Lubrication during colonoscopy: a forgotten factor.
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Colonoscopy↗
Biomedical subjects
M Bonora
Publications and source records attributed to M Bonora.
Oil-lubricated colonoscopy: easier and less painful?
BACKGROUND AND STUDY AIMS: Methods of lubrication are rarely considered to be a matter for study in gastrointestinal endoscopy. We evaluated a new technique, i. e. the release of seed oil in discrete amounts from the tip of the scope during colonoscopy. PATIENTS AND METHODS: 346 consecutive patients prospectively underwent colonoscopy with a standard lubricating method (using water-soluble jelly; group A) or with the standard method plus seed oil (corn oil) instillations through the biopsy channel (group B). The following variables were evaluated in the two groups: the success rate for total intubation, and the time required to reach the cecum; the time needed to examine the colon at withdrawal; the detection rates for colorectal diseases; the level of pain and degree of difficulty associated with the examination. Patients in whom total colonoscopy was not achieved were asked to undergo a further examination in which the other lubricating technique was used. RESULTS: Successful intubation to the cecum was significantly more frequent ( P < 0.005) in the oil lubrication group (group B, 159/168) than in the control group (group A, 145/170), and less time was needed ( P < 0.001). No significant differences were found with regard to time for examination at withdrawal and detection rates for colorectal diseases. Level of pain and degree of difficulty during colonoscopy were significantly lower in the oil group ( P < 0.001). In the cross-over examinations done in patients in whom total colonoscopy was not achieved, no statistical difference was found between the two groups. We observed no side effects for patients or damage to the instrument. CONCLUSIONS: The proposed technique could be a simple, safe, and inexpensive method for easier and less painful colonoscopy; moreover, it might facilitate difficult examinations. Further studies are needed to confirm our data and to ensure that the use of this technique is not liable to damage the scope.
Adult↗
Zollinger-Ellison syndrome. Diagnosis and therapy.
Zollinger-Ellison syndrome (ZES) is characterised by refractory peptic ulcer disease, severe diarrhoea and gastric acid hypersecretion associated with an islet-cell tumor of the pancreas (gastrinoma). ZES is sporadic in 62-80% of cases and in 20-38% of cases is associated with multiple endocrine neoplasia type 1 (MEN 1). The diagnosis of ZES is certain when the plasma gastrin is >1000 pg/mL and the basal acid output is >15 mEq/h in patients with an intact stomach, >5 mEq/h in gastrectomised patients, or when the hypergastrinemia is associated with a pH <2. Treatment is based on the control of gastric acid hypersecretion and of the malignant tumor and its possible metastases. Proton pump inhibitors are the most effective antisecretory drugs and can be administered at high dosages without drug-related adverse effects. All sporadic, localised gastrinomas should be excised if possible. When liver metastases are also present, their debulking may improve symptoms and survival, and facilitate medical treatment. There is some controversy as to the surgical approach for gastrinomas associated with MEN 1. Somatostatin analogues can be useful in reducing gastric acid hypersecretion, serum gastrin and gastric enterochromaffin-like cells, and can thus contribute to treating the disease more effectively. Their antiproliferative effect can be used in treating liver metastases. Chemotherapy and/or interferon are indicated only in patients with malignant progressive disease. Embolisation and chemoembolisation are effective in controlling clinical symptoms; however, they do not seem to improve survival.
Biomarkers↗
Endoscopic signs in celiac disease.
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Adolescent↗
Hunting for celiac patients.
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Celiac Disease↗
New materials for ESR dosimetry.
New materials for electron spin resonance (ESR) dosimetry have been investigated with the aim to find systems more sensitive than L-alanine accepted as a standard for high dose determinations. Among the investigated systems ammonium tartrate, 2-methylalanine, salts of formic acids and dithionates have been found to be more sensitive than alanine by a factor 2-10. The lower limit applies to tissue equivalent materials, while much higher sensitivities were obtained with formates and dithionates containing heavier atoms. The increased sensitivity was mainly attributed to suitable ESR properties of the room temperature stable radicals as regards spectral shape (narrow lines, little or no hyperfine structure) and microwave saturation properties (short relaxation times). The radical structures have when necessary been clarified by ENDOR spectroscopy, while the saturation properties have been screened by pulsed ESR measurements.
Alanine↗
Ventilation, EELV and diaphragmatic activity in rats during the early phase of normobaric hypoxia.
We tested whether the enhancement of end-expiratory activity of the diaphragm (DE) induced by acute hypoxia persists during long-lasting hypoxia and participates in the enlargement of end-expiratory lung volume (EELV). We thus measured these two parameters together with ventilation (VE) in 30 rats, either awake or anesthetized, exposed to (1) poikilocapnic hypoxia sustained for 2 or 3 h; or (2) chronic normobaric hypoxia for 7 days interrupted by short episodes of normoxia. Twelve control animals were also studied. (1) Sustained hypoxia induced a stable increase in DE, VE and EELV. (2) In awake rats, chronic hypoxia induced a transient increase in VE after 1 day of hypoxia, and an increase persisting during acute normoxia throughout the exposure. DE followed the same, although less pronounced, course as VE. In anesthetized animals, only EELV was increased in both chronic hypoxia and acute normoxia, but its enlargement in normoxia was not associated with a concomitant increase in DE. The transition from hypoxia to normoxia always induced a decrease in DE and EELV. Therefore, (1) during hypoxia sustained for 2 or 3 h, the ventilatory and diaphragmatic responses were stable; (2) during chronic hypoxia lasting 1 week, a ventilatory acclimatization was expressed by a transient increase in hypoxic VE and a hyperventilation continuing during acute normoxia; (3) EELV enlargement in chronic hypoxia was partly related to changes in DE and partly due to another mechanism possibly involving morphological adaptations.
Acclimatization↗
Ventilation, EELV and diaphragmatic activity in rats during chronic normobaric hypoxia.
We determined the effects of chronic hypoxia on end-expiratory lung volume (EELV), end-expiratory diaphragmatic activity (DE) and ventilation (VE) in 27 intact (awake and anesthetized) and six carotid body-denervated (CBD; anesthetized) rats. Twenty-nine control animals were also studied. Recordings were made during hypoxia and normoxia before and after 2 or 3 weeks of hypoxia (+3 days of recovery from chronic hypoxia). In awake rats, 2 weeks of chronic hypoxia increased only normoxic VE, while 3 weeks of chronic hypoxia did not change VE or DE. In anesthetized intact rats, after both exposures, hypoxic and normoxic VE tended to decrease, DE did not change and hypoxic and normoxic EELV were enlarged. In CBD animals, 2 weeks of chronic hypoxia did not affect hypoxic VE but decreased normoxic ventilation and enlarged EELV similar to the intact animals. After 3 days of recovery in normoxia, all parameters except EELV were restored to prehypoxic values. Also, transition from hypoxia to normoxia induced parallel changes in EELV and DE while chronic hypoxia increased only EELV. Therefore, chronic normobaric hypoxia induced, (1) an increase in normoxic ventilation reflecting a process of acclimatization; (2) an enlargement of EELV that did not depend on changes in DE and carotid chemoreceptors.
Acclimatization↗
Lung mechanics and end-expiratory lung volume during hypoxia in rats.
We investigated whether an hypoxia-induced increase in airway resistance mediated by vagal efferents participates in the increase in end-expiratory lung volume (EELV) observed in hypoxia. We also assessed the contribution of the end-expiratory activity of the diaphragm (DE) to this phenomenon. Therefore, we measured EELV, total lung resistance (RL), dynamic lung compliance (Cdyn), DE, and minute ventilation (VE) in anesthetized rats during normoxia and hypoxia (10% O(2)) before (control) and after administration of atropine or saline. In the control group, hypoxia increased EELV, Cdyn, DE, and VE but slightly decreased RL. These changes were unaffected by saline or atropine, except that, in the atropine-treated rats, hypoxia did not change RL. These results suggest that 1) the increase in EELV observed in hypoxia cannot result from an increase in airway resistance; 2) the increased and persistent activity of inspiratory muscles during expiration is the most likely cause of the increase in EELV during hypoxia; and 3) the decrease in RL induced by hypoxia could result from the increase in lung volume including EELV.
Airway Resistance↗
Diaphragmatic activity during biphasic ventilatory response to hypoxia in rats.
To determine its role in the biphasic ventilatory response to hypoxia, we examined the diaphragmatic activity at its peak (DI), at the end of expiration (DE), and ventilation in adult anesthetized rats: (1) after 10 min of graded levels of poikilocapnic hypoxia (16, 14, 12, 10% O2); (2) at 1, 5 and 10 min of steady hypoxia (10% O2) in intact and vagotomized rats. (1) Gradual hypoxia progressively increased VE and DE but DI only at 10% O2; (2) 10% O2 induced an initial increase in ventilation followed by its consistent decline. VT, DI and DE at first increased, then VT and DI decreased, while DE remained augmented. VT and phasic activation of the diaphragm (DI - DE) decreased in parallel. Bilateral vagotomy did not affect the biphasic response of Ve. These results suggest that (1) the increased end-expiratory activity of the diaphragm limits its phasic inspiratory activation and thus contributes to the biphasic character of the ventilatory response to sustained hypoxia; (2) vagal input does not play a major role in this phenomenon.
Animals↗
Ventilatory and metabolic responses to ambient hypoxia or hypercapnia in rats exposed to CO hypoxia.
We have investigated at ambient temperatures (Tam) of 25 and 5 degrees C the effects of ambient hypoxia (Hxam; fractional inspired O2 = 0.14) and hypercapnia (fractional inspired CO2 = 0.04) on ventilation (V), O2 uptake (VO2), and colonic temperature (Tc) in 12 conscious rats before and after carotid body denervation (CBD). The rats were concomitantly exposed to CO hypoxia (HxCO; fractional inspired CO = 0.03-0.05%), which decreases arterial O2 saturation by approximately 25-40%. The results demonstrate the following. 1) At Tam of 5 degrees C, in both intact and CBD rats, V/VO2 is larger when Hxam or CO2 is associated with HxCO than with normoxia. At Tam of 25 degrees C, this is also the case except for CO2 in CBD rats. 2) At Tam of 5 degrees C, the changes in VO2 and Tc seem to result from additive effects of the separate changes induced by Hxam, CO2, and HxCO. It is concluded that, in conscious rats, central hypoxia does not depress respiratory activity. On the contrary, particularly when VO2 is augmented during a cold stress, both V/VO2 during HxCO and the ventilatory responses to Hxam and CO2 are increased. The mechanisms involved in this relative hyperventilation are likely to involve diencephalic integrative structures.
Animals↗
Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity.
The possible role of pulmonary C fibers in the hypoxia-induced concomitant increases in end-expiratory lung volume (EELV) and in the activity of the diaphragm at the end of expiration (DE) were evaluated by measuring the effects of hypoxia (10% O2) on ventilation, EELV, and DE in eight chloralose-urethan anesthetized rats. Recordings were made before and after blocking vagal C fibers and after bilateral vagotomy. C-fiber conduction was blocked by applying capsaicin perineurally to the cervical vagi. The efficiency of C-fiber blockade was tested with intravenous capsaicin and its selectivity by the Hering-Breuer reflex. Perineural capsaicin abolished the reflex apnea induced by intravenous capsaicin and transiently reduced Hering-Breuer reflex. Perineural capsaicin affected neither ventilation, DE, and EELV in air nor the hypoxia-induced increases in these parameters. Vagotomy caused the typical changes of breathing pattern in air, but the ventilatory response to hypoxia was unchanged. Vagotomy performed during hypoxia resulted in large decreases in DE and EELV. Hypoxia increased DE and EELV in vagotomized rats but less than in intact rats. We conclude that the hypoxia-induced increases in EELV and diaphragmatic activity are probably not mediated by vagal C fibers and that vagal afferents are involved but not fully responsible for this phenomenon.
Anesthesia↗
Pyrazole-related nucleosides. 4. Synthesis and antitumor activity of some 1-tetrahydropyranyl-4-substituted pyrazoles.
Continuing our studies on the structure-activity relationships of some pyrazole nucleosides (1a-h) structurally related to ribavirin, tiazofurin and selenazofurin, we describe here the synthesis and antitumor/antiviral/antimicrobial activity of a new series of 1-tetrahydropyranyl-4-substituted pyrazoles. In this study, the tetrahydropyranyl moiety (THP), designed as a mimic of the glycosidic portion of the parent compounds 1a-h, has led to a few derivatives with moderate cytotoxic activity against leukemia/lymphoma and solid tumor-derived cell lines (IC50 14-100 microM). The compounds obtained through substitution of the ribofuranosyl moiety by the THP moiety were still active, the free heterocyclic bases were devoid of any activity.
Animals↗
Ventilatory response to CO2 and hypoxia during cold exposure in awake rats.
Recently, we have described the effects of hypoxia and of hypercapnia on the metabolic (VO2) and ventilatory responses to cold in unanesthetized intact and carotid body-denervated (CBD) rats (Gautier et al., J. Appl. Physiol. 73: 847-854, 1992 and 75: 2570-2579, 1993). In the present paper, we have reanalyzed the above results for a more detailed study of the interactions of hypoxia (FIO2 = 0.12), hypercapnia (FICO2 = 0.04) and changes in VO2 with the ventilatory control. The results show that: (1) Compared to normoxia, in hypoxia increments in V and VT are proportional to VO2 whereas in hypercapnia increments in ventilation (V) and tidal volume (VT) are independent of VO2. In both hypoxia and hypercapnia, increases in respiratory frequency (fR) are independent of VO2; and (2) Interactions of hypoxia, hypercapnia and VO2 with control of V persist in CBD rats but, for a given VO2, V, VT and fR are lower than in intact rats. These interactions are essentially similar to those observed during muscular exercise performed in normoxia, hypoxia or hypercapnia. It is suggested that during cold exposure or muscular exercise, resulting both in increased VO2, there are common integrative structures probably located in the hypothalamus which are involved in the control of breathing.
Animals↗
Changes in end-expiratory lung volume and diaphragmatic activity during hypoxia and hypercapnia in cats.
To assess the role of diaphragmatic activity at the end of expiration (DE) in the control of end-expiratory lung volume (EELV), 1) these two parameters were correlated in anesthetized cats breathing different gas mixtures; and 2) expiratory flow volume curves in normoxia and hypoxia together with changes in esophageal pressure were measured. The influence of volume feedback on DE control was tested by applying positive end-expiratory pressure (PEEP). The effect of anesthesia was determined by measuring DE in unanesthetized cats. In hyperoxia, DE (but not EELV) decreased. In hypocapnic hypoxia (12, 10, and 8% O2), both DE and EELV gradually increased, and these changes were significantly correlated. When normocapnia was restored in 8% O2, DE and EELV decreased but remained higher than in air. Hypercapnia affected neither DE nor EELV. PEEP blocked the hypoxia-induced increase in DE. Hypoxia decreased expiratory flow and esophageal pressure. Finally, the increases in DE at 12 and 10% O2 were more pronounced when the cats were unanesthetized. These results suggest that the increase in diaphragmatic activity induced by hypocapnic hypoxia during expiration affects expiratory flow and thoracic volume and, therefore, plays a major role in increasing EELV. This phenomenon may also be controlled by volume feedback.
Animals↗
Ventilatory and metabolic responses to cold and CO-induced hypoxia in awake rats.
Experiments were carried out in awake rats to compare the effects of ambient and CO-induced hypoxia on thermoregulation and ventilatory control. Measurements of metabolic rate (VO2), ventilation (V), shivering (EMG) and colonic temperature (Tc) were made at fixed ambient temperature (Ta) of 25, 15 and 5 degrees C. Animals were exposed to ambient hypoxia (FIO2 of 21, 17, 14, 12 and 10%) or to CO hypoxia (FICO of 0.03% in air). The results show that: (1) Both ambient and CO-induced hypoxia provoked decreases in VO2 and Tc which were more marked at low Ta values; non-shivering thermogenesis was depressed with both types of hypoxia, whereas shivering was depressed only with ambient hypoxia; (2) Ventilatory response to ambient hypoxia was blunted at low Ta values and CO-induced hypoxia did not affect ventilation. It is concluded that: (1) hypoxia affects markedly the control of Tc by altering thermogenesis: inhibition of non-shivering thermogenesis seems to result from a decrease in CaO2 whereas inhibition of shivering seems to result from a decrease in PaO2; (2) during hypoxia, ventilation is controlled by the opposite stimulation from chemoreceptors and inhibition from hypometabolism. However, as revealed by CO-induced hypoxia, another stimulatory factor may also interact with the control of breathing.
Animals↗
Effects of hypercapnia and hypoxia on inspiratory and expiratory diaphragmatic activity in conscious cats.
The influence of steady-state changes in chemical stimuli on ventilation and electromyographic activity of the diaphragm during both inspiration (total DI) and expiration (total DE) was studied in unanesthetized intact adult cats before and after carotid denervation. In intact animals, during hypercapnia (2 4, and 6% CO2), tidal volume (VT) and total DI increase, whereas total DE did not consistently change. During ambient hypocapnic hypoxia (14, 12, and 10% O2), VT increased only at 10% O2, whereas total DI increased at all levels studied. Total DE increased substantially at 14% O2, persisting up to the end of expiration with 12 and 10% O2. This effect was markedly attenuated during normocapnic hypoxia. During CO hypoxemia (1,700 ppm in air), VT as well as total DI and total DE decreased because of a large reduction in inspiratory and expiratory time elicited by tachypneic breathing. The effects of hypercapnia and hypoxia persisted after carotid denervation. Therefore, 1) in contrast to hypercapnia, hypoxia markedly enhances the expiratory diaphragmatic activity, 1) this expiratory braking mechanism depends on the severity of hypoxia and is partly due to hypocapnia secondary to hypoxia; and 3) because this effect was observed after carotid denervation and during CO hypoxemia, it may arise in the central nervous system, possibly in bulbopontine structures.
Animals↗
Ventilatory strategy in hypoxic or hypercapnic newborns.
In conscious newborns, the ventilatory response to hypoxia is characterized by precocious hyperventilation followed by tardive hypoventilation, the latter disappearing with age. The hypoventilation could be mainly related to a weak peripheral drive and to the persistence of the diaphragmatic activity during expiration. Also, a decrease in metabolic rate and body temperature interferes with the response. The hyperventilation in response to hypercapnia increases as maturation proceeds and the maturation of the peripheral chemoreceptors contribute to this effect, as during hypoxia. The responses to both stimuli depend on many factors such as sleep state, anesthesia or ambient temperature.
Animals↗