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Sleep-stage-dependent Cheyne-Stokes respiration after cerebral infarct: a case study.

Polysomnographic studies of nocturnal sleep were performed on a 63-year-old women. Sleep-onset and sleep-maintenance insomnia dated back to a cerebral infarction at age 53, which resulted in bilateral cerebral injury. Two patterns of respiration were observed, and both were sleep-stage-dependent. Classic Cheyne-Stokes respiration predominated during slow-wave sleep and stages 1 and 2. REM sleep, in contrast, was associated almost exclusively with normal respiration. Recurrent brief arousals, temporally linked to the Cheyne-Stokes pattern of respiration, markedly disturbed sleep stages 1 and 2 and appeared related to the patient's subjective sleep complaints. During waking, REM, and NREM sleep, respiration is known to have different sensitivity to CNS and peripheral controls. The selective association of Cheyne-Stokes respiration with NREM sleep in this patient supports the view that anatomically separate CNS mechanisms regulate respiration in REM and NREM sleep.

Cerebral Infarction↗

[Effect of forced respiration on the stress on puncture channels of sutures in transverse laparotomies of the upper abdomen; experimental studies in the anesthesized dog].

In 11 mongrel dogs in propiophenylpromazine-pentobarbital-anaesthesia the influence of forced respiration on the load of puncture channels of a suture was investigated. For this horizontal suture in the upper abdominal wall, threads No. 3 USP and round needles No. ECT-4 were used. The experiments were carried out in supine position with stretched hindlegs, in supine position with relaxed hindlegs, in lateral position, and in hanging abdominal position. Measurements were performed with a selfconstructed resistance strain gauge element. Rising forced respiration pressure increased the inspiratory load of puncture channels, but there were no significant differences between spontaneous breathing and forced respiration with pressure of 10 cm H2O. In contrary to this there were highly significant differences between spontaneous breathing and forced respiration with pressure of 20 and 30 cm H2O (multiple variance analysis). For instance the load during forced respiration with a pressure of 30 cm H2O in supine position with relaxed hindlegs rose about 67% above pressure values of spontaneous breathing. It could be shown that the expiratory load in the puncture channels was not influenced by forced respiration pressure, but depended on the body position; in dogs it was minimal in side position (45-48 g), higher in supine position with relaxed hindlegs (67-71 g), even higher in supine position with stretched hindlegs (88-92 g), and maximal in hanging abdominal position (109-113 g). By this investigation the increase of load in the puncture channels during forced respiration with pressures of 20 and 30 cm H2O was quantified.

Abdomen↗

The effect of buprenorphine and benzodiazepines on respiration in the rat.

Methadone and buprenorphine are the two main opioid substitution treatments for heroin dependence currently offered in Australia. A number of publications have implicated buprenorphine as being potentially dangerous in combination with benzodiazepines but no comparison has been made to the relative dangers of benzodiazepines combined with buprenorphine or methadone. The effect of i.v. methadone and buprenorphine on respiration was investigated by evaluating arterial blood pCO2, pO2 and pH, and measuring respiratory rate in rats. Measurements were taken at 0, 15, 30, 60, 120, 180 and 240 min after i.v. administration of methadone or buprenorphine. Effects on respiration were greatest 15 min after i.v. drug administration. The effect of methadone and buprenorphine on respiration was compared with and without diazepam pretreatment (20 mg/kg). Buprenorphine alone exhibited a bell shaped dose response inhibition of respiration; however the plateau of the dose response inhibition on respiration was lost when administered in combination with diazepam. Methadone showed a dose-dependent inhibitory effect on respiration, which was potentiated with diazepam pretreatment. While the effect of diazepam pretreatment was the abolishment of the protective bell shaped dose response effect on respiration, the effect of buprenorphine and diazepam was not greater than methadone and diazepam.

Animals↗

Study of regulation of mitochondrial respiration in vivo. An analysis of influence of ADP diffusion and possible role of cytoskeleton.

The purpose of this work was to investigate the mechanism of regulation of mitochondrial respiration in vivo in different muscles of normal rat and mice, and in transgenic mice deficient in desmin. Skinned fiber technique was used to study the mitochondrial respiration in the cells in vivo in the heart, soleus and white gastrocnemius skeletal muscles of these animals. Also, cardiomyocytes were isolated from the normal rat heart, permeabilized by saponin and the "ghost" (phantom) cardiomyocytes were produced by extraction of myosin with 800 mM KCl. Use of confocal immunofluorescent microscopy and anti-desmin antibodies showed good preservation of mitochondria and cytoskeletal system in these phantom cells. Kinetics of respiration regulation by ADP was also studied in these cells in detail before and after binding of anti-desmine antibodies with intermediate filaments. In skinned cardiac or soleus skeletal muscle fibers but not in fibers from fast twitch skeletal muscle the kinetics of mitochondrial respiration regulation by ADP was characterized by very high apparent Km (low affinity) equal to 300-400 microM, exceeding that for isolated mitochondria by factor of 25. In skinned fibers from m. soleus, partial inhibition of respiration by NaN3 did not decrease the apparent Km for ADP significantly, this excluding the possible explanation of low apparent affinity of mitochondria to ADP in these cells by its rapid consumption due to high oxidative activity and by intracellular diffusion problems. However, short treatment of fibers with trypsin decreased this constant value to 40-70 microM, confirming the earlier proposition that mitochondrial sensitivity to ADP in vivo is controlled by some cytoplasmic protein. Phantom cardiomyocytes which contain mostly mitochondria and cytoskeleton and retain the normal shape, showed also high apparent Km values for ADP. Therefore, they are probably the most suitable system for studies of cellular factors which control mitochondrial function in the cells in vivo. In these phantom cells anti-desmin antibodies did not change the kinetics of respiration regulation by ADP. However, in skinned fibers from the heart and m. soleus of transgenic desmin-deficient mice some changes in kinetics of respiration regulation by ADP were observed: in these fibers two populations of mitochondria were observed, one with usually high apparent Km for ADP and the second one with very low apparent Km for ADP. Morphological observations by electron microscopy confirmed the existence of two distinct cellular populations in the muscle cells of desmin-deficient mice. The results conform to the conclusion that the reason for observed high apparent Km for ADP in regulation of oxidative phosphorylation in heart and slow twitch skeletal muscle cells in vivo is low permeability of mitochondrial outer membrane porins but not diffusion problems of ADP into and inside the cells. Most probably, in these cells there is a protein associated with cytoskeleton, which controls the permeability of the outer mitochondrial porin pores (VDAC) for ADP. Desmin itself does not display this type of control of mitochondrial porin pores, but its absence results in appearance of cells with disorganised structure and of altered mitochondrial population probably lacking this unknown VDAC controlling protein. Thus, there may be functional connection between mitochondria, cellular structural organisation and cytoskeleton in the cells in vivo due to the existence of still unidentified protein factor(s).

Adenosine Diphosphate↗

Selective inhibition of mitochondrial respiration and glycolysis in human leukaemic leucocytes by methylglyoxal.

The effect of methylglyoxal on the oxygen consumption of mitochondria of both normal and leukaemic leucocytes was tested by using different respiratory substrates and complex specific artificial electron donors and inhibitors. The results indicate that methylglyoxal strongly inhibits mitochondrial respiration in leukaemic leucocytes, whereas, at a much higher concentration, methylglyoxal fails to inhibit mitochondrial respiration in normal leucocytes. Methylglyoxal strongly inhibits ADP-stimulated alpha-oxoglutarate and malate plus NAD+-dependent respiration, whereas, at a higher concentration, methylglyoxal fails to inhibit succinate and alpha-glycerophosphate-dependent respiration. Methylglyoxal also fails to inhibit respiration which is initiated by duroquinone and cannot inhibit oxygen consumption when the N,N,N', N'-tetramethyl-p-phenylenediamine by-pass is used. NADH oxidation by sub-mitochondrial particles of leukaemic leucocytes is also inhibited by methylglyoxal. Lactaldehyde, a catabolite of methylglyoxal, can exert a protective effect on the inhibition of leukaemic leucocyte mitochondrial respiration by methylglyoxal. Methylglyoxal also inhibits l-lactic acid formation by intact leukaemic leucocytes and critically reduces the ATP level of these cells, whereas methylglyoxal has no effect on normal leucocytes. We conclude that methylglyoxal inhibits glycolysis and the electron flow through mitochondrial complex I of leukaemic leucocytes. This is strikingly similar to our previous studies on mitochondrial respiration, glycolysis and ATP levels in Ehrlich ascites carcinoma cells [Ray, Dutta, Halder and Ray (1994) Biochem. J. 303, 69-72; Halder, Ray and Ray (1993) Int. J. Cancer 54, 443-449], which strongly suggests that the inhibition of electron flow through complex I of the mitochondrial respiratory chain and inhibition of glycolysis by methylglyoxal may be common characteristics of all malignant cells.

Adenosine Triphosphate↗

Modulation of the stretch reflex of jaw-closing muscles in different modes and phases of respiration.

The objective of this study was to investigate whether and how changes in the mode of respiration affect the electromyographic activity of human jaw-closing muscles. Fifteen men were examined in this study. A pair of surface electrodes was attached bilaterally to the masseter and anterior and posterior temporalis muscles for electromyographic recording. Respiratory movements of the chest wall and nasal airflow were recorded simultaneously. Recordings were performed with subjects in the sitting position during quiet nasal and oral respiration. The stretch reflex of jaw-closing muscles was elicited by randomly tapping the chin with an impulse hammer. In 11 subjects, we measured nasal resistance with a rhinomanometer. The amplitude of electromyographic activities of the masseter and anterior temporalis muscles during oral respiration was significantly less than that during nasal respiration, whereas that of the posterior temporalis muscle showed no significant difference between the different modes of respiration. Furthermore, the reduction in the amplitude of the electromyographic activity was more evident in the inspiratory phase during oral respiration. There was a significant positive correlation between the ratio of the reflex amplitude during inspiration in the 2 respiratory modes and nasal resistance for the masseter muscle, but not for the anterior temporalis muscle. These results suggest that the reflexive electromyographic activity of some human jaw-closing muscles is modulated during oral respiration.

Adult↗

Inhibition of brain mitochondrial respiration by dopamine: involvement of H(2)O(2) and hydroxyl radicals but not glutathione-protein-mixed disulfides.

Examination of the downstream mediators responsible for inhibition of mitochondrial respiration by dopamine (DA) was investigated. Consistent with findings reported by others, exposure of rat brain mitochondria to 0.5 mm DA for 15 min at 30 degrees C inhibited pyruvate/glutamate/malate-supported state-3 respiration by 20%. Inhibition was prevented in the presence of pargyline and clorgyline demonstrating that mitochondrial inhibition arose from products formed following MAO metabolism and could include hydrogen peroxide (H(2) O(2) ), hydroxyl radical, oxidized glutathione (GSSG) or glutathione-protein mixed disulfides (PrSSG). As with DA, direct incubation of intact mitochondria with H(2) O(2) (100 microm) significantly inhibited state-3 respiration. In contrast, incubation with GSSG (1 mm) had no effect on O(2) consumption. Exposure of mitochondria to 1 mm GSSG resulted in a 3.3-fold increase in PrSSG formation compared with 1.4- and 1.5-fold increases in the presence of 100 microm H(2) O(2) or 0.5 mm DA, respectively, suggesting a dissociation between PrSSG formation and effects on respiration. The lack of inhibition of respiration by GSSG could not be accounted for by inadequate delivery of GSSG into mitochondria as increases in PrSSG levels in both membrane-bound (2-fold) and intramatrix (3.5-fold) protein compartments were observed. Furthermore, GSSG was without effect on electron transport chain activities in freeze-thawed brain mitochondria or in pig heart electron transport particles (ETP). In contrast, H(2) O(2) showed differential effects on inhibition of respiration supported by different substrates with a sensitivity of succinate > pyruvate/malate > glutamate/malate. NADH oxidase and succinate oxidase activities in freeze-thawed mitochondria were inhibited with IC(50) approximately 2-3-fold higher than in intact mitochondria. ETPs, however, were relatively insensitive to H(2) O(2). Co-administration of desferrioxamine with H(2) O(2) had no effect on complex I-associated inhibition in intact mitochondria, but attenuated inhibition of rotenone-sensitive NADH oxidase activity by 70% in freeze-thawed mitochondria. The results show that DA-associated inhibition of respiration is dependent on MAO and that H(2) O(2) and its downstream hydroxyl radical rather than increased GSSG and subsequent PrSSG formation mediate the effects.

Animals↗

Quantitative fit testing of personnel utilizing a mouthpiece respirator.

A respirator test facility using Refrigerant 12 as a challenge gas has been developed. More than 6000 people have received training in the effective use of mouthpiece respirators. Leakage is determined by the use of a halide detection meter analyzing the exhaled breath. The facilities have been used to provide training and quantitative fit testing for practically all types of respiratory protective equipment. An actual use investigation was made to determine the suitability of the mouthpiece respirator for use in a chlorine producing plant work situation. The mouthpiece respirator was compared with a group of half-face respirators. A clear distinction was made: the half-face respirator offered less protection than the mouthpiece respirator.

Chemical Industry↗

Respirator fit factor performance while sweating.

The extent to which sweat accumulation inside respirators affects respirator fit has not been quantified. This study represents an attempt to measure facial sweating and to quantify its effects on fit factors of negative pressure, full-facepiece respirators. Respirator fit factor (FF) data were obtained while 14 subjects completed 30 minutes of treadmill walking at an intensity of 75% of age-predicted maximal heart rate in an aerosol test chamber under ambient environmental conditions. Subject facial and whole body sweat production were also measured. Statistical analysis of the treadmill FF results showed that respirator fit was significantly (p < 0.05) degraded after 14 minutes of exercise. Sweat accumulation inside the respirator facepiece averaged 30.9 +/- 15.5 g. However, no significant correlation of subject facial sweat production with overall FF values measured during exercise was found. The results of this study indicate that respirator FFs degrade significantly over time under moderate exercise and environmental conditions and suggest that facial sweat accumulation alone does not account for the reduced FF levels.

Adult↗

Alterations in physiological and perceptual variables during exhaustive endurance work while wearing a pressure-demand respirator.

The purpose of this investigation was to describe the time course of changes in physiological and perceptual variables during exhaustive endurance work with and without an air-supplied, full-facepiece, pressure-demand respirator. Thirty-eight healthy subjects (24 to 51 years of age) volunteered for this study. Treadmill speed was set at 5.5 kph (3.4 mph) and elevation was set at a level calculated to elicit 70% of a previously determined maximal aerobic capacity (VO2max). Subjects continued at this rate to exhaustion. Despite a constant work rate, VO2 and %VO2max increased during exercise and were significantly greater with the respirator (34.4 +/- 1.1 mL/kg.min; 84% VO2max) than without the respirator (31.9 +/- 1.1 mL/kg.min; 76% VO2max) at the "final" measurement point prior to termination of exercise by each subject. The final values for ventilation volume (VE) also were significantly greater with the respirator (89.2 +/- 3.4 L/min) than without (73.4 +/- 3.7 L/min). At the conclusion of the endurance walk, dyspnea index (VE/MMV.25) remained well below maximal values (with = 58.6 +/- 2%; without = 44.6 +/- 2%; p less than 0.001). Also, at the final period, no significant differences occurred in the subjects' perceptual ratings of work of breathing, yet work performance time was significantly reduced (p less than 0.0001) from 69.1 +/- 4.4 min (without) to 55.6 +/- 3.8 min (with). A significantly greater swing in peak pressure (maximum pressure measured within the facepiece of respirator), however, from inspired (PPi) to expired (PPe) occurred with the respirator (13.42 cmH2O) than without the respirator (9.25 cmH2O).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Physiological and subjective responses to working in disposable protective coveralls and respirators commonly used by the asbestos abatement industry.

The physiological and subjective effects of working with different respirators while wearing lightweight disposable (Tyvek 1412 polyolefin) coveralls commonly used by the asbestos abatement industry were studied. Nine healthy men (mean age = 27.3 yr, weight = 76.9 kg) each performed a series of four exercise tests with four different respirator ensembles in counterbalanced order. Treadmill work was performed at a set walking speed of 4 kph (2.5 mph), 0 percent elevation (220 kcal/hr), a controlled environmental temperature of 33.9 degrees C, and 50% relative humidity. Each test continued up to 120 min, with repeated work/rest intervals of 26 min of work and 4 min of rest. Tyvek disposable coveralls and hoods were worn with each of these four different respirator ensembles: (1) control--a lightweight, low resistance mask; (2) HEPA--an air purifying, full facepiece respirator with dual high efficiency filters; (3) SAR--a supplied-air, pressure-demand respirator with escape filter; (4) SCBA--an open circuit, pressure-demand, self-contained breathing apparatus. Physiological measurements obtained every minute during each test included heart rate and skin and rectal temperatures. Subjective evaluations of clothing, respirator, and facepiece comfort, ease of breathing, temperature and perspiration in the mask and clothing, and respirator load also were measured at the end of the test. Data were analyzed using an analysis of variance. Results indicated that heart rate at the end of the test differed by less than 8 BPM between the control condition and the SCBA (heaviest) condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The course of respiration during the life cycle of Chlorella cells.

Endogenous and glucose respiration were studied during the life history of Chlorella pyrenoidosa. A generalized picture of the course of respiration during the life cycle is suggested. At the liberation of daughter cells from the wall of the mother cell, or soon after, the respiration rate reaches its lowest level. If the daughter cells are placed in light the respiration rate rapidly increases with time, soon reaches a maximum, and then declines slowly. Two factors are important in the initial increase-the early developmental stage of the cells and the influence of light. In autotrophically developing algae the parts played by developmental processes and by light have not been separated. Direct activation of respiratory enzymes by light, in addition to the level of respiratory substrate, cannot be excluded. The decline of respiration rate over most of the cell history seems to have no connection with light and is probably bound to the developmental processes per se. Darkening the suspension interrupts growth and induces liberation of daughter cells, with concomitant faster decrease in respiration rate. The rate of respiration of small daughter cells decreases in darkness only slowly with time. Illumination seems necessary to bring these cells back to a high level of respiratory activity.

Cell Respiration↗

Variations in dark respiration and mitochondrial numbers within needles of Pinus radiata grown in ambient or elevated CO2 partial pressure.

Within-leaf variations in cell size, mitochondrial numbers and dark respiration rates were compared in the most recently expanded tip, the mid-section and base of needles of Pinus radiata D. Don trees grown for 4 years in open-top chambers at ambient (36 Pa) or elevated (65 Pa) carbon dioxide partial pressure (p(CO2)a). Mitochondrial numbers and respiratory activity varied along the length of the needle, with the highest number of mitochondria per unit cytoplasm and the highest rate of respiration per unit leaf area at the base of the needle. Regardless of the location of the cells (tip, middle or basal sections), needles collected from trees grown in elevated p(CO2)a had nearly twice the number of mitochondria per unit cytoplasm as those grown in ambient p(CO2)a. This stimulation of mitochondrial density by growth at elevated p(CO2)a was greater at the tip of the needle (2.7 times more mitochondria than in needles grown in ambient CO2) than at the base of the needle (1.7 times). The mean size of individual mitochondria was unaffected either by growth at elevated p(CO2)a or by position along the needle. Tree growth at elevated p(CO2)a had a variable effect on respiration per unit leaf area, significantly increasing respiration in the tip of the needles (+25%) and decreasing respiration at the mid-section and base of the needles (-14% and -25%, respectively). Although a simple relationship between respiration per unit leaf area and mitochondrial number per unit cytoplasm was found within each CO2 treatment, the variable effect of growth at elevated p(CO2)a on respiration along the length of the needles indicates that a more complex relationship must determine the association between structure and function in these needles.

Carbon Dioxide↗

Estimating stem respiration in trees by a mass balance approach that accounts for internal and external fluxes of CO2.

The respiration rate of a tree stem has commonly been estimated from measurements of CO2 efflux to the atmosphere. These estimates assume that all CO2 efflux originates from respiration of local tissues and that all CO2 produced by local tissues escapes to the atmosphere through the bark. However, dissolved CO2 can be transported in the xylem stream, and CO2 concentration ([CO2]) in xylem can be up to three orders of magnitude greater than that of the atmosphere, suggesting that measurements of CO2 efflux do not account for all CO2 produced by respiration. Here, we propose a new mass balance approach for estimating the respiration rate of tree stems that accounts for both external and internal fluxes of CO2. We demonstrate this approach using measurements of CO2 efflux, sap flux and internal [CO(2)] to calculate the rate of CO2 production of a segment of stem tissue in situ. At different times of the day, CO2 produced by respiration of stem tissues followed different flux pathways. During daylight hours when sap was flowing, a large proportion of respired CO2 was carried away in the xylem stream, whereas at night, most respiratory CO2 escaped to the atmosphere through the bark. Our calculations showed errors in efflux-based estimates of respiration of up to 76% compared with estimates that include both internal and external fluxes.

Carbon Dioxide↗

Respiration rate in maize roots is related to concentration of reduced nitrogen and proliferation of lateral roots.

The relationship between specific rate of respiration (respiration rate per unit root dry weight) and concentration of reduced nitrogen was examined for maize (Zea mays L.) roots. Plants with 2 primary nodal root axes were grown for 8 days in a split-root hydroponic system in which NO3- was supplied to both axes at 1.0 mol m-3, to one axis at 1.0 mol m-3 and the other axis at 0.0 mol m-3, or to both axes at 0.0 mol m-3. Respiration rates and root characteristics were measured at 2-day intervals. Specific rate of respiration was positively correlated in a nonlinear relationship with concentration of reduced nitrogen. The lowest specific rates of respiration occurred when neither axis received exogenous NO3- and the concentration of reduced nitrogen in the axes was less than 9 mg g-1. The greatest rates occurred in axes that were actively absorbing NO3- and contained more than 35 mg g-1 of reduced nitrogen. At 23 mg g-1 of reduced nitrogen, below which initiation of lateral branches was decreased by 30-50%, specific rate of respiration was 17% greater for roots actively absorbing NO3- than for roots not absorbing NO3-. Increases in specific rate of respiration associated with concentrations of reduced nitrogen greater than 23 mg g-1 were concluded to be attributable primarily to proliferation of lateral branches.

Carbon Dioxide↗

Doxorubicin-induced thiol-dependent alteration of cardiac mitochondrial permeability transition and respiration.

Doxorubicin (DOX) is a highly effective treatment for several forms of cancer. However, clinical experience shows that DOX induces a cumulative and dose-dependent cardiomyopathy that has been ascribed to redox-cycling of the drug on the mitochondrial respiratory chain generating free radicals and oxidative stress in the process. Mitochondrial dysfunction including induction of the mitochondrial permeability transition (MPT) and inhibition of mitochondrial respiration have been implicated as major determinants in the pathogenesis of DOX cardiotoxicity. The present work was aimed at investigating whether the inhibition of mitochondrial respiration occurs secondarily to MPT induction in heart mitochondria isolated from DOX-treated rats and whether one or both consequences of DOX treatment are related with oxidation of protein thiol residues. DOX-induced oxidative stress was associated with the accumulation of products of lipid peroxidation and the depletion of alpha-tocopherol in cardiac mitochondrial membranes. No changes in mitochondrial coenzyme Q9 and Q10 concentrations were detected in hearts of DOX-treated rats. Cardiac mitochondria from DOX-treated rats were more susceptible to diamide-dependent induction of the MPT. Although DOX treatment did not affect state 4 respiration, state 3 respiration was decreased in heart mitochondria isolated from DOX-treated rats, which was reversed in part by adding either cyclosporin A or dithiothreitol, but not Trolox. The results suggest that in DOX-treated rats, (i) induction of the MPT is at least in part responsible for decreased mitochondrial respiration, (ii) heart mitochondria are more susceptible to diamide induced-MPT, (iii) thiol-dependent alteration of mitochondrial respiration is partially reversible ex vivo with dithiothreitol. Collectively, these data are consistent with the thesis that thiol-dependent alteration of MPT and respiration is an important factor in DOX-induced mitochondrial dysfunction.

Animals↗

Influence of forced respiration on nonlinear dynamics in heart rate variability.

Although it is doubtful whether the normal sinus rhythm can be described as low-dimensional chaos, there is evidence for inherent nonlinear dynamics and determinism in time series of consecutive R-R intervals. However, the physiological origin for these nonlinearities is unknown. The aim of this study was to test whether the known nonlinear input from spontaneous respiration is a source for the nonlinearities in heart rate variability. Twelve healthy subjects were examined in supine position with 3-h electrocardiogram recordings during both spontaneous and forced respiration in accordance with a metronome set to 12 min(-1). Nonlinear dynamics were measured as the correlation dimension and the nonlinear prediction error. Complexity expressed as correlation dimension was unchanged from normal respiration, 9.1 +/- 0.5, compared with forced respiration, 9.3 +/- 0.6. Also, nonlinear determinism expressed as the nonlinear prediction error did not differ between spontaneous respiration, 32.3 +/- 3.4 ms, and forced respiration, 31.9 +/- 5.7. It is concluded that the origin of the nonlinear dynamics in heart rate variability is not a nonlinear input from the respiration into the cardiovascular oscillator. Additional studies are needed to elucidate the mechanisms behind the nonlinear dynamics in heart rate variability.

Adolescent↗

Theophylline therapy for near-fatal Cheyne-Stokes respiration. A case report.

BACKGROUND: Cheyne-Stokes respiration is characterized by periodic breathing that alternates with hypopnea or apnea. OBJECTIVE: To describe the effect of theophylline on near-fatal Cheyne-Stokes respiration. DESIGN: Case report. SETTING: Tertiary referral center. PATIENT: A 48-year-old diabetic woman with a history of three cardiorespiratory arrests, a normal coronary arteriogram, normal left ventricular function, and severe Cheyne-Stokes respiration. MEASUREMENTS: Oxygen saturation, intra-arterial blood pressure, central venous pressure, chest wall movement, electrocardiography, electromyography, electroencephalography, electro-oculography, minute ventilation, arterial blood gases, and serum theophylline levels. RESULTS: After intravenous administration of 1.2 mg of theophylline at 0.6 mg/kg per hour (serum level, 5.6 microg/mL), both Cheyne-Stokes respiration and oxygen desaturation were markedly attenuated. After infusion of 2.4 mg of theophylline (serum level, 11.6 microg/mL), Cheyne-Stokes respiration resolved completely. No change was seen with placebo. Cheyne-Stokes respiration did not recur during outpatient treatment with oral theophylline. CONCLUSION: Theophylline may be a rapid and effective therapy for life-threatening Cheyne-Stokes respiration.

Blood Pressure↗