Effects of hyper- and hypoventilation on gastric and sublingual PCO(2). (1/152)

We investigated the effects of hyper- and hypoventilation on gastric (Pg(CO(2))) and sublingual (Psl(CO(2))) tissue PCO(2) before, during, and after reversal of hemorrhagic shock. Pg(CO(2)) was measured with ion-sensitive field-effect transistor sensor and Psl(CO(2)) with a CO(2) microelectrode. Under physiological conditions and during hemorrhagic shock, decreases in arterial (Pa(CO(2))) and end-tidal (PET(CO(2))) PCO(2) induced by hyperventilation produced corresponding decreases in Pg(CO(2)) and Psl(CO(2)). Hypoventilation produced corresponding increases in Pa(CO(2)), PET(CO(2)), Pg(CO(2)), and Psl(CO(2)). Accordingly, acute decreases and increases in Pa(CO(2)) and PET(CO(2)) produced statistically similar decreases and increases in Pg(CO(2)) and Psl(CO(2)). No significant changes in the tissue PCO(2)-Pa(CO(2)) gradients were observed during hemorrhagic shock in the absence or in the presence of hyper- or hypoventilation. Acute changes in Pg(CO(2)) and Psl(CO(2)) should, therefore, be interpreted in relationship with concurrent changes in Pa(CO(2)) and/or PET(CO(2)).  (+info)

Hyperbaric bradycardia and hypoventilation in exercising men: effects of ambient pressure and breathing gas. (2/152)

We sought to determine whether hydrostatic pressure contributed to bradycardia and hypoventilation in hyperbaria. Eight men were studied during exercise at 50, 150, and 250 W while breathing 1) air at 1 bar, 2) helium-oxygen (He-O(2)) at 5.5 bar, 3) sulfur hexafluoride-oxygen (SF(6)-O(2)) at 1.3 bar, and 4) nitrogen-oxygen (N(2)-O(2)) at 5.5 bar. Gas densities were pairwise identical in 1) and 2), and 3) and 4), respectively. Increased hydrostatic pressure to 5.5 bar resulted in a modest but significant relative bradycardia on the order of 6 beats/min, in both the absence [1) vs. 2), P = 0. 0015] and presence [3) vs. 4), P = 0.029] of gases that are both denser than normal and mildly narcotic. In contrast, ventilatory responses appeared not to be influenced by hydrostatic pressure. Also, the combined exposure to increased gas density and mild-to-moderate inert gas narcosis at a given hydrostatic pressure [1) vs. 3), 2) vs. 4)] caused bradycardia (P = 0.032 and 0.061, respectively) of similar magnitude as 5.5-bar hydrostatic pressure. At the same time there was relative hypoventilation at the two higher workloads. We conclude that heart rate control, but not ventilatory control, is sensitive to relatively small increases in hydrostatic pressure.  (+info)

Structural abnormalities underlying alveolar hypoventilation and fluid imbalance in the dystrophic hamster lung. (3/152)

Bio 14.6 dystrophic hamsters exhibit alveolar hypoventilation and increased lung hydration. This study evaluated whether age- and genotype-related morphometric differences in lungs exist and correlate with the development of lung pathophysiology. Morphometry was used to characterize lungs of young (Y) and mature (M) control (C) and dystrophic (D) hamsters. With age, both C and D had increased barrier surface area [S(a-b,p)] and morphometric diffusing capacity index [mdci], and decreased harmonic thickness. In C but not D, mean capillary diameter [d(c)] and parenchymal volume density [V(v)(p,L)] increased with age, whereas barrier arithmetic thickness decreased. Chord length increased with age, whereas the ratio of parenchymal surface area to airspace volume [S/V] and the intersection density of the air-blood interface [I(v)(a-b,s)] decreased in D but not C. At both ages, lung volume relative to body mass was greater in D than C. With that exception, no genotype differences were found in young hamsters. Mature D displayed lower V(v)(p,L), S/V, d(c), I(v)(a-b,s), S(a-b,p), and mdci than mature C. Independent of age, chord length was greater but arithmetic thickness, airspace surface density, frequency of type II cells, and lamellar body area and volume density were lower in D than C. We conclude: 1) lung volume relative to body growth was greater in dystrophics than controls; 2) parenchymal remodeling was delayed or abnormal in dystrophics; 3) lower diffusing capacity in mature dystrophics may effect alveolar hypoventilation; 4) lower tissue volume, surface area, and the type II cell abnormalities in dystrophics could reduce sodium and water transport leading to greater lung hydration.  (+info)

Muscimol dialysis in the retrotrapezoid nucleus region inhibits breathing in the awake rat. (4/152)

Under anesthesia, inactivation of the retrotrapezoid nucleus (RTN) region markedly inhibits breathing and chemoreception. In conscious rats, we dialyzed muscimol for 30 min to inhibit neurons of the RTN region reversibly. Dialysis of artificial cerebrospinal fluid had no effect. Muscimol (1 or 10 mM) significantly decreased tidal volume (VT) (by 16-17%) within 15 min. VT remained decreased for 50 min or more, with recovery by 90 min. Ventilation (VE) decreased significantly (by 15-20%) within 15 min and then returned to baseline within 40 min as a result of an increase in frequency. This, we suggest, is a compensatory physiological response to the reduced VT. Oxygen consumption was unchanged. In response to 7% CO(2) in the 1 mM group, absolute VE and change in VE were significantly reduced (by 19-22%). In the 10 mM group, the response to dialysis included a time-related increase in frequency and decrease in body temperature, which may reflect greater spread of muscimol. In the awake rat, the RTN region provides a portion of the tonic drive to breathe, as well as a portion of the response to hypercapnia.  (+info)

Ventilatory responses to hypercapnia and hypoxia in relatives of patients with the obesity hypoventilation syndrome. (5/152)

BACKGROUND: It is unclear why some morbidly obese individuals have waking alveolar hypoventilation while others with similar obesity do not. Some evidence suggests that patients with the obesity hypoventilation syndrome (OHS) may have a measurable premorbid impairment of ventilatory chemoresponsiveness. Such an impairment of ventilatory chemoresponsiveness in OHS, however, may be an acquired and reversible consequence of severe obstructive sleep apnoea (OSA). We hypothesised that, in patients with OHS who do not have coincident severe OSA, there may be a familial impairment in ventilatory responses to hypoxia and hypercapnia. METHODS: Sixteen first degree relatives of seven patients with OHS without severe OSA (mean (SD) age 40 (16) years, body mass index (BMI) 30 (6) kg/m(2)) and 16 subjects matched for age and BMI without OHS or OSA were studied. Selection criteria included normal arterial blood gas tensions and lung function tests and absence of sleep apnoea on overnight polysomnography. Ventilatory responses to isocapnic hypoxia and to hyperoxic hypercapnia were compared between the two groups. RESULTS: The slope of the ventilatory response to hypercapnia was similar in the relatives (mean 2.33 l/min/mm Hg) and in the control subjects (2.12 l/min/mm Hg), mean difference 0.2 l/min/mm Hg, 95% confidence interval (CI) for the difference -0.5 to 0.9 l/min/mm Hg, p=0.5. The hypoxic ventilatory response was also similar between the two groups (slope factor A: 379.1 l/min * mm Hg for relatives and 373.4 l/min * mm Hg for controls; mean difference 5.7 l/min * mm Hg; 95% CI -282 to 293 l/min * mm Hg, p=0.7; slope of the linear regression line of the fall in oxygen saturation and increase in minute ventilation: 2.01 l/min/% desaturation in relatives, 1.15 l/min/% desaturation in controls; mean difference 0. 5 l/min/% desaturation; 95% CI -1.7 to 0.7 l/min/% desaturation, p=0. 8). CONCLUSION: There is no evidence of impaired ventilatory chemoresponsiveness in first degree relatives of patients with OHS compared with age and BMI matched control subjects.  (+info)

Relation of ventricular fibrillation threshold to heart rate during normal ventilation and hypoventilation in female Wistar rats: a chronophysiological study. (6/152)

The aim of our study was to verify the relationship between heart rate (HR) and ventricular fibrillation threshold (VFT) during different types of ventilation in female Wistar rats from the circadian point of view. The experiments were performed under pentobarbital anesthesia (40 mg/kg i.p., adaptation to a light-dark cycle 12:12 h, open chest experiments) and the obtained results were averaged independently of the seasons. The VFT measurements were performed during normal ventilation (17 animals) and hypoventilation (10 animals). The HR was recorded immediately before the rise of ventricular arrhythmias. Results are expressed as arithmetic means -/+ S.D. and differences are considered significant when p<0.05. The basic periodic characteristics were calculated using single and population mean cosinor tests. The results from our experiments have demonstrate that 1) the VFT and HR respond identically to hypoventilation by a decrease in the light and also in the dark phases, and 2) hypoventilation changes the 24-h course of the VFT without a change in the 24-h rhythm of the HR. It is concluded that the HR and VFT behave as two independent functional systems without apparent significant circadian dependence during both types of ventilation.  (+info)

Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain. (7/152)

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.  (+info)

Hyperventilation and loss of hemolymph Na+ and Cl- in the freshwater amphipod Gammarus fossarum exposed to acid stress: a preliminary study. (8/152)

The effect of acidification on the acid-sensitive species Gammarus fossarum was investigated in the laboratory. The results showed that as mortality increased, mean hemolymph chloride and sodium concentrations decreased rapidly. Concomitantly, organisms hyperventilated during the first 24 h and then started to hypoventilate. These results demonstrated that exposure to acid stress in the acid-sensitive species G. fossarum led to ion-regulatory and respiratory failure as previously reported in fish and crayfish exposed to acid stress.  (+info)