baumgartner ◽  
S. F. Ciricillo ◽  
...  
Keyword(s):  
Ventral Surface ◽  
High Pco2 ◽  
Nerve Roots ◽  
Arterial Pco2 ◽  
Glass Bulb ◽  
Response Slope ◽  
Left Posterior ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Ph Electrodes

In castrated male goats, two flexible catheters, one open ended for reference and the other ending in a 1-mm-diam glass bulb pH electrode, were advanced ventrally through a left posterior fossa craniotomy into the subarachnoid space between the 9th and 10th cranial nerve roots, passing medially into cerebrospinal fluid (CSF) over the medullary ventral surface (MVS). They were anchored to dura and fascia, tunneled under the scalp, and terminated in connectors on the left horn. After several days for recovery, while the animals were awake, the effects of CO2 and hypoxia on pH of the film of CSF between the pia and arachnoid (pHMVS) were recorded along with end-tidal PCO2 and PO2 (mass spectrometer), ventilation (pneumotachometer) through a permanent tracheostomy, and, when possible, ear arterial O2 saturation (SaO2). High PCO2 acidified MVS as expected: delta pH MVS/delta log PCO2. = -0.64 +/- 0.14, producing a ventilatory response slope delta VI/delta pHMVS = 372 l/min. Hypoxia resulted in acid shifts even when PCO2 was allowed to fall. The development of hypoxic acidosis was related to the location of pH electrodes determined at necropsy. In isocapnic hypoxia, pH over putative chemoreceptor surfaces fell in proportion to desaturation: delta pHMVS = 0.0033(SaO2)-0.34, r = 0.80, Sy.x = 0.025. With uncontrolled arterial PCO2, similar acidosis occurred when SaO2 fell below 85–90%: delta pHMVS = 0.0039(SaO2)-0.34, r = 0.88, Sy.x = 0.032. With constant hypoxia, pH fell (tau = 3.7 +/- 2.2 min) to a plateau after 10–20 min and showed rapid recovery (tau = 2.0 +/- 1.3 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Validation of a maskless CO2-response test for sleep and infant studies

1988 ◽  
Vol 64 (1) ◽  
pp. 391-396 ◽  
Author(s):  
K. H. Naifeh ◽  
J. W. Severinghaus
Keyword(s):  
Steady State ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Response Test ◽  
Response Slope ◽  
Fractional Increase ◽  
The Subject ◽  
End Tidal ◽  
Co2 Electrode ◽  
Co2 Excretion

The Hazinski method is an indirect, noninvasive, and maskless CO2-response test useful in infants or during sleep. It measures the classic CO2-response slope (i.e., delta VI/delta PCO2) divided by resting ventilation Sr = (VI''--VI')/(VI'.delta PCO2) between low (')- and high ('')-inspired CO2 as the fractional increase of alveolar ventilation per Torr rise of PCO2. In steady states when CO2 excretion (VCO2') = VCO2'', Hazinski CO2-response slope (Sr) may be computed from the alveolar exchange equation as Sr = (PACO2'--PICO2')/(PACO2'--PICO2'') where PICO2 is inspired PCO2. To avoid use of a mask or mouthpiece, the subject breathes from a hood in which CO2 is mixed with inspired air and a transcutaneous CO2 electrode is used to estimate alveolar PCO2 (PACO2). To test the validity of this method, we compared the slopes measured simultaneously by the Hazinski and standard steady-state methods using a pneumotachograph, mask, and end-tidal, arterial, and four transcutaneous PCO2 samples in 15-min steady-state challenges at PICO2 23.5 +/- 4.5 and 37 +/- 4.1 Torr. Sr was computed using PACO2 and arterial PCO2 (PaCO2) as well as with the four skin PCO2 (PSCO2) values. After correction for apparatus dead space, the standard method was normalized to resting VI = 1, and its CO2 slope was designated directly measured normalized CO2 slope (Sx), permitting error to be calculated as Sr/Sx.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of plasma carbonic anhydrase on ventilation in exercising dogs

1980 ◽  
Vol 49 (4) ◽  
pp. 708-714 ◽  
Author(s):  
S. M. Lewis ◽  
E. P. Hill
Keyword(s):  
Carbonic Anhydrase ◽  
Partial Pressure ◽  
Reaction Rate ◽  
Control Period ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Ventilatory Parameters ◽  
Activity Measurements ◽  
End Tidal ◽  
Ph Electrodes

Recent studies suggest pH sampled by arterial chemoreceptors may not equal that sampled by external pH electrodes, because the uncatalyzed hydration of CO2 in plasma is a slow reaction (t 1/2 approximately 9 S). The importance of this reaction rate to ventilatory control (particularly during exercise) is not known. We studied the effect of catalyzing the CO2-pH reaction in three awake exercising dogs with chronic tracheostomies and carotid loops; the dogs were trained to run on a treadmill. Respiration frequency, tidal volume, total ventilation, and end-tidal partial pressure of CO2 (PCO2) were continuously monitored. Periodically, carotid artery blood was drawn and analyzed for partial pressure of O2 (PO2), PCO2, pH, and plasma carbonic anhydrase (CA) activity. Measurements were made during steady-state exercise (3 mph and 10% grade), during a control period, after injection of a 5 ml bolus of saline, and after injection of 5 mg/kg of bovine CA dissolved in 5 ml of saline. This dose of CA increased the reaction rate by more than 80-fold. Neither the control nor the CA injections significantly altered the ventilatory parameters. Saline and CA date differed by less than 5% in ventilation, 1 Torr in arterial PCO2, 0.01 in pH units, and 1.5 Torr in end-tidal PCO2. Thus the of CO2 hydration in plasma is not a significant factor in ventilatory control.

Topography of cat medullary ventral surface hypoxic acidification

1992 ◽  
Vol 73 (6) ◽  
pp. 2631-2637 ◽  
Author(s):  
F. Xu ◽  
M. Sato ◽  
M. J. Spellman ◽  
R. A. Mitchell ◽  
J. W. Severinghaus
Keyword(s):  
Spinal Cord ◽  
Parietal Cortex ◽  
Acute Hypoxia ◽  
Extracellular Fluid ◽  
Ventral Surface ◽  
Brain Surface ◽  
Alkaline Shift ◽  
Steel Tubing ◽  
Arterial O2 Saturation ◽  
Ph Electrodes

The topographic relationship between previously identified medullary ventral surface respiratory chemosensitive regions and brain surface extracellular fluid (ECF) acid production during acute hypoxia was explored in anesthetized, paralyzed, and artificially ventilated cats. Glass pH electrodes (0.8-mm diam, sheathed in stainless steel tubing) were mounted in mechanical contact with surfaces of medullary surface or adjacent pyramids, pons, spinal cord, or parietal cortex. Isocapnic hypoxia of 5 min [at arterial O2 saturation (SaO2) = 48 +/- 10%] reduced pH over rostral (Mitchell) and caudal (Loeschcke) areas by 0.12 +/- 0.09 and 0.07 +/- 0.04, respectively (n = 10, P < 0.05). Change in pH (delta pH) was proportional to desaturation with slopes 100 delta pH/delta SaO2 of 0.45 (rostral) and 0.20 (caudal) (R = 0.91 and 0.88, respectively). pH drop usually began within 3 min of hypoxia, became stable between 5 and 15 min, began to rise within 2 min of reoxygenation, and returned to control within 10 min. During equally hypoxic tests, intermediate area (Schlafke), pons, and spinal cord surfaces showed no significant acid shift. Parietal cortex ECF pH dropped more slowly but steadily by 0.079 +/- 0.034 during 20 min at SaO2 = 50% after a small but significant initial alkaline shift, and acidification of cortical surface continued for > 5 min after reoxygenation. We conclude that medullary ventral chemosensitive regions produce more lactic acid during hypoxia than neighboring brain surfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory control during experimental maldistribution of VA/Q in the dog

1982 ◽  
Vol 52 (1) ◽  
pp. 245-253 ◽  
Author(s):  
C. E. Juratsch ◽  
B. J. Whipp ◽  
D. J. Huntsman ◽  
M. M. Laks ◽  
K. Wasserman
Keyword(s):  
Steady State ◽  
Early Phase ◽  
Main Pulmonary Artery ◽  
State Regulation ◽  
Balloon Inflation ◽  
Peripheral Chemoreceptors ◽  
Arterial Pco2 ◽  
Bilateral Carotid ◽  
End Tidal ◽  
Transient Elevation

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5–2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5–2.0 min) of acute maldistribution of VA/Q.

Developmental pattern of hypercapnic and hypoxic ventilatory responses from childhood to adulthood

1994 ◽  
Vol 76 (1) ◽  
pp. 314-320 ◽  
Author(s):  
C. L. Marcus ◽  
W. B. Glomb ◽  
D. J. Basinski ◽  
S. L. Davidson ◽  
T. G. Keens
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Body Size ◽  
Respiratory Rate ◽  
Body Surface ◽  
Vital Capacity ◽  
Developmental Pattern ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

The developmental pattern of ventilatory responses, through childhood and puberty into adulthood, is not known. Therefore we studied hypercapnic (HCVR) and hypoxic ventilatory responses (HOVR) in 59 subjects (29 males and 30 females) 4–49 yr of age, of whom 35 were children ( < 18 yr old). There was a significant correlation between HCVR and weight (r = 0.33, P < 0.02), vital capacity (r = 0.30, P < 0.05), and body surface area (r = 0.30, P < 0.05) but not height (r = 0.22, NS). There was no correlation between HOVR and any of the correcting factors. To account for disparities in body size, volume-related results were scaled for body weight. The HCVR corrected for weight (HCVR/WT) decreased with age (r = -0.57, P < 0.001). HCVR/WT was significantly higher in children than in adults (0.056 +/- 0.024 vs. 0.032 +/- 0.015 l.kg-1 x min-1. Torr end-tidal PCO2-1, P < 0.001). The (tidal volume/inspiratory duration)/weight, respiratory rate, and heart rate responses to hypercapnia were increased in the children, and the CO2 threshold was lower (36 +/- 5 vs. 40 +/- 6 Torr, P < 0.05). Similarly, the HOVR corrected for weight (HOVR/WT) decreased with age (r = 0.34, P < 0.05), and HOVR/WT was significantly higher in children than in adults (-0.035 +/- 0.017 vs. -0.024 +/- 0.016 l.kg-1 x min-1.% arterial O2 saturation-1, P < 0.02). The respiratory rate and heart rate responses to hypoxia were increased in the children. We conclude that rebreathing HCVR and HOVR are higher during childhood than during adulthood.

Infrared end-tidal CO2 measurement does not accurately predict arterial CO2 values or end-tidal to arterial PCO2, gradients in rabbits with lung injury

1994 ◽  
Vol 17 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Andrew O. Hopper ◽  
Gerald A. Nystrom ◽  
Douglas D. Deming ◽  
Wesley R. Brown ◽  
Joyce L. Peabody
Keyword(s):  
Lung Injury ◽  
Arterial Pco2 ◽  
End Tidal ◽  
End Tidal Co2

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Maturation of steady-state CO2 sensitivity in vagotomized anesthetized lambs

1992 ◽  
Vol 72 (4) ◽  
pp. 1255-1260 ◽  
Author(s):  
A. H. Jansen ◽  
S. Ioffe ◽  
V. Chernick
Keyword(s):  
Steady State ◽  
Test Procedure ◽  
Nerve Section ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Co2 Sensitivity ◽  
Carotid Bodies ◽  
Before And After ◽  
End Tidal ◽  
Respiratory Sensitivity

The maturation of the respiratory sensitivity to CO2 was studied in three groups of anesthetized (ketamine, acepromazine) lambs 2–3, 14–16, and 21–22 days old. The lambs were tracheostomized, vagotomized, paralyzed, and ventilated with 100% O2. Phrenic nerve activity served as the measure of respiration. The lambs were hyperventilated to apneic threshold, and end-tidal PCO2 was raised in 0.5% steps for 5–7 min each to a maximum 7–8% and then decreased in similar steps to apneic threshold. The sinus nerves were cut, and the CO2 test procedure was repeated. Phrenic activity during the last 2 min of every step change was analyzed. The CO2 sensitivity before and after sinus nerve section was determined as change in percent minute phrenic output per Torr change in arterial PCO2 from apneic threshold. Mean apneic thresholds (arterial PCO2) were not significantly different among the groups: 34.8 +/- 2.08, 32.7 +/- 2.08, and 34.7 +/- 2.25 (SE) Torr for 2- to 3-, 14- to 16-, and 21- to 22-day-old lambs, respectively. After sinus denervation, apneic thresholds were raised in all groups [39.9 +/- 2.08, 40.9 +/- 2.08, and 45.3 +/- 2.25 (SE) Torr, respectively] but were not different from each other. CO2 response slopes did not change with age before or after sinus nerve section. We conclude that carotid bodies contribute to the CO2 response during hyperoxia by affecting the apneic threshold but do not affect the steady-state CO2 sensitivity and the central chemoreceptors are functionally mature shortly after birth.

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