Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a small, but significant, increase in frequency during hypercapnia in vagotomized, anesthetized animals, indicating involvement of an extravagal mechanism in the response. The intent of this study was to determine the source of this second mechanism regulating frequency during hypercapnia. Experiments were performed on 22 vagotomized, anesthetized (Dial) cats. Frequency (f), inspiratory time (ti) and expiratory time (te) responses to CO2 were monitored before and after sectioning of afferent nerves from the carotid bodies (carotid sinus nerve section), chest wall (dorsal rhizotomies, T1-T12) and diaphragm (dorsal rhizotomies. C4-C7). Most vagotomized animals responded to 6% CO2 with an increased frequency, decreased ti and no consistent change in te. The responses to CO2 were essentially unaltered following chest wall and diaphragm deafferentation. Sodium cyanide stimulation of the carotid bodies produced similar respiratory pattern changes as CO2; furthermore, the f and ti changes with CO2 were still present following carotid body deafferentiation. The results of this study suggest that: (1) afferents from chest wall and diaphragm mechanoreceptors are not responsible for the vagal-like effects on ti and f during hypercapnia, (2) afferents from lung mechanoreceptors, via the vagus nerves, are the only inputs from respiratory mechanoreceptors causing an increased f during hypercapnia, (3) the extravagal mechanism responsible for the decreased ti and increased f during hypercapnia is inherent to the medullary-pontine rhythm generator, and (4) input from the chemoreceptors can elicit the response.
 ...
PMID:Respiratory frequency control during hypercapnia in vagotomized, anesthetized cats. 97 52

Previously we have demonstrated that continuous positive pressure breathing (PB) depresses diaphragm activity and excites expiratory activity in the abdominal muscle (AMR) via vagal proprioceptive impulses. During prolonged PB the AMR persists at a constant level whereas inhibition of the diaphragm wanes, possibly as a result of CO2 retention. This study measures CO2 retention during PB and compares the responses of the abdominal muscle and diaphragm to chemostimulation alone and to chemostimulation and PB in combination. Continuous recordings of minute ventilation, integrated EMGs of the diaphragm and abdominal muscle, and mass spectrometer analysis of airway gases were obtained during PB on air, 5.25 percent CO2 and 12.4 percent O2 in eight Dial-anaesthetized cats. Between 0 and 15 cm H2O the steady-state end-tidal CO2 rises about 0.6 mm Hg/km H2O, diaphragm activity decreases and AMR increases exponentially with each increment in PB. When 5.25 percent CO2 is inspired, diaphragm activity is augmented at every pressure suggesting algebraic summation of proprioceptive and chemoreceptive effects at the respiratory centre. In contrast, the AMR is not significantly altered by hypercapnia. The absence of all abdominal muscle expiratory activity after bilateral vagotomy suggests that the role of active expiration is to regulate thoracic-lung volume, not blood gases.
 ...
PMID:Comparative influence of proprioceptors and chemoreceptors in the control of respiratory muscles. 426 86

Single motor unit potentials from the eighth internal intercostal (IIC) muscle were recorded along with tracheal pressure and end-tidal CO2 (PETCO2) in spontaneously breathing, Dial-urethane anesthetized cats during hypercapnia (3, 5, or 7% CO2) and during lung inflation (LI, 100 ml above functional residual capacity) before and after vagotomy. Hypercapnia depressed IIC activity in 5 of 7 cats; the higher the PETCO2, the lower was the firing rate and the fewer the number of spikes per breath. LI evoked an initial silent phase (ISP) in 6 of 10 cats followed by a prolonged IIC burst. Hypercapnia combined with LI abolished or diminished the ISP and shortened the prolonged burst with an increase in firing rate and a recruitment of new units. Vagotomy silenced IIC activity in 7 of 10 cats, but LI after vagotomy activated IIC activity in 10 of 10 cats, though neither an ISP nor prolonged activity occurred. Our data suggest that major factors in controlling IIC activity are reciprocal inhibition from bulbospinal inspiratory neurons, excitatory and inhibitory inputs mediated by vagal afferents, and a modulation of IIC activity via gamma-loop. Hypercapnia affects the former two factors.
 ...
PMID:Responses of cat's internal intercostal motor units to hypercapnia and lung inflation. 640 90

The steady-state ventilatory and end-tidal PCO2 (PETCO2) responses to low-level CO2 inhalation have been studied in four awake cats. Four cats anesthetized with Dial-urethane were also studied before and after vagal section or blockade. Awake cats breathed gas mixtures with FICO2 equal to 0.0015 (control), 0.01 and 0.03 in oxygen or 0.0015, 0.01 and 0.02 in air, while anesthetized cats inhaled FICO2 of 0.0000 (control), 0.005 and 0.01 in oxygen. In order to obtain accurate, unbiased determinations of the respiratory system responses to small increases of FICO2 above control values, we used a protocol in which control conditions preceded and followed each CO2 test. The pairwise response for each variable was calculated from the mean of the two 'bracketing' control values. We found that low-level CO2 inhalation in the cat resulted in consistent and significant increases in PETCO2 (82 of 86 trials) and VT (76 of 86 trials) but inconsistent changes in TTOT. We conclude that low-level CO2 inhalation in the cat results in hypercapnia detectable by a replicated, unbiased experimental design.
 ...
PMID:Ventilatory responses to low levels of CO2 inhalation in the cat. 642

Proximal tubular cell membrane potentials were measured in rat kidney in vivo and the response to luminal perfusion of 2mmolar phosphate (Pi) was studied. Pi transport was preferentially rheogenic at low pH (cotransport of 1H2PO2- plus 2Na+) but preferentially electroneutral at high pH (cotransport of 1HPO4--plus 2Na+). The potential response as a function of pH conformed to a model which transports both H2PO4- and HPO4--indiscriminately and whose maximal transport capacity increases with increasing pH. Further kinetic experiments are required to definitely exclude separate transport systems for both ionised forms. Hypercapnic phosphaturia may be explained by a decreased maximal transport capacity of Pi at low luminal pH.
Proc Eur Dial Transplant Assoc 1983
PMID:pH--dependence of phosphate absorption in rat renal proximal tubule. 687 64

The impact of autonomic neuropathy (common in patients on haemodialysis) on ventilatory response to hypercapnia has been studied. We investigated cardiac reflex tests in 20 patients on chronic haemodialysis (8 patients were found with and 12 without neuropathy of the autonomic nervous system). Using the hyperoxic CO2-rebreathing method (according to Read), we tested the above-mentioned two groups of patients and compared them with 14 healthy control subjects. Accumulation of CO2 in blood with hyperoxic CO2 rebreathing stimulates central chemoreceptors, and therefore causes a progressive rise in minute ventilation. In patients with autonomic neuropathy (n = 8), ventilatory response to increasing pCO2 was significantly lower than that in the controls (1.7 +/- 0.3 versus 3.2 +/- 0.5 l/min/mmHg, P < 0.001). On the other hand ventilatory response in patients without autonomic damage (n = 12) showed no significant difference when compared to controls (3.1 +/- 0.8 l/min/mmHg). There were no differences in lung function, arterial blood gas analysis, blood chemistry, duration on dialysis, and demographic data when comparing the patients with and those without autonomic damage. Our analysis shows different patterns of ventilatory response to increasing pCO2 in patients on haemodialysis. Autonomic neuropathy has to be considered when rebreathing tests are interpreted. The clinical relevance of these findings needs further investigation.
Nephrol Dial Transplant 1995
PMID:Effect of autonomic neuropathy on ventilatory response to progressive hypercapnia in dialysis patients. 756 11

Videolaparoscopic techniques are an increasingly used modality for peritoneal dialysis catheter implant and rescue procedures. The greatest impediment for acceptance of the laparoscopic approach has been the necessity of general anesthesia because peritoneal insufflation of CO2 gas produces pain. In addition, complications of CO2 pneumoperitoneum include hypercarbia, acidosis, and cardiac arrhythmias. Renal failure patients commonly have severe coexisting medical conditions that make them an unacceptable risk for both general anesthesia and CO2 peritoneal insufflation. From December 1996 through November 1997, laparoscopy was performed utilizing nitrous oxide (N2O) as the insufflation gas. Since N2O produces neither pain nor metabolic effects, the laparoscopic procedure was safely performed under local anesthesia. Thirty-one patients have had laparoscopic implantation of peritoneal dialysis catheters under local anesthesia with 22 procedures performed on an ambulatory basis. The remaining cases were already hospitalized for complications of their renal failure. Four laparoscopic rescue procedures for catheter dysfunction were performed under local anesthesia with 3 cases as outpatients. Surgical laparoscopy under local anesthesia with N2O insufflation is a safe approach for both implantation procedures and salvaging of malfunctioning catheters. The procedure can be performed on an outpatient basis, frequently without delay in initiation or interruption of peritoneal dialysis.
Adv Perit Dial 1998
PMID:Videolaparoscopic peritoneal dialysis catheter implant and rescue procedures under local anesthesia with nitrous oxide pneumoperitoneum. 1064 98

Acid-base alterations in patients with kidney failure and on hemodialysis (HD) treatment contribute to (1) intradialytic hypercapnia and hypoxia, (2) hemodynamic instability and cardiac arrhythmia, (3) systemic inflammation, and (4) a number of associated electrolyte alterations including potentiating effects of hypokalemia, hypocalcemia and, chronically, soft-tissue and vascular calcification, imparting poor prognosis and mortality. This paper discusses acid-base regulation and pathogenesis of dysregulation in patients with kidney failure. Major organ and systemic effects of acid-base perturbations with a specific focus on kidney failure patients on HD are emphasized, and potential mitigating strategies proposed. The high rate of HD-related complications, specifically those that can be accounted for by rapid and steep acid-base perturbations imposed by HD treatment, attests to the pressing need for investigations to establish a better dialysis regimen.
Semin Dial 2018 05
PMID:Acid-base alterations in ESRD and effects of hemodialysis. 2914 94