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Biomedical subjects

M P Habib

Publications and source records attributed to M P Habib.

At least 19 recordsLinked to original sources
PubMed2001

Management of clinical failures in non-ICU patients with chronic obstructive pulmonary disease exacerbations.

Clinical failure after initial treatment for exacerbations of chronic obstructive pulmonary disease (COPD) occurs in 10-25% of cases. Once the original diagnosis is confirmed, there is a need to optimise therapy, including introducing bronchodilators and corticosteroids. The use of aggressive antibiotic treatment is recommended for patients with risk factors (elderly, more than four exacerbations per year, underlying cardiopulmonary disease) and more severe disease. Fluoroquinolones are a good choice for those patients who failed initial therapy and who require antimicrobials, including those with simple exacerbations, complicated cases with comorbidity, or those with bronchiectasis. Consideration of less common pathogens, such as Pseudomonas aeruginosa infection, should also be considered. Bacteria usually associated with exacerbations are becoming increasingly resistant, and this needs to be considered when deciding on appropriate antibiotic treatment.

Adrenal Cortex Hormones↗
PubMed1999

Effect of vitamin E on exhaled ethane in cigarette smokers.

STUDY OBJECTIVES: We hypothesized that micronutrient antioxidant intake may be one factor determining the development of significant COPD. Vitamin E was administered to smokers to determine if exhaled ethane was reduced and if ethane correlated with measures of lung function. STUDY DESIGN: Longitudinal placebo lead-in trial with posttreatment observation period. SETTING: Tucson Veterans Affairs Medical Center. PARTICIPANTS: Twenty-nine current stable smokers having no interest in smoking cessation. INTERVENTIONS: Spirometry, exhaled breath ethane measurements, and vitamin E and [-carotene plasma levels followed by 3 weeks of placebo with repeat plasma vitamin levels and ethane measurements; next, 3 weeks of vitamin E (dl-a-tocopherol), 400 IU po bid followed by plasma vitamin levels and breath ethane measurements; finally, 3 weeks without vitamins followed by breath ethane and plasma vitamin levels. RESULTS: Vitamin E treatment did not reduce ethane significantly. Exhaled ethane levels (mean + SD: pm/min/kg) were as follows: baseline, 7.39 + 5.39; after run-in period, 6.86 + 4.09; after vitamin E, 6.36+/-3.02; and final, 7.23+/-4.63. After vitamin E therapy, a significant negative correlation existed between exhaled ethane and FEV1/FVC. Pack-years of smoking at baseline and after vitamin E were significantly associated with ethane exhaled. Initial lung function was not significantly negatively associated with vitamin E-induced changes in exhaled ethane but a negative trend was found. CONCLUSIONS: Vitamin E alone, unlike the combination of vitamins C, E, and beta-carotene, failed to reduced exhaled ethane in cigarette smokers. Exhaled ethane was correlated with pack-years of smoking. Smokers whose ethane values were found to fall the most tended to have better preserved lung function.

Adult↗
PubMed1996

Exhaled ethane and antioxidant vitamin supplements in active smokers.

To determine the effect of nutritional agents on lipid peroxidation, 10 smokers were given 6 mg beta carotene, 200 IU vitamin E, and 250 mg vitamin C 4 times daily for 3 weeks. Lipid peroxidation was assessed by measuring baseline and postsupplementation levels of exhaled ethane. There was a 29% decrease in mean (+/-SD) exhaled ethane (4.06 +/- 1.49 vs 2.90 +/- 1.29 pmol.kg-1.min-1), with individual levels decreasing in 8 of the 10 smokers (p < 0.05, Wilcoxon sign rank test). Three nonsmokers had very low baseline levels of ethane that did not change with supplementation. Ethane production correlated with active (packs per day) and lifelong (pack-years) tobacco consumption. Also, a strong correlation was found between the decline in ethane output after micronutrient supplementation and the presupplement FEV1. Therefore, antioxidant vitamin supplementation resulted in attenuation of smoking-related lipid peroxidation, and the decreases in ethane production appears to be associated with preserved lung function.

Antioxidants↗
PubMed1995

The early pattern of conjugated dienes in liver and lung after endotoxin exposure.

If lipid peroxidation (LP) contributes to organ dysfunction in sepsis rather than simply reflecting established injury, it should occur soon after the onset of the septic insult, and it may not progress uniformly in all organs. We assessed whether LP occurs within 90 min after onset of continuous intravenous endotoxin (E. coli 055:B5) infusion in rats, using second-derivative spectroscopy to semiquantitatively assess conjugated dienes (CD) in lung, liver, and plasma phospholipids. Measurements were also made after 90-min infusions with saline or 1 mM H2O2. Both the quantity and spectrophotometric patterns of CD differed between the three groups. Compared with saline controls, lung lipid CD increased after both H2O2 and endotoxin. Venous plasma CD were elevated only after H2O2, while arterial plasma and liver lipid CD were not different between the three groups. Exhaled ethane (an indicator of peroxidation of omega-3 fatty acids) did not differ between groups. Wet-to-dry lung weights were significantly increased after endotoxin compared with that after saline controls. Our results indicate that tissue-specific LP occurs within 90 min of endotoxin or H2O2 intravenous infusion.

Animals↗
PubMed1995

Cigarette smoking and ethane exhalation in humans.

The time course of exhaled ethane gas was determined in the alveolar expirate of healthy, fasting smokers and nonsmokers after smoking a cigarette. Baseline ethane was measured by gas chromatography and corrected for background ethane after a 2-min washout using purified air. Ethane was measured immediately after smoking and hourly thereafter. Ethane was highest immediately after smoking, reflecting ethane in cigarette smoke. An exponential decline of ethane in smokers returned ethane to baseline within 3 h. Ethane in nonsmokers also peaked immediately after smoking but returned to baseline by 1 h. Ethane from smokers, measured 3 h after the last cigarette, was compared with ethane from healthy ex-smokers and nonsmokers. Mean (+/- SEM) baseline ethane in smokers was 2.90 +/- 0.52 pmol/min/kg, 1.55 +/- 0.36 pmol/min/kg in ex-smokers and 1.11 +/- 0.26 pmol/min/kg in nonsmokers (p < 0.05). Ethane in two smokers measured before and after a week of oral beta carotene supplementation (60 mg/d) fell by 80 and 35%. We conclude that cigarette smokers have increased baseline ethane in exhaled breath compared with non-smokers. Trials with antioxidant agents are warranted to assess their ability to reduce expired ethane levels.

Breath Tests↗
PubMed1994

Effect of diabetes, insulin, and glucose load on lipid peroxidation in the rat.

Lipid peroxidative activity in rats made diabetic with streptozocin and rats made acutely hyperglycemic by intraperitoneal dextrose administration was determined by measurement of exhaled ethane during exposure in vivo to ethane-free air (EFA). Diabetic rats demonstrated increased ethane in the expired breath while breathing EFA (5.82 +/- 0.56 pmol/min/100 g) compared with control rats (4.02 +/- 0.23 pmol/min/100 g). Insulin treatment of diabetic rats attenuated the ethane produced (4.88 +/- 0.23 pmol/min/100 g). Acute hyperglycemia increased exhaled ethane to levels higher than those seen in diabetic rats (9.87 +/- 0.98 pmol/min/100 g). Saline injected intraperitoneally to control rats produced ethane levels similar to those of untreated nondiabetic controls (4.11 +/- 0.52 pmol/min/100 g). Chronic uncontrolled hyperglycemia and acute hyperglycemia are associated with increased in vivo ethane production.

Animals↗
PubMed1994

Effect of simple carbohydrates, casein hydrolysate, and a lipid test meal on ethane exhalation rate.

To determine the potential differences in the effect of various nutrients on lipid peroxidation, the ethane exhalation (EE) rate, an index of lipid peroxidation, was measured in rats at 4 (young), 18 (intermediate age), and 24 (aged) mo of age at fasting conditions and after acute ingestion of various test meals. The EE rate (means +/- SD) after a 15-h fast was significantly reduced in 24-mo-old rats (2.45 +/- 0.44 pmol.min-1.100 g body wt-1) and 18-mo-old rats (3.51 +/- 0.55 pmol.min-1.100 g body wt-1) compared with 4-mo-old rats (4.44 +/- 0.66 pmol.min-1.100 g body wt-1; P < 0.01). The EE rate significantly increased in 4-mo-old rats after ingestion of 50% (wt/vol) dextrose (8.59 +/- 2.9 pmol.min-1.100 g body wt-1), 50% casein hydrolysate (6.77 +/- 1.23 pmol.min-1.100 g body wt-1), and 20% neutral lipid emulsion (7.33 +/- 1.96 pmol.min-1.100 g body wt-1; P < 0.01). The response of aged rats to these nutrients compared with young rats was reduced by approximately 50%. A 25% dextrose solution or a 50% solution of sucrose, fructose, maltose, or galactose did not significantly alter EE rate. It is concluded that various macronutrients have a diverse potential of inducing lipid peroxidation. The responsiveness of aged rats to meal-induced enhancement of EE and presumably lipid peroxidation is significantly reduced.

Aging↗
PubMed1994

Effect of age on L-3,5,3'-triiodothyronine-induced ethane exhalation.

The effect of age on thyroid hormone-induced lipid peroxidation in rats was determined by measuring ethane exhalation (EE) rate. The mean basal EE rates (in pmol.min-1 x 100 g-1) at room air in 25-mo-old aged rats [3.07 +/- 0.26 (SE)] and in intermediate age (18-mo-old) rats (3.42 +/- 0.18) were significantly lower than that in young (3- to 5-mo-old) rats (4.44 +/- 0.27) (P < 0.01). After 8 days of L-3,5,3'-triiodothyronine (T3) administration, EE rates in aged rats (4.10 +/- 0.25) and in intermediate-age rats (4.16 +/- 0.35) were significantly lower than that in young rats (5.61 +/- 0.36) (P < 0.01). T3-treated young rats pair-fed with aged rats for 2 wk had EE rates (5.53 +/- 0.18) comparable to ad libitum-fed young rats, although the basal rate of EE was significantly reduced with partial food restriction (4.44 +/- 0.27 vs. 3.50 +/- 0.24) (P < 0.01). These observations indicate that reduced food intake with age cannot account for the age-related changes in T3-stimulated peroxidation rate of lipids.

Aging↗
PubMed1993

Vitamin A pretreatment and bleomycin induced rat lung injury.

Possible antioxidant effects of pretreatment with vitamin A on bleomycin-induced rat lung injury were studied. Intratracheal bleomycin was administered to rats pretreated with vitamin A (50,000 IU/day) or vehicle control. Analysis of bronchoalveolar lavage fluid (BAL) total and differential cell counts, lung weight, lung pathology, and alveolar macrophage superoxide anion production were performed before and at various time points after the instillation of bleomycin. Bleomycin with vehicle raised total BAL cell count and the per cent of BAL neutrophils at day 7 post injury. The percent of lung involved with pneumonitis, the lung wet weight/body weight ratio and the alveolar macrophage superoxide anion production were also increased after bleomycin alone compared to the group pretreated with vitamin A. Rats pretreated with vitamin A demonstrated a statistically significant reduction in total BAL cell count and in alveolar macrophage superoxide anion production 7 days after bleomycin compared with vehicle control. Lung wet weight/body weight ratio 7 days after bleomycin was reduced in the vitamin A treated rats. There was a trend to less pneumonitis in the vitamin A pretreated group. These data suggest that vitamin A attenuates bleomycin induced pulmonary damage by a mechanism which involves inhibition of bleomycin-induced alveolar macrophage superoxide anion production.

Animals↗
PubMed1991

Expiratory computed tomography for assessment of suspected pulmonary emphysema.

Results of computed tomography of the lung performed at two levels in upper lung zones at full inspiration and full expiration were compared with results of tests of ventilatory function, lung mechanics, and single breath carbon monoxide diffusing capacity in 64 subjects, many of whom had some form of airflow obstruction. From the CT scans, the mean percentage of pixels in the range -900 to -1,024 Hounsfield units, or pixel index, was determined for each subject. The highest correlations of pixel index with physiologic variables consistent with a diagnosis of emphysema were observed for CT taken at full expiration. In some subjects, the inspiratory CT would give a "false positive" for emphysema when the hyperaeration observed at inspiration was not observed at expiration. We believe that the CT scan taken at full expiration can effectively reveal the abnormal permanent enlargement of airspaces which defines emphysema and provides a noninvasive method of assessing lung morphology in the living human subject.

Adult↗
PubMed1990

Ethane production rate in vivo is reduced with dietary restriction.

Dietary restriction without malnutrition prolongs life and has a beneficial effect on age-related diseases and metabolic derangements. To test the effect of food restriction on ethane production rate, ethane exhalation was measured in rats with partial food restriction. Ethane production rate in room air in rats fed 60% of food consumed by ad libitum-fed animals for 2 wk was significantly reduced (3.50 +/- 0.25 vs. 5.21 +/- 0.34 pmol.min-1.100 g body wt-1, P less than 0.01). In 100% oxygen, ethane production in food-restricted rats was not different from that of ad libitum-fed rats (21.81 +/- 1.25 vs. 19.57 +/- 1.89 pmol.min-1.100 g-1). Fifteen hours of fasting compared with ad libitum feeding reduced ethane production modestly in room air (4.37 +/- 0.45 vs. 5.21 +/- 0.34 pmol.min-1.100 g-1) and more significantly in 100% oxygen (12.37 +/- 0.78 vs. 19.57 +/- 1.89 pmol.min-1.100 g-1). Thus, in 100% oxygen, 15 h of fasting, compared with ad libitum feeding, resulted in an approximately 40% decrease in ethane production rate. It is concluded that short-term food restriction significantly reduces ethane exhalation rate in rats when measured in room air.

Animals↗
PubMed1990

Ethane production in copper-deficient rats.

Evidence is accumulating which indicates that copper-deficient animals are prone to oxidative damage. To investigate this possibility further, we measured the production of breath ethane, a hydrocarbon by-product of lipid peroxidation, in copper-deficient rats. Male, weanling Sprague-Dawley rats were fed either a purified diet which was deficient in copper (CuD) or the same diet made sufficient with 5 ppm of copper (CuS). After 33 to 34 days the rats were placed individually in gastight metabolic cages through which ethane-free air or 100% O2 was passed. Expired ethane was absorbed onto cold, activated charcoal, liberated by heating, and measured by gas chromatography. Ethane production rates (pmoles/min/100 g +/- SD) were 3.3 +/- 0.8 (CuS-air), 4.3 +/- 1.4 (CuD-air), 8.3 +/- 2.5 (CuS-O2), and 12.2 +/- 4.3 (CuD-O2). Repeated measures analysis of variance indicated that both copper deficiency (P less than 0.01) and breathing 100% O2 (P less than 0.0001) enhanced ethane production, with no interaction between treatments. This finding complements previous evidence that increased lipid peroxidation occurs in copper-deficient rats.

Animals↗
PubMed1989

Ethane production rates and minute ventilation.

Ethane quantitated in the expired alveolar gas is a noninvasive measure of free radical activity. This method has been criticized for lack of control of minute ventilation (VE) in spontaneously breathing animals, although ethane, which is poorly soluble in tissues, should not be affected by changes in VE. We measured ethane elimination rates in six strain 13 guinea pigs (GP13) during spontaneous room air breathing and in six room air breathing, pentobarbital-anesthetized, tracheostomized, externally warmed, mechanically ventilated GP13s at various levels of VE. In the ventilated animals, weight0.75/VE (metabolic activity corrected for VE) was a linear function of arterial CO2 tension (PaCO2) drawn from arterial line (r = 0.72, P less than 0.005). However, weight0.75/VE did not correlate with ethane elimination rates (r = 0.12, not significant). The mean (+/- SD) ethane elimination rates in the spontaneously breathing animals was 3.15 +/- 0.96 pmol.min-1.100 g-1 and was not significantly different from the mean rate in the mechanically ventilated animals (3.11 +/- 1.37) over a range of VE's. These data demonstrate that ethane elimination rates are not affected by changes in VE and are unaffected by pentobarbital anesthesia.

Animals↗
PubMed1989

Source of ethane in expirate of rats ventilated with 100% oxygen.

Ethane in alveolar expirate may have its source in organs other than the lung and be transported to the lung for elimination. We determined ethane production rates in rats (group I) ventilated with hydrocarbon-free air (HFA) before and after exsanguination. To determine whether the lung is the source of increased ethane production during exposure to 100% O2, we measured ethane in the expirate of nine exsanguinated, Sprague-Dawley rats (group II) mechanically ventilated with HFA and then with 100% O2. In all nine animals, ethane elimination rates on 100% O2 increased compared with HFA values. In five of the nine rats, HFA ventilation was reinstated after O2 (group III). In all five, ethane elimination fell with HFA ventilation compared with the value on 100%. Six rats with circulation intact were ventilated with HFA and then 100% O2 (group IV). Ethane production rate for group IV animals breathing HFA was not significantly different from the exsanguinated animals in group II while ventilated with HFA. The mean increase in ethane production for the group II animals was not significantly different from the group IV animals. Lung slices from four other rats (group V) were incubated in saline at 37 degrees C with FeCl2 (10 mg) added to enhance free radical formation. Paired lung samples from the same rat were incubated with either HFA or 100% O2. Headspace gas was analyzed chromatographically for ethane at 120 min. Mean ethane in the O2 samples was higher than for HFA. Rat lung tissue is the main source of increased ethane production during 100% O2 exposure.

Animals↗
PubMed1988

Immunoglobulin E anaphylaxis in rabbits: mechanisms of pulmonary resistance and compliance changes.

Factors causing changes in pulmonary resistance and dynamic compliance with immunoglobulin (Ig) E anaphylaxis in spontaneously breathing rabbits were assessed in ventilated rabbits using tantalum bronchography and wet-to-dry wt ratios. Ventilated rabbits demonstrated changes in resistance and compliance similar to spontaneously breathing rabbits. Chlorpheniramine pretreatment prevented increases in resistance but not decreases in compliance. Anaphylaxis constricted small (less than 1 mm) airways 20.9 +/- 16.0% (mean +/- SD) and intermediate (between 1 and 3 mm) airways 21.8 +/- 19.8%. Chlorpheniramine (10 mg/kg) prevented small airway changes and attenuated those in intermediate airways. Chlorpheniramine prevented histamine-induced constriction of small (23.6 +/- 15.7%) and intermediate (17.6 +/- 15.0%) airways. Lung wet-to-dry wt ratios were unchanged. Changes in resistance and compliance during rabbit IgE anaphylaxis are not due to changes in tidal volume or frequency. Histamine, via H1 receptors, is the principal mediator of pulmonary resistance increases but not dynamic compliance reductions. Chlorpheniramine-sensitive increases in resistance are caused by constrictions of intermediate and small airways, whereas the chlorpheniramine-resistant decrease in compliance is not caused directly by constriction of the smallest measurable airways (0.25 mm) or changes in lung water.

Airway Resistance↗
PubMed1988

Ethane production rate in rats exposed to high oxygen concentration.

Production rates for ethane gas, a hydrocarbon byproduct of lipid peroxidation, measured from the ethane present in the exhaled breath of rats, were used to determine changes in oxygen-free radical activity. Rates of ethane production were measured in rats housed in metabolic chambers and exposed to room air and to high oxygen concentrations. Expired ethane, adsorbed onto activated charcoal and then liberated by heating, was measured by gas chromatography. Ethane production rates in groups of 8 rats increased during 8 h of 100% oxygen exposure from a mean (+/- SE) room air value of 11.30 +/- 1.15 to 27.85 +/- 2.93 pmol/min/100 g rat (p less than 0.005). The mean (+/- SE) percent increases in ethane production after exposure to 100% oxygen in 8 rats pretreated with 0.1 mg/100 g of vitamin E in corn oil vehicle (0.1 ml/100 g) injected intraperitoneally and in a group of 5 rats injected with vehicle alone averaged 157.16 +/- 37.83% and 150.98 +/- 25.19%, respectively. The percent changes noted were not significantly different as measured by analysis of variance. These data indicate that lipid peroxidative activity, hence oxygen-free radical activity, increases in normally fed rats exposed to hyperoxia at a time prior to the previously reported neutrophil influx into the lungs of similarly exposed rats and that it is not attenuated by pretreatment with vitamin E.

Analysis of Variance↗
PubMed1988

Pressure support compensation for inspiratory work due to endotracheal tubes and demand continuous positive airway pressure.

We evaluated the use of pressure support to compensate for the added inspiratory work of breathing due to the resistances of endotracheal tubes and a ventilator demand-valve system for continuous positive airway pressure (CPAP). A mechanical model was used to simulate spontaneous breathing at five respiratory rates through 7-mm, 8-mm, and 9-mm endotracheal tubes with and without a ventilator demand CPAP circuit. Added work was measured as the integral of the product of airway pressure and volume during inspiration. Additional work was a function of the tube's size, and each 1-mm decrease in the tube's diameter resulted in a 67 to 100 percent increase in work. Adding the ventilator CPAP circuit further increased work and was responsible for 30 to 50 percent of the total work resulting from a tube and CPAP circuit together. Pressure support was added to a level at which net work on the airway was zero, and a relationship between mean inspiratory flow (VT/TI) and the optimal level of pressure support was established for each endotracheal tube. The inspiratory work of breathing was then measured in normal subjects breathing with and without each endotracheal tube plus the demand CPAP circuit. Work per liter of minute ventilation due to the endotracheal tube and CPAP circuit was increased from 54 to 240 percent over levels measured while breathing through an open airway. For each endotracheal tube and VT/TI, a level of pressure support (range, 2 to 20 cm H2O) was found which eliminated added work in the spontaneously breathing subject. This level correlated well with that predicted from the data derived using the mechanical model. We conclude that when adjusting for an endotracheal tube's diameter and VT/TI, pressure support can be used to compensate for the added inspiratory work due to artificial airway resistances.

Airway Resistance↗