PubMed Health⌕ Search

Biomedical subjects

H Sahebjami

Publications and source records attributed to H Sahebjami.

At least 19 recordsLinked to original sources
PubMed2000

Influence of body weight on the severity of dyspnea in chronic obstructive pulmonary disease.

A substantial number of patients with COPD are underweight (UW); they comprise the clinical subtype of "dyspneic" or emphysematous. To determine whether these patients are more dyspneic than normal weight (NW) patients with COPD, we quantitated the severity of dyspnea, using a modified Medical Research Council (MRC) dyspnea scale, in 33 UW and 57 NW patients and compared their pulmonary function tests (PFTs), arterial blood gases (ABGs), and respiratory muscle strength as estimated by maximum static inspiratory (PI(max)) and expiratory (PE(max)) mouth pressures (all as means +/- SEM). Body mass index was 18.7 +/- 1.2 and 24.5 +/- 1.8 kg/m(2) in UW and NW patients, respectively (p < 0.0001). The MRC dyspnea scale was 3. 1 +/- 0.9 in UW and 2.5 +/- 1.2 in NW groups (p = 0.035). All PFT and ABG parameters were similar in the two groups except for DCO (36 +/- 11% in UW and 57 +/- 17% in NW, p < 0.001) and PI(max) (55 +/- 18 mm Hg in UW and 66 +/- 19 mm Hg in NW, p = 0.020). In a stepwise multiple regression model, %DCO and %MVV combined were the best predictors of dyspnea severity (R(2) = 0.30, p = 0.001). We conclude that UW patients with COPD are more dyspneic than NW patients. Although the origin of dyspnea in COPD is multifactorial, changes in DCO and respiratory muscle strength may contribute to its intensity.

Aged↗
PubMed1998

Dyspnea in obese healthy men.

STUDY OBJECTIVES: To determine whether obese, apparently healthy individuals experience dyspnea at rest and, if so, whether their pulmonary function test (PFT) profile and maximal respiratory pressures are different from obese, healthy subjects without dyspnea. DESIGN: Prospective, open. SETTING: Pulmonary function test laboratory, Veterans Administration Medical Center. PATIENTS: Twenty-three obese male subjects (each with a body mass index [BMI] of > 28 kg/m2) with an FEV1 level and an FEV1/FVC ratio > or = 80% of predicted and no coexisting conditions. Fifteen complained of dyspnea, where eight denied having it, at rest. MEASUREMENTS AND RESULTS: Standard PFT parameters and maximum static inspiratory (P(Imax)) and expiratory (P(Emax)) mouth pressures were determined. Subjects with dyspnea had similar age and height but larger body weight (113.9+/-5.0 vs 97.4+/-2.6 kg, p = 0.03) and BMI (37.4+/-1.6 vs 31.8+/-0.7 kg/m2, p = 0.02) than subjects without dyspnea, and a greater number of them were current or previous smokers. Forced expiratory flow at 75% vital capacity (54.9+/-6 vs 75.5+/-7% predicted, p = 0.05), maximum voluntary ventilation (MVV; 90.2+/-3.8 vs 107.8+/-9.3% predicted, p = 0.05), and P(Emax) (77+/-2 vs 97.8% predicted, p = 0.007) were significantly reduced in the group of subjects with dyspnea. Large airway function (FVC, FEV1, and FEV1/FVC ratio), lung volumes, and gas exchange parameters were similar between the two groups. CONCLUSIONS: Some obese, but otherwise healthy, individuals experience dyspnea at rest. Reduced P(Emax) and MVV combined with greater body mass and peripheral airway disease are most likely responsible for the sensation of dyspnea in these individuals.

Dyspnea↗
PubMed1996

Pulmonary function in obese subjects with a normal FEV1/FVC ratio.

STUDY OBJECTIVE: To determine pulmonary function test (PFT) profile and respiratory muscle strength (RMS) of a group of obese individuals who did not have evidence of obstructive airway disease or other underlying diseases affecting their respiratory system. DESIGN: Prospective, open. SETTING: PFT laboratory, VA Medical Center. PARTICIPANTS: Sixty-three consecutive obese (body mass index greater than 27.8 kg/m2) male subjects without overt obstructive airway disease (FEV1/FVC ratio greater than 80%). MEASUREMENTS AND RESULTS: Standard PFTs and maximum static inspiratory (PImax) and expiratory (PEmax) mouth pressures were determined. RMS was calculated from the following formula: (PImax+PEmax):2. Two distinct groups were identified, those with normal maximum voluntary ventilation (MVV) (> 80% predicted) and those with low MVV. Both inspiratory and expiratory flow rates (FVC, FEV1, forced expiratory flow at 50% vital capacity [V50], maximum inspiratory flow rate [MIFR]), lung volumes (vital capacity [VC], inspiratory capacity [IC], expiratory reserve volume), PImax, and RMS were significantly lower, and residual volume/total lung capacity (RV/TLC) ratio was significantly higher in obese subjects with low MVV compared with those in whom MVV was normal. MVV correlated significantly with FVC, FEV1, V50, MIFR, TLC, VC, IC, RV/TLC, and RMS; the strongest correlation was with MIFR (r = 0.76, p < 0.0001). CONCLUSIONS: Standard PFTs allow recognition of a subgroup of obese subjects without overt obstructive airway disease who have more severe lung dysfunction, the marker of which is a low MVV. Peripheral airway abnormalities may be responsible for these observations.

Adult↗
PubMed1994

Hemodynamic and oxygen transport characteristics of common ventilatory modes.

We studied hemodynamic and oxygen transport parameters in 12 stable critically ill patients on assist control (ACV), synchronized intermittent mandatory (SIMV), and pressure support (PSV) ventilatory modes. Patients were optimally ventilated on ACV, were awake, and capable of spontaneous breathing. After baseline measurements on ACV, patients were placed on SIMV and PSV for 30 min each and measurements were repeated at the end of each period. The SIMV rate (f) was 75 percent of the rate on ACV. The PSV was set at a level enough to maintain a tidal volume (VT) equal to that on ACV. The FIo2 was kept constant on all three modes. Patients on SIMV and PSV maintained similar minute ventilation as when on ACV but with significantly lower peak and mean inspiratory pressures than on ACV. However, f increased and VT decreased significantly on SIMV. Hemodynamic and oxygen transport parameters were not significantly different among the three groups, although there was a tendency toward higher cardiac index, oxygen transport, and oxygen consumption on SIMV and PSV. We conclude that in stable critically ill patients, SIMV and PSV used according to our study protocol for 30 min can provide adequate ventilation with lower airway pressure and possibly less adverse effects on hemodynamic and tissue oxygenation parameters compared with ACV. Because of a significant decrease in VT and an increase in f seen with SIMV, PSV may be a more desirable mode for ventilatory support.

Critical Care↗
PubMed1992

Effects of repeated cycles of starvation and refeeding on lungs of growing rats.

Adult male rats were subjected to four cycles of mild starvation (2 wk) and refeeding (1 wk) and were compared with a fed group. Starvation was induced by giving rats one-third of their measured daily food consumption. During each starvation cycle, rats lost approximately 20% of their body weight. Despite catch-up growth and overall weight gain, starved rats had lower final body weight than fed rats. Lung dry weight and lung volumes were also reduced in the starved group. The mechanical properties of air- and saline-filled lungs did not change significantly with repeated cycles of starvation. Mean linear intercept was similar in the two groups, but alveolar surface area was reduced in the starved rats. Total content of crude connective tissue and concentration per lung dry weight of hydroxyproline and crude connective tissue were reduced in starved rats. We conclude that lung growth is retarded in growing rats subjected to repeated cycles of mild starvation and refeeding, as manifested by smaller lung volume and reduced alveolar surface area. Because alveolar size is unchanged, a reduced number of alveoli is most likely responsible for decreased lung volumes.

Animals↗
PubMed1989

Effects of starvation and refeeding on elastase-induced emphysema.

Adult rats received pancreatic elastase (75 U/100 g) intratracheally and were divided into three groups: fed, starved, and refed. Starved rats received one-third of their measured daily food consumption until they lost 40% body weight. The refed group was fed after 40% weight loss. A control group received saline intratracheally. Saline volume-pressure curve was shifted more significantly to the left of the control group in starved than in fed rats and was superimposed in refed and fed groups. Mean linear intercept was larger and alveolar surface area was smaller in starved than in fed rats compared with the control group; both were similar in fed and refed rats. Protein and hydroxyproline content of the lung were higher in fed than in control and in starved groups; after refeeding these returned to the control values. We conclude that starvation aggravates elastase-induced injury and that refeeding results in the complete recovery of the mechanical but only partial recovery of the morphometric changes induced by starvation.

Animals↗
PubMed1989

Effects of postnatal dexamethasone treatment on development of alveoli in adult rats.

We compared the effects of dexamethasone given to rats from age 4 to 14 days, on alveolar development at age 99 days. Judged by similar nose-to-tail length and body weight, somatic growth was not altered by dexamethasone treatment. Lung volumes in both air- and saline-filled lungs and mean chord length (Lm) were increased, whereas alveolar surface area (Sa) and surface-to-volume ratio (S/V) were diminished in dexamethasone-treated adult rats. These changes were associated with a significant reduction in DNA content and concentration but larger protein/DNA and RNA/DNA ratios in the lungs of treated rats. We conclude that dexamethasone treatment during the critical period of septation in rats impairs alveolar formation, which persists until adulthood and leads to larger and less complex gas-exchange regions. Inhibition of DNA synthesis due to dexamethasone may be responsible for its effects on alveolar development. Larger lung volumes in treated rats are, most likely, related to larger air space dimensions.

Animals↗
PubMed1988

Effects of streptozotocin-induced diabetes on lung mechanics and biochemistry in rats.

Young and adult rats were given a single intraperitoneal injection of 75 mg/kg streptozotocin in citrate buffer and were compared with age- and weight-matched controls that received an equal volume of buffer alone. Studies done 8 wk after the injections showed that final body weight, lung dry weight, lung DNA content, and air and saline lung volumes were significantly lower in both young and adult diabetic rats compared with the controls. In young diabetic rats, volume-pressure (V-P) curves expressed as percent maximal lung volume (%MLV) were shifted downward and to the right of those in young control rats at 5 cmH2O transpulmonary pressure (PL) for air and at 4, 6, and 8 cmH2O PL for saline-filled lungs; specific lung compliance (CL) values obtained from both air and saline V-P curves were significantly reduced, and concentration of hydroxyproline relative to DNA was significantly increased. In adult diabetic rats, V-P curves expressed in %MLV, CL values, and concentrations of protein and hydroxyproline were similar to those in adult control rats. We conclude that in both young and adult rats, diabetic state leads to somatic and lung growth retardation. In addition in young diabetic rats lung distensibility is decreased. An increase in the concentration of some connective tissue proteins may be responsible for the latter observation.

Animals↗
PubMed1987

Lung mechanics and connective tissue proteins in diabetic Bio-Breeding/Worcester Wistar rats.

We studied lungs of spontaneously diabetic Bio-Breeding/Worcester (BB/W) Wistar rats which resemble human insulin-dependent diabetes mellitus. Compared with the age-matched control group, the body weight of the diabetic rats tended to be smaller and lung wet and dry weight were similar, but lung dry weight, relative to body weight and to lung wet weight, was significantly larger. Both air and saline lung volumes were reduced in the diabetic rats, and volume-pressure (V-P) curves expressed as a percent of maximal lung volume were significantly shifted downward and to the right of those in the control group over the midportion. Total DNA and RNA contents were similar in both groups, whereas protein content and concentration and protein/DNA and RNA/DNA ratios were significantly reduced in the diabetic rats. In contrast, content and concentration of 4-hydroxy-L-proline, elastin, and crude connective tissue were significantly higher in the diabetic group. We conclude that the increase in connective tissue proteins in the BB/W rats is most likely responsible for the shift in the V-P curves.

Animals↗
PubMed1986

Nutrition and the pulmonary parenchyma.

Fasting and starvation affect various aspects of lung structure and function in experimental animals. Short-term food deprivation influences lung metabolism and biochemistry; prolonged partial food restriction affects lung structure and mechanics as well. This article provides a historical review of the topic and summarizes data obtained in humans and animals.

Adolescent↗
PubMed1986

Effects of postnatal starvation and refeeding on rat lungs during adulthood.

Rats approximately 3 wk of age were given one half of their measured daily food consumption for 4 to 5 wk until they lost approximately 25% of their initial body weight (starved group) and were compared with an age-matched fed group 20 wk after the beginning of the study. Final body weight and nose-to-tail length were significantly lower in the starved group, whereas dry and wet weights of the lung were similar in both groups. The maximal and minimal lung volumes and specific lung compliance in air- and saline-filled lungs were similar in both groups, but in starved rats the volume-pressure curve was shifted significantly downward and to the right of that of the fed group at 70 and 60% maximal lung volume with air and at 90% maximal lung volume with saline. Total lung content of protein, DNA, RNA, hydroxyproline, and elastin were similar in fed and starved groups. It appears that moderate weight loss during the postnatal period leads to somatic growth retardation but to insignificant changes in the lungs of adult rats.

Age Factors↗
PubMed1985

Effects of starvation on lung mechanics and biochemistry in young and old rats.

Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.

Age Factors↗
PubMed1984

Serial studies of pulmonary function in continuous ambulatory peritoneal dialysis. A prospective study.

Continuous ambulatory peritoneal dialysis (CAPD) produces a nearly continuous state of iatrogenic ascites which may interfere with respiratory excursions of the diaphragm and compromise ventilatory function. Sitting and supine studies of pulmonary function and arterial blood gas analyses done serially in 13 patients undergoing CAPD showed a significant decline in pulmonary volumes immediately after the institution of CAPD; however, the decline was not accompanied by abnormalities in gas transfer. Pulmonary volumes returned to baseline values within two weeks in all patients, including those with preexisting mild chronic obstructive pulmonary disease (COPD). It is concluded that CAPD does not compromise pulmonary function in patients with normal pulmonary function or in those with mild COPD.

Adult↗