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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three types of catheters, the Arrow multi-orifice catheter, the American Edwards 7 Fr Swan-Ganz catheter and the Cook Bunegin-Albin multi-orifice CVP catheter were evaluated for their ability to retrieve venous air emboli and effect on the success rate of resuscitation from venous air emboli. The catheters were inserted in dogs anesthetized with isoflurane (1.7%, inspired) and N2O (66%) in O2 and placed in the sitting position with the head 90 degrees to the horizontal. Swan-Ganz catheters were positioned with the right atrial (RA) port just above the junction of the superior vena cava (SVC) and the RA and the pulmonary artery (PA) port in the pulmonary artery. The Arrow and Bunegin-Albin multi-orifice catheters were placed with the proximal orifice just above the SVC-RA junction and the distal orifice near the mid-RA. Dogs were then given a predetermined lethal dose of air (5 ml.kg-1) over 30 sec via the jugular vein. Attempts to aspirate venous air emboli were begun with the first decrease in expired CO2. Both RA and PA ports of the Swan-Ganz catheter were used for aspiration. The amounts of gas retrieved expressed as a percent of the injected air and the incidence of successful resuscitation were compared. Significantly greater percentages of injected venous air were retrieved with the Bunegin-Albin catheter (63 +/- 14%, mean +/- SEM) than with the Arrow multi-orifice catheter (6 +/- 2%) or the Swan-Ganz catheter (14 +/- 5%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bunegin-Albin catheter improves air retrieval and resuscitation from lethal venous air embolism in upright dogs. 291 70

Inspiratory mechanical loads were applied to the airway continuously for 5 min in healthy young adult volunteers maintained in a near steady-state of halothane anesthesia 1.1 MAC. The loads, both flow resistive and elastic in nature, had been selected to reduce the first loaded tidal volume approximately 10, 30 or 50%--these being designated "small," "medium," and "large" loads, respectively. The actual magnitudes of resistive load were 8 +/- 1, 21 +/- 3, and 48 +/- 6 cmH2O X l-1 X s, and of elastic load 6 +/- 1, 18 +/- 1, and 41 +/- 5 cmH2O X l-1 (mean +/- SEM). All loads caused an immediate reduction of ventilation proportional to the size of the load. This was followed by a gradual recovery of ventilation toward control values over approximately 2 min and then nearly stable ventilation for the rest of the loading period. Respiratory frequency was unchanged throughout. At 5 min of loading, ventilation and PaCO2 had been nearly steady for 3 min and O2 uptake and CO2 output at the airway were unchanged from control, suggesting the establishment of a near steady respiratory state. With the small and medium loads of both types, ventilation and PaCO2 in this near steady-state were not detectably different from control. With the large loads, however, ventilation was significantly reduced and PaCO2 slightly increased. The end-expiratory position of the chest wall and the relative contributions of the rib cage and abdomen-diaphragm to ventilation, as estimated by anteroposterior chest wall magnetometers, were not consistently altered by any load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory compensation for continuous inspiratory resistive and elastic loads during halothane anesthesia in humans. 293 23

beta-Endorphin (beta-EP) and methionine-enkephalin (Met-Enk) have been detected in human follicular fluid in concentrations several times higher than those in plasma. These data stimulated us to study the possible physiological role of ovarian opioids. We, therefore, determined the effects of both beta-EP and Met-Enk, alone or in combination with naloxone, on FSH-induced progesterone (P) secretion by cultured granulosa cells. Granulosa cells were collected from follicular fluid recovered at laparoscopy in seven superovulated women. The cells were preincubated with RPMI-1640 medium containing 20% fetal calf serum in 5% CO2 for 48 h, followed by the addition of 100 mU purified FSH and the various test substances for 48 more h. beta-EP (10 nM to 1 pM) had no effect on P secretion either alone or in combination with FSH and/or naloxone. Micro- to picomolar amounts of Met-Enk increased FSH-induced P secretion up to 186.9 +/- 35.1% (+/- SEM). Met-Enk had no affect in the absence of FSH, and its action was significantly blunted by the concomitant addition of 10(-5) M naloxone. These data provide evidence for a dose-dependent naloxone-reversible synergistic action of Met-Enk and FSH on P secretion by cultured granulosa cells. This finding supports the hypothesis of the existence of an ovarian opioid system.
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PMID:Met-enkephalin enhances follicle-stimulating hormone-dependent progesterone production from cultured granulosa cells. 294 12

The electromyograms of the rectus abdominis, external oblique, and transversus abdominis muscles were recorded in eight lightly anesthetized, spontaneously breathing dogs. During quiet breathing in the supine posture seven animals invariably had a phasic expiratory activity in the transversus, whereas only two animals had invariable expiratory activity in the external oblique. An intermittent expiratory activity in the rectus was recorded in only one animal. The degree of activation, expressed as a percentage of the activity detected during breathing with 25 cm H2O positive end-expiratory pressure (PEEP), was also significantly greater (P less than 0.05) for the transversus (mean +/- SEM: 29.4 +/- 8.6%) than the external oblique (5.5 +/- 2.3%). Head up tilting and progressive hypercapnia elicited substantial increases in transversus and external oblique expiratory activity in all animals, whereas head down tilting caused marked decreases in expiratory activity. In each posture and at any given end-tidal CO2, however, the amount of transversus activity was larger than the amount of external oblique activity. The rectus was usually silent in all the conditions. Bilateral cervical vagotomy suppressed external oblique activity in most supine animals, and the muscle was no longer recruited by PEEP, head up tilting, or hypercapnia. In contrast, there was residual transversus expiratory activity in all supine animals (11.1 +/- 3.1%), as well as some expiratory recruitment during PEEP, head up tilting, and hypercapnia. These results indicate that: (1) the transversus is the primary abdominal muscle of expiration in the anesthetized dog; and (2) its behavior resembles that of the triangularis sterni, although it is more dependent on vagal afferent pathways. The present findings also strengthen the important fact that spontaneous quiet expiration in the dog is an active rather than passive process.
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PMID:Abdominal muscle use during breathing in the anesthetized dog. 295 99

Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0 meq/liter). Hypoxic rats also showed evidence of tissue hypoxia; liver tryptophan oxygenase levels were increased to 21 +/- 2 nmole/min/mg protein. In the hypoxic animals there was decreased jejunal mucosal (Na+-K+)-ATPase activity and an inhibition of active intestinal transport of sodium, glucose, 3-O-methylglucose, galactose, tyrosine, phenylalanine, and glycine as determined by in vivo perfusion studies. Jejunal fructose transport, which has a large passive component, was unaffected by hypoxia. The electrolyte, carbohydrate, and amino acid transport alterations produced by hypoxia were seen in the absence of an effect on jejunal cell number, DNA synthesis, or cell turnover. There was also no evidence of histological or ultrastructural damage. Furthermore, studies with a luminal macromolecular tracer, horseradish peroxidase, indicated that the jejunal lumen-to-blood barrier to macromolecules was also unaltered in these hypoxic animals. In vitro local oxygenation of the jejunum, by bubbling of 95% O2:5% CO2, markedly improved sodium and glucose (but not 3-O-methylglucose) absorption in hypoxic rats and control rats. The (Na+-K+)-ATPase activity of the jejunal mucosa of hypoxic rats was significantly enhanced by the local bubbling of 95% O2:5% CO2. Overall, our data indicate that during relatively mild conditions of hypoxia there is an inhibition of jejunal (Na+-K+)-ATPase activity and related transport processes that is prevented by in situ oxygenation.
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PMID:Alterations in jejunal transport and (Na+-K+)-ATPase in an experimental model of hypoxia in rats. 300 54

To determine whether the stimulatory effect of CO2 on the peripheral chemoreceptors is due to molecular CO2, H+ or both we measured steady-state ventilation (Ve) during normoxia in 9 and during hypoxia in 5 chloralose-urethane anaesthetized cats using the artificial brain stem perfusion technique. This technique allows one to manipulate independently the PaCO2, PaO2 and the pHa of the blood in the systemic circulation (peripheral) and the blood perfusing the brain stem (central). Keeping the central conditions constant the H+ and CO2 concentrations in the systemic circulation were changed by i.v. infusion of 0.3 M HCl or 0.6 M NaHCO3 and by giving the animal different CO2 mixtures to inhale. The peripheral H+ concentration ([H+]p) range covered was from 27 to 103 nmol X 1(-1); the peripheral arterial CO2 tension (PaPCO2) ranged from 2.3 kPa to 8.4 kPa. Fitting the data with the function VE = a[H+]p + bPaPCO2 + c revealed that the coefficient b was not significantly different from zero at the 0.05 level during normoxia and hypoxia. The mean value (+/- SEM) found for the coefficient a was 33.0 +/- 3.6 at normoxia and 36.0 +/- 15.4 ml X min-1 X nM-1 at hypoxia. We conclude that the steady-state ventilatory response due to the stimulation of the peripheral chemoreceptors with CO2 is mediated by H+. The effects of molecular CO2 are negligible.
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PMID:Effects of CO2 and H+ on the ventilatory response to peripheral chemoreceptor stimulation. 308 87

One hypothesis that could account for the anxiogenic response to breathing air supplemented with carbon dioxide seen in panic anxiety patients is that panic patients might have abnormally high central medullary chemoreceptor sensitivity. Chemoreceptor sensitivity was assessed by using a rebreathing technique to measure the ventilatory response to CO2 in 14 medication-free patients with agoraphobia and panic attacks and 23 healthy subjects. Ventilatory response to CO2 was similar in patients and controls (mean +/- SEM, 1.58 +/- 0.16 vs 1.58 +/- 0.14 L/min/mm Hg), suggesting that abnormal chemoreceptor sensitivity does not explain the behavioral sensitivity of panic patients to CO2. Anxiety ratings increased markedly during rebreathing both in patients and controls; anxiety increases were significantly greater in patients than in healthy subjects matched for age, sex, and rebreathing duration. Alprazolam treatment in eight patients markedly attenuated anxiety increases during rebreathing. Differences in anxiogenic sensitivity to CO2 between patients and controls may be due to differences in the regulation of noradrenergic or other neuronal systems.
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PMID:Carbon dioxide sensitivity in panic anxiety. Ventilatory and anxiogenic response to carbon dioxide in healthy subjects and patients with panic anxiety before and after alprazolam treatment. 309 80

Nineteen subjects with the obstructive sleep apnea syndrome (10 with daytime arterial CO2 tension 44 mm Hg or higher) were treated with long-term nocturnal continuous positive airway pressure. The ventilatory response to CO2 (Read's method) was measured in triplicate prior to treatment and after 1, 2, 3, 7, and 14 or more nights of therapy. Seven subjects were tested on at least 4 occasions. For each test, slope of the response line and position of the response line (ventilation at a PCO2 of 60 mm Hg) were calculated. The subjects with initial high daytime CO2 showed no change in slope of response with treatment but showed a progressive increase in ventilation at any given degree of PCO2. Ventilation at a PCO2 of 60 mm Hg increased from a mean of 20.0 +/- 1.3 SEM L/min by 8.0 +/- 2.5 SEM L/min after 2 nights of therapy (p less than 0.05, two-way analysis of variance), and by 16.2 +/- 1.9 L/min after 2 wk or more (p less than 0.01). On average, there was no significant change in either slope or position of response in the subjects with initially normal daytime PCO2. We conclude that airway obstruction in sleep (in obstructive sleep apnea syndrome) leads in some subjects to respiratory failure in the daytime, with a left shift in the ventilatory response to CO2, and that this changes is usually reversible during the next several days.
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PMID:Time course of change in ventilatory response to CO2 with long-term CPAP therapy for obstructive sleep apnea. 309 16

To determine the relative importance of the peripheral and central chemoreceptors in the ventilatory response to acute metabolic acid-base disturbances we measured the normoxic ventilatory response to acute respiratory and metabolic acidosis and alkalosis in 10 chloralose-urethane anesthetized cats using a technique of vertebral artery perfusion that allows one to independently manipulate the PaCO2, PaO2 and the H+ concentration of the blood in the systemic circulation (peripheral) and the blood perfusing the brain stem (central) (Berkenbosch et al., 1979). The ventilation could be satisfactorily described by a linear function of the peripheral and central arterial H+ concentration and the central PaCO2. Mean values (+/- SEM) found for the peripheral arterial H+ sensitivity and the isocapnic central arterial H+ sensitivity were 26.0 +/- 3.2 and 12.7 +/- 1.8 ml X min-1 X nM-1, respectively; the isohydric central arterial CO2 sensitivity was 545.9 +/- 96.7 ml X min-1 X kPa-1. We conclude that in the ventilatory response to an acute metabolic acid-base disturbance both the peripheral and central chemoreceptors play a role. However, the sensitivity of the peripheral chemoreceptors to isocapnic changes in the arterial H+ concentration is twice as large as the sensitivity of the central chemoreceptors. It is argued that in the adaptation of the ventilation to an acute metabolic acidosis the stimulatory effect of the peripheral chemoreceptors is counteracted by a diminished stimulation of the central chemoreceptors.
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PMID:Ventilatory responses to respiratory and metabolic acid-base disturbances in cats. 310 86

Intracellular pH (pHi) and buffering power of type 1 and type 2 fibres from the iliofibularis muscle of the clawed frog, Xenopus laevis, have been measured using pH-sensitive microelectrodes. In phosphate buffered Ringer's solution (extracellular pH 7.25, 20-22 degrees C), mean pHi and its variance were similar in the two fibre types (6.86 +/- SD 0.15 +/- SEM 0.03, n = 24, type 1, and 6.86 +/- SD 0.12 +/- SEM 0.03, n = 15, type 2). On changing to Ringer's solution containing CO2 and HCO3- (extracellular pH 7.25, 20-22 degrees C), pHi became more acid in both fibre types. Although H+ ions were not at electrochemical equilibrium across the surface membrane, active transport did not return pHi to its original value during exposure to CO2. The buffering powers calculated from the changes in pHi were not significantly different, 41.6 mmol X l-1 per pH unit (+/- SEM 4.0, n = 17) for type 1 and 49.3 mmol X l per pH unit (+/- SEM 7.2, n = 11) for type 2 fibres. Thus differences in the mechanical properties of these fibre types are not due simply to a difference of the intracellular pH or buffering of resting fibres. Other possible explanations are discussed for the changes in some contractile properties that occur when pHi is acidified.
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PMID:Intracellular pH and buffer power of type 1 and 2 fibres from skeletal muscle of Xenopus laevis. 310 53


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