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Biomedical subjects

J Ali

Publications and source records attributed to J Ali.

At least 109 records · Page 6Linked to original sources
PubMed1986

Changes in human milk vitamin E and total lipids during the first twelve days of lactation.

Our previous study showed vitamin E deficiency in newborns (69.7%) and mothers at term (85.9%) when the ratio between serum vitamin E in mg/dl and total lipids in g/dl was used as an indicator of vitamin E status. This study was conducted to determine the human milk content of vitamin E. During the first 12 days of lactation milk vitamin E levels remained almost constant (day 1, 0.68 mg/dl; day 12, 0.65 mg/dl), milk total lipid levels increased daily (day 1, 1.11 g/dl; day 12, 3.60 g/dl), and the ratio between milk vitamin E and total lipids dropped steadily (day 1, 1.3; day 12, 0.2). In spite of this drop in vitamin E status, it is unlikely that vitamin E availability will be affected in neonates, because normal neonates absorb milk fats well and this ability increases with age.

Computers↗
PubMed1986

Factors affecting perfusion distribution in canine oleic acid pulmonary edema.

Factors affecting perfusion distribution in oleic acid pulmonary edema were examined in 28 anesthetized open-chest dogs. Sixteen had unilobar oleic acid edema produced by left lower lobe pulmonary artery infusion of 0.03 ml/kg of oleic acid, and 12 had the same amount of edema produced by left lower lobe endobronchial instillation of hypotonic plasma. Lobar perfusion (determined from flow probes) and lobar shunt (determined from mixed venous and lobar venous blood) were measured at base line, 1.5 h after edema, and 10 min after 10 cmH2O positive end-expiratory pressure (PEEP). Fourteen dogs (8 oleic acid, 6 plasma) received sodium nitroprusside (11.72 +/- 7.10 micrograms X kg-1 X min-1). Total and lobar shunts increased to the same extent in all animals. Lobar perfusion decreased by 49.8 +/- 4.8% without nitroprusside and 34.0 +/- 3.6% with nitroprusside in the oleic acid group, corresponding values being 40.3 +/- 0.8% and 26.4 +/- 1.7% in the hypotonic plasma group. PEEP returned perfusion and shunt to base line. In oleic acid edema, most of the decreased perfusion results from mechanical effects of the edema, a smaller fraction results from other vascular effects of the oleic acid, and approximately 30% is reversible by nitroprusside. PEEP normalizes the perfusion distribution.

Animals↗
PubMed1985

Lethality in mice and rats exposed to 2450 MHz circularly polarized microwaves as a function of exposure duration and environmental factors.

Adult male CD-1 mice and CD rats were used to determine LD50/24 h lethality rates from exposure to 2450-MHz circularly polarized microwaves. Groups of 16 mice or six rats were exposed in each of 32 combinations of nominal power density (10, 25, 50 or 75 mW cm-2), exposure duration (1 or 4 h), and environmental temperature (20 or 30 degrees C) and relative humidity (35 or 80%). An analysis of variance probit model was used to determine the influence each variable had on the probability of death. Significant factors in lethality were nominal power density, exposure duration and environmental temperature, but not environmental relative humidity. The estimated power density (mW cm-2) required to kill 50% of the animals in 24 h is halved when the environmental temperature is increased from 20 to 30 degrees C. Similarly, only 20-25% of the power density is required when the exposure duration is increased from 1 to 4 h. The use of nominal power density as a predictor of the probability of death was more efficient than specific absorption rate estimated experimentally by twin-well calorimetry. The exposure of one mouse at a time, instead of 16, did not alter the predicted death rate.

Animals↗
PubMed1985

The acute effects of intralipid on lung function.

To determine whether the oleic acid contained in intralipid injures the lung, we measured fractional lobar perfusion, lobar shunt, and edema (wet to dry weight ratios, W/D) in 20 open-chested mechanically ventilated dogs. Five dogs received oleic acid 0.03 g/kg injected into a lower lobe pulmonary artery. Ten received 0.5 cc/kg of 20% intralipid which contains the equivalent amount of oleic acid, five of these animals being heparinized. The same dose of oleic acid was also suspended in intralipid and administered to five heparinized dogs. Shunt and edema were measured in another five heparinized closed-chested dogs receiving 2 g/kg of intralipid IV over 1 hr. Half hour after intralipid or oleic acid, shunts did not change. At 2 1/2 hr, oleic acid alone increased lobar shunt from 4.6 +/- 1.4 to 40.8 +/- 24.9% while intralipid shunt remained unchanged with and without heparin. Lobar perfusion fell significantly with oleic acid from 29.3 +/- 2.3 to 17.8 +/- 5.6% while showing no change in the lobes not receiving oleic acid. When oleic acid was suspended in intralipid, shunt and perfusion changed less than with oleic acid alone. Mean W/D of the oleic acid lower lobe exceeded (P less than 0.05) W/D of the other lobes, including the lobe receiving oleic acid suspended in intralipid which had a W/D greater than the lobes receiving intralipid only. We conclude that intralipid has no acute deleterious effects on pulmonary gas exchange, blood flow distribution, or edema. Our data suggest that intralipid may protect the lung from the deleterious effects of fatty acids.

Animals↗
PubMed1984

High-frequency ventilation in lung edema: effects on gas exchange and perfusion.

In six open-chest dogs, unilobar pulmonary edema was induced by injection of oleic acid into a lower lobe pulmonary arterial branch. Two hours later, intermittent positive-pressure ventilation (IPPV) and high-frequency oscillatory ventilation (HFOV) at matched mean alveolar pressures (MAP) were compared at 30-min intervals. The edematous lobar venous admixture (Qva/QT) increased by 0.14 (P less than 0.1) and its relative perfusion (QL/QT) decreased by 0.03. (P less than 0.1) during HFOV compared with IPPV. In another six dogs the MAP was increased by 1.5 cmH2O during HFOV; now the edematous lobar Qva/QT decreased by 0.15 (P less than 0.03) and QL/QT increased by 0.03 (P less than 0.03) during HFOV compared with IPPV. Greater MAP during HFOV also improved the edematous lobar ventilation (lobar venous PCO2) during HFOV compared with IPPV. Conceivably, the increase in MAP inflated collapsed, flooded regions, and thereby increased their O2 transfer, perfusion, and ventilation. Whole-lung Qva/QT was similar during IPPV and HFOV in both groups because of the opposing effects of lobar Qva/QT and QL/QT. We conclude that HFOV supports cardiovascular-respiratory function in open-chest unilobar pulmonary edema compared with IPPV at similar MAP; gas exchange and perfusion of edematous units may be sensitive to small changes in MAP, and we detected no intrinsic effects of HFOV on these variables. We speculate that similar beneficial effects in diffuse pulmonary edema may be effected by small variations in MAP during HFOV without the barotrauma side effects sometimes observed when MAP is increased during IPPV.

Animals↗
PubMed1984

Pulmonary vascular effects of furosemide on gas exchange in pulmonary edema.

To test the hypothesis that pulmonary vasoactivity of furosemide redistributes blood away from edematous lung, thus improving gas exchange, we studied two groups of 10 dogs each with unilobar oleic acid edema, treating one group with 1 mg/kg furosemide 2 h after the oleic acid. Pulmonary perfusion distribution was determined with radio microspheres. Shunts of the injured lobe, measured from O2 contents of lower lobar pulmonary venous blood, increased significantly (P less than 0.05) at 2 h after injury in both groups. Within 0.5 h after furosemide the lobar shunt decreased in the treated animals from 40.1 +/- 20.6 to 28.6 +/- 20.1% and increased from 21.4 +/- 14.0 to 53.8 +/- 26.9% in the control group (P less than 0.05). Mean fractional lobar perfusion to the injured lobe increased from 18.2 +/- 4.8 to 21.6 +/- 6.4% (P less than 0.05) in the furosemide group but decreased from 20.1 +/- 3.5 to 16.1 +/- 4.4% (P less than 0.05) in the controls. Wet lung-to-body weight ratios of the edematous lobes did not differ between the two groups. Our data suggest the possibility that, before decreasing edema, furosemide improved shunt through pulmonary vascular effects by preferential perfusion of nonflooded alveolar units.

Animals↗
PubMed1984

How does positive end-expiratory pressure reduce intrapulmonary shunt in canine pulmonary edema?

We ventilated separately the right and left lungs of seven dogs having thoracotomies and catheters in both lower lobe veins. Two hours after right atrial injection of oleic acid, shunt (Qs/QT) in each lower lobe increased from 0.10 to 0.47. Ten minutes after positive end-expiratory pressure (PEEP) was increased from 3 to 13 cmH2O in one lung, mean lobar Qs/QT decreased to 0.06 with no change in its fraction of pulmonary blood flow measured by microsphere techniques. At the same time mean Qs/QT in the other lower lobe was 0.48. At end expiration each lower lobe hilum was then clamped, and the excised lobe was quickly frozen over liquid N2. There was no difference in the extravascular lung liquid per gram blood-free dry lobe between the lower lobes (7.5 +/- 2.6 ml/g), but perivascular cuff liquid was greater in the lower lobe with PEEP (3.8 +/- 2.8 ml/g) than in the lower lobes without PEEP (2.4 +/- 1.7 ml/g). Light microscopy revealed that 77.8 +/- 9.0% of the alveoli were flooded in the lobe without PEEP, but only 22.2 +/- 11.8% were flooded in the lobe with PEEP. The mean linear intercepts of the flooded alveoli were not different between lower lobes, and both were reduced to about 50% of the size of adjacent unflooded units in the same lobe. Alveolar septum thickness was greater without PEEP. We conclude that PEEP reduces Qs/QT by inflating previously flooded and collapsed air spaces and by redistributing the excess alveolar water into the compliant perivascular space, thus eliminating the obstacle to pulmonary O2 transfer.

Animals↗
PubMed1984

Effect of postoperative intermittent positive pressure breathing on lung function.

Thirty patients undergoing elective cholecystectomy were randomly assigned to two groups. Fifteen patients received postoperative intermittent positive pressure breathing (IPPB) for four days together with physiotherapy while the other 15 had the same postoperative care but without IPPB. Vital capacity (VC), functional residual capacity (FRC) and PO2 were measured preoperatively and on days 0, 1, 3, and 5 postoperatively. The incidence of postoperative pulmonary complications utilizing chest x-ray films, sputum analysis, temperature, and clinical assessment was determined. Both groups had significant deterioration in pulmonary function but did not differ except for a greater depression in VC in the IPPB group (p less than .05). In patients receiving postoperative physiotherapy, the addition of IPPB did not usually result in improved pulmonary function.

Adult↗
PubMed1983

The effect of lung edema on pulmonary vasoactivity of furosemide.

Previous data suggest that furosemide improves gas exchange in pulmonary edema by preferential perfusion of nonedematous lung units. To test whether this is a direct effect of furosemide on the pulmonary vasculature as opposed to a secondary phenomenon resulting from the known peripheral effects of this drug, the effect of furosemide on the pressure-flow characteristics of the pulmonary vasculature was studied in six isolated perfused canine lungs with different degrees of gravimetrically determined edema. Furosemide shifted the pressure-flow curve by decreasing the mean intercept or average closing pressure of the pulmonary vascular bed from 13.8 +/- 5.3 to 9.5 +/- 5.4 cm H2O and the zero-flow critical closing pressure from 9.3 +/- 4.3 to 4.7 +/- 3.5 cm H2O (P less than 0.05). The slopes of these curves did not change between control and furosemide treatment. The decrease in intercept and the decrease in zero-flow critical closing pressures were closely correlated with the increase in edema (r = 0.895 for average closing pressure and r = -0.928 for critical closing pressure) (P less than 0.05). Furosemide doubled the pulmonary blood flow in the isolated lobe for the same driving pressure and the greater the amount of lobar edema the less pronounced was this furosemide-associated increase in blood flow. This direct effect of furosemide on the pulmonary vasculature could explain the improved gas exchange seen before a decrease in pulmonary edema, since this pulmonary vasoactivity would result in preferential perfusion of nonflooded alveolar units.

Animals↗
PubMed1983

Does increased pulmonary blood flow redistribute towards edematous lung units?

Unilobar pulmonary edema secondary to increased capillary permeability was produced utilizing oleic acid infusion into the left lower lobe pulmonary artery of seven dogs. This model was used to determine whether random changes in cardiac output produced by opening and closing arteriovenous fistulae were associated with changes in fractional perfusion to the edematous lobe (as determined by differentially labeled radiomicrospheres) thus explaining changes in intrapulmonary shunt. With an increase in cardiac output from a mean (+/- SD) of 1.6 +/- 0.5 liters/min to 2.6 +/- 0.8 liters/min (P less than 0.01), mean (+/- SD) injured lobar shunt as measured from O2 contents of lower lobar pulmonary venous blood and mixed venous blood increased from 54.4 +/- 3.0% to 74.4 +/- 22.1% while total intrapulmonary shunt increased from 12.0 +/- 4.0% to 16.0 +/- 3.7% (P less than 0.01). This increase in intrapulmonary shunt was, however, not associated with preferential perfusion of the edematous lobe, the mean (+/- SD) of the perfusion to the edematous lobe expressed as a percentage of the cardiac output being 16.6 +/- 1.6% at the low cardiac output and 16.9 +/- 1.4% at the high cardiac output. It is concluded that redistribution of blood flow towards the edematous lobe does not occur with increases in cardiac output and therefore does not account for the increased intrapulmonary shunt.

Animals↗
PubMed1982

How does increased cardiac output increase shunt in pulmonary edema?

In pulmonary edema, the relationship between cardiac output (QT) and shunt (QS/QT) may be due to a diffusion barrier for O2 transfer (incomplete alveolar-capillary equilibration) or to redistribution of increased pulmonary blood flow toward edematous units. We compared transfer of O2 and multiple inert gases in the left (LLL) and right (RLL) lower lobes and in the whole lungs of eight dogs having oleic acid edema in LLL. When mean QT was increased from 3.0 to 5.5 l X min-1 during O2 ventilation, relative perfusion of LLL did not increase but QS/QT increased because LLL shunt increased from 56 to 78%. We conclude that increased pulmonary blood flow is not redistributed toward edematous regions, but we cannot exclude such redistribution within LLL and other slightly edematous lobes. In LLL, inert gas shunt and O2 shunt were not systematically different during O2 ventilation, and lobar venous PO2 measured during air ventilation was not different from that predicted by inert gas transfer. We conclude that diffusion limitation for O2 does not contribute to QS/QT or to the increase in QS/QT when QT increases. Conceivably, increased QT increased QS/QT by increasing edema or hematocrit in edematous regions.

Animals↗
PubMed1981

The effect of transcutaneous electric nerve stimulation on postoperative pain and pulmonary function.

Surgery on the upper abdomen is associated with marked postoperative pulmonary dysfunction that results largely from restriction of lung expansion secondary to incisional pain. This study, utilizing three groups of patients (a control group, a sham group, and a group receiving transcutaneous electric nerve stimulation [TENS] for pain control), was designed to determine whether this modality is effective in alleviating postoperative pain. Spirometry, arterial blood gases, clinical as well as radiologic evidence of postoperative pulmonary complications, and the frequency of analgesic requests were determined. Of the 40 patients studied, the 15 receiving TENS required only 4.7 +/- 2.5 doses of narcotic analgesics in the first 72 hours as opposed to 10.1 +/- 2.7 and 10.4 +/- 2.7 in the other two groups (P less than 0.005). There were a total of six postoperative pulmonary complications, all occurring in the groups not receiving TENS. Postoperative arterial Po2, vital capacity, and functional residual capacity were least depressed in the TENS group. The data suggest that TENS minimizes the tendency toward postoperative alteration in respiratory mechanics and decreases the incidence of pulmonary complications by alleviating incisional pain.

Abdomen↗