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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By means of ultrasonic method, used in acute experiments on cats with closed abdominal cavity under nembutal narcosis, we studied the linear and volumetric blood flow velocity in the left phrenic artery, vascular resistance, systemic blood pressure, lung ventilation, arterial blood gases during different degrees of hypoxia and hypercapnia. It was shown that hypoxia and hypercapnia resulted in a decrease of the phrenic artery vascular resistance and an increase of the blood flow in the phrenic artery, not always proportional to hypoxia and hypercapnia degree. The correlation of an increase of the lung ventilation with an increase of the blood flow in the phrenic artery depends on the factor causing activation of the diaphragm performance. Some extreme conditions (prolonged asphyxia, blood loss, the exposure to 3% O2) lower phrenic vascular resistance, providing maximal blood supply of the diaphragm.
Biull Eksp Biol Med 1992 Dec
PMID:[Diaphragmatic blood flow in hypoxia and hypercapnia]. 129 76

In an attempt to elucidate the role of cholinergic mechanism in respiratory chemosensitivity to CO2 in humans, we examined 17 healthy male volunteers for ventilatory responses to hyperoxic progressive hypercapnia and isocapnic progressive hypoxia on three separate days in a randomized, double-blind fashion. Pirenzepine, a M1 muscarinic antagonist which does not cross the blood-brain barrier, biperiden, another M1 muscarinic antagonist which is expected to penetrate into the central nervous system, or placebo was intravenously preinjected before the measurement of ventilatory responses. There were no significant differences in the mean magnitude of ventilatory responses among the three experimental days. However, despite the poor correlation between the magnitude of ventilatory response to hypercapnia in the placebo and pirenzepine studies, there was a significant correlation between them when the value in the pirenzepine study was expressed as % of control, value i.e., subjects with greater hypercapnic ventilatory response in the placebo study showed greater declines with biperiden. Since these relations were seen only for the ventilatory response to hypercapnia with biperiden, we suggest that a cholinergic mechanism, particularly the M1 muscarinic receptor, may be involved in chemoreception to CO2 in the central nervous system and constitute the neurochemical background for the interindividual variation in hypercapnic ventilatory response in humans.
Nihon Kyobu Shikkan Gakkai Zasshi 1992 Dec
PMID:[Involvement of cholinergic mechanism in respiratory chemosensitivity to CO2 in humans]. 130 11

Whether the change of lung volume affect ventilatory responsiveness to chemical stimuli has not been studied in patients with interstitial lung disease (ILD). We measured the responses of minute ventilation (VE), tidal volume (VT), and occlusion pressure (P0.1) to hypercapnia (HCVR) and hypoxia (HVR) in these patients. Breathing efficiency (delta VE/delta P0.1) and effective compliance (delta VT/delta P0.1) were also measured under the same stimuli. 1) HCVR and HVR were measured in one female patient with hypersensitivity pneumonitis. VE responses during low VC phase (VC; 71% of predicted value) were similar to that during increased VC phase (VC; normal level) in both HCVR and HVR. However, VT responses of low VC phase were lower than those of increased phase, and P0.1 responses of low VC phase were higher than those of increased VC phase. Both breathing efficiency and effective compliance of low VC phase were lower than those of increased VC phase. 2) Thirty one patients with ILD were divided into two groups: low VC group; VC < 80% of predicted value, and normal VC group; VC > 80% of predicted value. HCVR and HVR were compared between two groups. Mean values of VE response to hypercapnia and hypoxia in low VC group were lower than those of in normal group, although they were not significantly different. VT response to hypercapnia and hypoxia were significantly lower of low VC group than those of normal VC group. Mean values of P0.1 responses to hypercapnia and hypoxia of low VC group were higher than those of normal VC group, although they were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
Nihon Kyobu Shikkan Gakkai Zasshi 1992 Dec
PMID:[Respiratory control in diffuse interstitial lung disease]. 130 13

In patients with chronic obstructive pulmonary disease (COPD), we examined ventilatory responses to hypercapnia (HCVR) and hypoxia (HVR). HVR was with normal limits, although HCVR was decreased in half of the patients. The patients with COPD often developed oxygen desaturation during sleep. Also, they had severe hypoxemia during exercise. High responders both to HCVR and HVR had no hypoxic episode during sleep or exercise. We conclude that hypoxemia during sleep or exercise may be related to both HCVR and HVR.
Nihon Kyobu Shikkan Gakkai Zasshi 1992 Dec
PMID:[Hypercapnic and hypoxic ventilatory responses in patients with chronic obstructive pulmonary disease]. 130 14

Results from previous studies have suggested that the hypothalamus modulates cardiorespiratory responses to hypoxia and/or hypercapnia. Many neurons in the caudal hypothalamus are stimulated by hypercapnia and hypoxia in vivo; however, it is not known if these responses are dependent upon input from other areas. Whole-cell patch and extracellular recordings from a brain slice preparation were used in the present study to determine the direct effects of hypoxia (5% CO2/95% N2 or 10% O2/5% CO2/85% N2) and hypercapnia (7% CO2/93% O2) on caudal hypothalamic neurons in vitro. Coronal sections (400-500 microns) were obtained from young Sprague-Dawley rats and placed in a recording chamber that was perfused with nutrient media equilibrated with 95% O2/5% CO2. Extracellular recordings demonstrated that hypoxia stimulated over 80% of the neurons tested; the magnitude of the response was dependent upon the degree of hypoxia. In addition, over 80% of cells that were excited by hypoxia retained this response during synaptic blockade. Hypercapnia increased the discharge frequency of 22% of the caudal hypothalamic neurons that were studied. A second set of caudal hypothalamic neurons were studied with whole-cell patch recordings; the mean resting membrane potential of these neurons was -51.8 +/- 1.0 mV with an average input resistance of 399 +/- 49 M omega. Hypoxia produced a depolarization in 76% of these neurons; a poststimulus hyperpolarization often occurred. A depolarization and/or increase in discharge rate during hypercapnia was observed in 35% of the neurons tested. Only 10% of all neurons studied were excited by both hypoxia and hypercapnia. These findings suggest that separate subpopulations of caudal hypothalamic neurons are sensitive to hypoxia and hypercapnia. Thus, this hypothalamic area may be a site of central hypoxic and hypercapnic chemoreception.
Neuroscience 1992 Dec
PMID:In vitro responses of caudal hypothalamic neurons to hypoxia and hypercapnia. 133 28

A 46-year-old man underwent cosmetic facial surgery under general anesthesia. He was ventilated by mask with an oxygen-enriched gas mixture for 4 to 6 h and monitored by pulse oximetry. Despite adequate arterial saturation (SaO2 > 90 percent) throughout the procedure, he remained in a deep coma after termination of anesthesia. Initial arterial blood gas analysis revealed a pH of 6.60 and a PaCO2 of 375 mm Hg. The patient was intubated and placed on mechanical ventilation. As his respiratory acidosis resolved, he regained consciousness quickly and recovered without any neurologic deficits. This case of record extreme hypercapnia and review of the literature demonstrates that survival is possible in acute severe respiratory acidosis as long as tissue anoxia and ischemia are prevented. We discuss the tissue effects of acute hypercapnia and newer aspects of the nature of intracellular pH regulation in critical tissues that afford considerable tolerance to acidosis. The dependence of these mechanisms upon active ion transport underscores the importance of adequate tissue oxygenation and perfusion.
Chest 1992 Dec
PMID:Resuscitation from severe acute hypercapnia. Determinants of tolerance and survival. 144 82

As sleep apnea is more prevalent in men and testosterone has known effects on sleep apnea and chemosensitivity, reduction of androgen activity may influence sleep-disordered breathing and respiratory control. We studied the effect of 1 wk of treatment with flutamide, a nonsteroidal antiandrogen, on sleep, respiration, and ventilatory control in eight men with sleep apnea. Results on flutamide were compared with two baseline studies performed before and after the drug treatment period. Although effective androgen blockade was achieved as evidenced by increased hormone levels, flutamide had no effect on sleep architecture or chemoresponsiveness to hypoxia and hypercapnia. There was a trend towards a reduction in respiratory disturbance index in both NREM and REM sleep (41 +/- 4 baseline versus 34 +/- 3 flutamide, p = 0.09 NREM; 53 +/- 4 baseline versus 48 +/- 3 flutamide, p = 0.16 REM), but this was not significant. Our results indicate that androgen blockade had no clinically significant effect on sleep, sleep-disordered breathing, or chemosensitivity in patients with moderate to severe sleep apnea. More specific blockers such as gonadotrophin-releasing hormone analogs may have more clinical effect or, alternatively, androgen blockade may be more beneficial in patients with milder sleep apnea.
Am Rev Respir Dis 1992 Dec
PMID:Androgen blockade does not affect sleep-disordered breathing or chemosensitivity in men with obstructive sleep apnea. 145 53

Theophylline is commonly believed to stimulate central respiratory centers. We studied the effect of oral theophylline therapy on ventilatory responses to hypercapnia and hypoxia during a double-blind placebo-controlled trial with a slow release oral theophylline preparation. We measured hypercapnic and hypoxic ventilatory responses using rebreathing techniques in 15 subjects (21 to 41 yr of age, with normal lung function) on three occasions: baseline, after 4 days of Drug 1, and after 4 days of Drug 2. For subjects receiving theophylline, the mean serum theophylline level was 11.3 + 1.3 (SE) micrograms/ml (range, 5.3 to 22.1). Unpleasant side effects were reported by 11 of the 15 subjects (nausea, jitteriness, and agitation) while receiving theophylline but not while receiving placebo. The mean hypercapnic ventilatory response with placebo was 4.3 +/- 0.9 L/min/mm Hg PACO2 and with theophylline it was 4.5 +/- 0.7 L/min/%SaO2 and with theophylline it was -2.7 +/- 0.4 L/min/%SaO2. Hypoxic responses for each subject were measured at similar PvCO2. There were no significant changes in ventilatory responses with theophylline. We conclude that theophylline use, at a dose sufficient to cause side effects, does not affect chemoreceptor responsiveness.
Am Rev Respir Dis 1992 Dec
PMID:Theophylline does not increase ventilatory responses to hypercapnia or hypoxia. 145 55

Ten survivors of double lung transplantation using a tracheal anastomosis underwent assessment of their ventilatory responses to hypercapnia (HCVR) at least 3 months postsurgery. At the time of HCVR testing, pulmonary functions were normal in four and abnormal in six patients who demonstrated degrees of obstruction, restriction, or mixed defects. Arterial blood gas measurements were normal. Postoperatively, hypercapnic responses were low or low normal. Mean changes in tidal volume and mean change in respiratory frequency in response to hypercapnia postoperatively were not different in patients with normocapnic versus hypercapnic preoperative blood gases. Neither postoperative resting PCO2 nor muscle strength (as measured by MIP) were predictive of the degree or character of the patients' ventilatory responses to hypercapnia. The factors resulting in the observed blunting of the hypercapnic response in this denervated population require further clarification; however, comparison of data between this patient population and recipients of heart-lung transplantation reported elsewhere suggests that alterations in pulmonary function correlate with the observed depression in HCVR.
Am Rev Respir Dis 1992 Dec
PMID:Hypercapnic ventilatory response in recipients of double-lung transplants. 145 85

Hypercarbia occurs during laparoscopy with carbon dioxide (CO2) insufflation. This may be due to increased ventilatory dead space after expansion of the peritoneal cavity with impairment of diaphragmatic excursion, or to increased absorption of CO2 from the peritoneum. To separate these effects, the authors examined the consequences of different insufflating gases and of diminished tissue perfusion on hypercarbia and dead space during pneumoperitoneum. Helium was chosen as an alternate insufflating gas because it is both inert and minimally absorbed. Eight swine (18 to 20 kg) were anesthetized, paralyzed, and mechanically ventilated at constant minute volume. Pneumoperitoneum with helium was maintained at 15 mm Hg for 45 minutes. After desufflation and stabilization for 1 hour, pneumoperitoneum was repeated with CO2. The sequence was again repeated after hemorrhagic shock to constant mean arterial pressure of 50 mm Hg. Data was analyzed by analysis of variance; significance levels are P < 0.01 unless otherwise listed. Arterial PCO2 increased significantly with CO2 insufflation within 15 minutes in normotensive animals and within 30 minutes during hypotension. Arterial pH decrease with CO2 pneumoperitoneum was significant in both groups at 30 minutes. Mixed venous PCO2 also increased with CO2 pneumoperitoneum within 30 minutes. Hypotension did not alter these changes. No significant changes were seen with helium pneumoperitoneum. Neither helium nor CO2 pneumoperitoneum significantly altered dead space. The authors make the following conclusions: 1) Absorption of CO2 from the abdomen during CO2 pneumoperitoneum produces respiratory acidosis, which is not seen with helium insufflation; 2) Pneumoperitoneum does not significantly increase dead space with either gas; 3) Transperitoneal absorption of CO2 is only partly related to perfusion because significant hypercarbia occurs during hemorrhagic shock.
Am Surg 1992 Dec
PMID:Effectors of hypercarbia during experimental pneumoperitoneum. 145 92


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