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J M Patel

Publications and source records attributed to J M Patel.

At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of nitrogen dioxide on surface membrane fluidity and insulin receptor binding of pulmonary endothelial cells.

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is known to peroxidize membrane lipids of lung cells. We evaluated the ability of NO2 to alter the surface membrane fluidity, lipid composition, and insulin receptor binding of porcine pulmonary artery endothelial cells in culture. After 3- to 24-hr exposure to 5 ppm NO2, cells were labeled with either 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH), a cationic fluorescent aromatic hydrocarbon that anchors at the lipid-water interface, or fluorescamine, a fluorescent molecular probe that covalently binds with amino groups of surface phospholipids and proteins. Membrane fluidity was measured by monitoring changes in the steady-state fluorescence anisotropies (rs) for TMA-DPH and fluorescamine. Insulin specific receptor binding was monitored by measuring time-dependent binding of 125I-insulin. Following NO2 exposure, rs values for TMA-DPH and fluorescamine were increased significantly in a time-dependent fashion, with maximum increases at 24 hr (P less than 0.001). Similar increases in rs values were observed in isolated plasma membranes as well as in lipid vesicles prepared from total lipid extracts of endothelial cells or their plasma membranes. Phosphatidylethanolamine plus phosphatidylserine content in lipid extracts from 24-hr but not 3- to 12-hr NO2-exposed cells was increased significantly (P less than 0.01) compared to control cells. Specific binding of 125I-insulin to cells exposed to NO2 for 12 and 24 hr (but not 3 and 6 hr) was reduced significantly (P less than 0.05) compared to binding in control cells. Scatchard analysis of the binding data indicated that NO2 exposure caused a 5-fold reduction in insulin receptor binding sites in endothelial cells. Recovery was achieved 24 hr after NO2 exposure with, but not without, changing culture medium. These results indicate that NO2 exposure causes reversible changes in the physical state of lipids in the superficial lipid domains of the pulmonary endothelial cell plasma membrane, and these alterations may interfere with plasma membrane-dependent functions such as receptor-ligand interaction.

Amino Acids↗
PubMed1988

Vitamin E, membrane order, and antioxidant behavior in lung microsomes and reconstituted lipid vesicles.

Vitamin E, a dietary antioxidant, is known to inhibit peroxidation of membrane lipids and to protect the lungs of vitamin E-deficient animals and to a lesser extent vitamin E-sufficient animals from oxidant injury. Since the protective interaction between vitamin E and biological membranes may be related to alterations in composition and physical state of membrane lipids, we evaluated the effect of vitamin E deficiency on lung microsomal lipids and membrane fluidity. Both intact microsomes and lipid vesicles prepared from the total lipid extracts of these microsomes were used. The percentage incorporation of vitamin E and cholesterol, membrane fluidity, and lipid peroxidation were measured in microsomes as well as their lipid vesicles. Fluidity was measured by monitoring changes in fluorescence anisotropy for 1,6-diphenyl-1,3,5-hexatriene (DPH). Lipid peroxidation was measured by thiobarbituric acid reaction. There were significant increases in the phospholipid (p less than 0.01), the total cholesterol (p less than 0.05), and the total saturated fatty acids (p less than 0.05) and decreases in total polyunsaturated fatty acid (p less than 0.01) content of vitamin E-deficient microsomes. There were no detectable peroxidative products in freshly isolated microsomes from either vitamin E-sufficient or -deficient lungs. However, lipids from vitamin E-deficient microsomal membranes were more susceptible to free radical initiated peroxidation than lipids from vitamin E-sufficient microsomes. Fluidity in vitamin E-deficient microsomes or in their lipid vesicles was significantly (p less than 0.05) decreased compared to the respective controls. In vitamin E-deficient microsomes or their lipid vesicles, the incorporation rate of vitamin E was two- to three-fold greater than in vesicles of vitamin E-sufficient microsomes or their lipid vesicles. However, the percentage incorporation of cholesterol was identical in both vitamin E-deficient and vitamin E-sufficient microsomes or in their respective lipid vesicles. As a result of vitamin E incorporation, fluidity was significantly decreased (p less than 0.05) in vitamin E-sufficient vesicles and was further decreased (p less than 0.001) in vitamin E-deficient vesicles. Incorporation of cholesterol also decreased fluidity in both vitamin E-deficient and vitamin E-sufficient vesicles but to the same extent (p less than 0.001). Lipid peroxide formation was two-fold greater in the vitamin E-deficient than in the vitamin E-sufficient vesicles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

The effect of oxidant gases on membrane fluidity and function in pulmonary endothelial cells.

Free radicals and oxidant gases, such as oxygen (O2) and nitrogen dioxide (NO2), are injurious to mammalian lung cells. One of the postulated mechanisms for the cellular injury associated with these gases and free radicals involves peroxidative cleavage of membrane lipids. We have hypothesized that oxidant-related alterations in membrane lipids may result in disordering of the plasma membrane lipid bilayer, leading to derangements in membrane-dependent functions. To test this hypothesis, we examined the effect of exposure to high partial pressures of O2 or NO2 on the physical state and function of pulmonary endothelial cell plasma membranes. Both hyperoxia (95% O2 at 1 ATA) and NO2 exposure (5 ppm) caused early and significant decreases in fluidity in the hydrophobic interior of the plasma membrane lipid bilayer and subsequent depressions in plasma membrane-dependent transport of 5-hydroxytryptamine. Lipid domains at the surface of pulmonary endothelial cell plasma membranes are more susceptible to NO2-induced injury than to hyperoxic injury. Alterations in the fluidity of these more superficial domains are associated with derangements in surface dependent functions, such as receptor-ligand interaction. These results support our hypothesis and advance our understanding of how the chemical events of free radical injury associated with high O2 and NO2 tensions are translated into functional manifestations of O2 and NO2-induced cellular injury.

Endothelium↗
PubMed1987

Stimulation of cyclophosphamide-induced pulmonary microsomal lipid peroxidation by oxygen.

Cyclophosphamide (CP) causes lung toxicity in a wide variety of animals including humans. Recent reports suggest that CP increases lipid peroxide formation in the lung, and that oxygen (O2) potentiates CP-induced lung toxicity. We hypothesized that CP, or one of its toxic metabolites, acrolein, stimulates lung lipid peroxide formation in the presence of high O2 tensions. To test this, rat lung microsomes were treated in vitro with CP or acrolein in the presence of NADPH and 0-100% O2 with and without superoxide dismutase (SOD), glutathione (GSH), dithiothreitol (DTT), and EDTA (agents which scavenge reactive O2 species and/or detoxify reactive metabolites). Lipid peroxide formation in untreated microsomes was increased 40, 39, and 37% in 60, 80 and 100% O2 respectively (P less than 0.02 vs. 21% O2 air). Lipid peroxide formation in microsomes treated with CP increased 2-3-fold under 21% O2 (P less than 0.05 vs. untreated under 21% O2). However, increases in lipid peroxide formation were 3-4 fold in CP treated microsomes under 40-100% O2 (P less than 0.001 vs. untreated at same % O2). CP and acrolein-stimulated lipid peroxidation with and without O2 exposure was significantly (P less than 0.05) reduced by prior addition of SOD, GSH, DTT, or EDTA to the lung microsomal suspension. These results indicate that lipid peroxide formation increases in CP and acrolein-treated lung microsomes, and high O2 tensions stimulate CP-induced lipid peroxidation. Stimulation of CP-induced microsomal lipid peroxidation appears to be mediated by reactive O2 species or metabolites.

Acrolein↗
PubMed1987

Bone growth and haemopoiesis: steroid reversible anaemia, myelofibrosis and increased bone formation in a child.

Factors regulating the interaction between bone marrow haemopoietic cells, stromal elements and bone growth are poorly understood. Disturbance in the equilibrium between these elements can occur as the result of metabolic bone disease, haematologic disorders, neoplasia and infections. The present report concerns a child with myelofibrosis, hypoplastic/dyserythropoietic anaemia, osteoblast proliferation and increased bone formation. A positive tuberculin skin test and elevated EB virus titre indicated previous exposure to Mycobacterium tuberculosis and Epstein-Barr virus. No active focus of infection was identified and no improvement occurred following anti-tuberculous therapy. A dramatic improvement occurred on corticosteroid therapy. Reticulocytosis was followed by an increase in haemoglobin and platelets and a decrease in ESR. Bone marrow fibrosis resolved and the marrow was repopulated with normal haemopoietic tissue. The bone abnormalities improved both radiologically and histomorphometrically. Relapse occurred when steroids were discontinued. Bone marrow tissue culture supernate from the patient during the active phase of the disease inhibited colony formation by normal marrow mononuclear cells. This was reversed by steroid therapy. It is postulated that EB virus may have triggered osteoblast proliferation with resultant bony and haematologic changes. Response to corticosteroids could be explained on the basis of suppression of osteoblast activity and correction of fibroblast mediated suppression of haemopoiesis.

Anemia, Aplastic↗
PubMed1987

Biochemical and metabolic response to nitrogen dioxide-induced endothelial injury.

Nitrogen dioxide (NO2), a major oxidant constituent of vehicle emissions, is toxic to lung cells including endothelial cells. Since NO2 is a reactive free radical, one of the postulated mechanisms of NO2-induced pulmonary injury involves the peroxidation of membrane lipids. Therefore, this study evaluated the dose- and time-dependent effects of nitrogen dioxide exposure by measuring the biochemical and biophysical parameters, as well as the metabolic function, in porcine pulmonary artery and aortic endothelial cells in monolayer cultures. To evaluate the biochemical changes, the antioxidant enzyme GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities, as well as the lipid peroxide formation, glutathione (GSH) content, and lactate dehydrogenase (LDH) release were measured. Biophysical changes were measured by monitoring lipid fluidity in both the hydrophobic and hydrophilic regions of the plasma membrane. The uptake of 5-hydroxytryptamine (5-HT) was measured as a metabolic function of endothelial cells. Confluent porcine pulmonary artery and aortic endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 hours. After 3-, 6-, or 12-hour exposures to 3 or 5 ppm NO2, the GSH-red and G6PDH activities, as well as the lipid peroxide formation and LDH release, were not different from those of controls in both pulmonary artery and aortic endothelial cells. Exposure of the cells to 3 or 5 ppm NO2 for 24 hours resulted in significant increases in GSH-red (p less than 0.05) and G6PDH (p less than 0.001) activities in both cell types. Exposure to 5 ppm NO2 for 24 hours significantly (p less than 0.05) increased lipid peroxide formation and increased (p less than 0.01) LDH release in both the pulmonary artery and aortic endothelial cells. GSH-per activity and GSH content in NO2-exposed pulmonary artery and aortic endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. Fluorescence spectroscopy was used to measure the membrane lipid fluidity. Membrane fluidity in the hydrophobic region was measured by 1,6-diphenyl-1, 3, 5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effect of NO2 exposure on antioxidant defense of endothelial cells.

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is toxic to lung cells. We evaluated the changes in antioxidant enzyme activities in porcine pulmonary artery (PA) and aortic (AO) endothelial cells in monolayer cultures. Confluent PA or AO endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 h and assayed for GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities as well as for intracellular GSH content. After 3, 6, or 12 h exposure to 3 or 5 ppm, GSH-red and G6PDH activities were not different from those of controls in both PA and AO endothelial cells. Exposure to 3 or 5 ppm NO2 for 24 h resulted in significant increases in GSH-red (P less than 0.05) and G6PDH (P less than 0.001) activities in both cell types. GSH-per activity and GSH content in NO2-exposed PA and AO endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. These results indicate that enzyme activities of G6PDH and GSH-red are increased in PA and AO endothelial cells exposed to NO2, and this response is comparable, in part, to that in the lungs from animals exposed to NO2.

Antioxidants↗
PubMed1986

The effect of site and technique of splenic tissue reimplantation on pneumococcal clearance from the blood.

The technique and site of reimplantation of splenic tissue influences survival of laboratory animals following intravenous injection of pneumococci. Splenic tissue was prepared by slicing, mincing, or grating the spleen. The tissue was placed subcutaneously, intraperitoneally, retroperitoneally, or in an omental pouch. This study was designed to determine the rate of pneumococcal clearance from the blood stream 16 weeks following splenic reimplantation by four different methods. All animals were challenged with an intravenous 1 mL bolus containing 10(7) bacteria. The New Zealand white rabbits were divided into six groups: intact spleen; splenectomized; spleen slices in an omental pouch; minced spleen in an omental pouch; splenic tissue implanted subcutaneously; and bits of spleen dropped into the peritoneal cavity. Animals with an intact spleen and those with spleen slices implanted into an omental pouch cleared bacteria during the first hour and all bacteria had disappeared at three hours. Bacteremia persisted longer than three hours in the other groups. Splenic tissue had regenerated in all animals with omental pouch implants, in four of six with minced spleen dropped into the peritoneal cavity but in only one with a subcutaneous implant. Reimplanted splenic tissue clears pneumococci from the blood stream best when thin slices of spleen are placed in an omental pouch. This technique also assures successful regeneration of splenic tissue.

Animals↗
PubMed1986

Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction.

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4-42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.

Adenosine Triphosphate↗
PubMed1986

Nitrogen dioxide-induced changes in cell membrane fluidity and function.

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is toxic to lung cells. One of the postulated mechanisms of NO2-induced pulmonary injury involves peroxidation of membrane lipids. Therefore, we evaluated the effect of 5 ppm NO2 exposure on membrane lipid fluidity, uptake of 5-hydroxytryptamine (5-HT), lactate dehydrogenase (LDH) release, and formation of lipid peroxides in porcine pulmonary artery and aortic endothelial cells in culture. After 3- to 24-h exposure, cells were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer of cell membranes. Membrane fluidity was monitored by measuring changes in rotational relaxation time (rho) for DPH by fluorescence spectroscopy. Reductions in membrane fluidity increase the value of rho. The 5-HT uptake was calculated from the disappearance of 1 X 10(-6) M 14C-5-HT from the medium, and LDH release and lipid peroxide formation were measured by spectrophotometric methods. The NO2 caused a significant increase in rhoDPH in both types of endothelial cells after 3 h and progressed with further exposure to NO2. Exposure to NO2 for 24 h, but not 3 or 12 h, significantly (p less than 0.05) reduced 5-HT uptake, increased (p less than 0.01) LDH release, and increased (p less than 0.05) lipid peroxide formation in both pulmonary artery and aortic endothelial cells. These results suggest that oxidant injury caused by NO changes the physical state of membrane lipids, impairs membrane function, and contributes to the biochemical and metabolic abnormalities in the cells.

Animals↗
PubMed1986

Endotoxin protects against hyperoxic decrease in membrane fluidity in endothelial cells but not in fibroblasts.

We evaluated the ability of endotoxin to protect against hyperoxic depression of plasma membrane fluidity in endothelial cells and fibroblasts in culture. Second- to-fifth passage porcine aortic endothelial cells and human newborn foreskin fibroblasts with 20 ng/ml of endotoxin or diluent in the culture medium were exposed to 20% O2 (control) or 95% O2 (hyperoxic) in 5% CO2 for 4 hours. After exposure, cells were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic core of lipid bilayer membranes, or transparinaric acid (TPA), a natural, conjugated fatty acid that orients parallel to fatty acyl chains of membrane phospholipids. Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropies (rs) for DPH and for TPA by using fluorescence spectroscopy. Reductions in membrane fluidity increase the value of rs. Addition of endotoxin to the culture medium of control endothelial cells and fibroblasts had no effect on rs for DPH or TPA. In hyperoxic endothelial cells, rs for DPH and rs for TPA were increased (p less than 0.001). Addition of endotoxin to the medium of hyperoxic endothelial cells prevented the increases in rs for DPH and TPA. Hyperoxia increased rs for DPH (p less than 0.003) but not rs to TPA in fibroblasts, and endotoxin failed to prevent this increase. These results indicate that hyperoxia decreases plasma membrane fluidity in endothelial cells and fibroblasts and demonstrate that endotoxin prevents the decrease in plasma membrane fluidity in endothelial cells, but not in fibroblasts. These membrane-protective effects may represent an alternative mechanism by which endotoxin protects against hyperoxic cellular injury, and this mechanism may be specific for hyperoxic injury to endothelial cells.

Animals↗
PubMed1985

Effect of oxygen and endotoxin on lactate dehydrogenase release, 5-hydroxytryptamine uptake, and antioxidant enzyme activities in endothelial cells.

We compared the effects of 95% O2 (hyperoxia) alone, endotoxin (20 ng/ml) alone, and 95% O2 plus endotoxin on the release of lactate dehydrogenase (LDH), uptake of 5-hydroxytryptamine (5-HT), and antioxidant enzyme activities in porcine pulmonary arterial and aortic endothelial cells in monolayer culture. Hyperoxia increased LDH release and decreased 5-HT in both endothelial cell types. Hyperoxia also caused a decrease in catalase (CAT) activity and an increase in total superoxide dismutase (SOD) and glutathione reductase (GSH-Red) activities in both cell types. Endotoxin alone had no effect on LDH release, 5-HT uptake, or antioxidant enzyme activities. However, endotoxin prevented the hyperoxic increase in LDH release and the hyperoxic decrease in 5-HT uptake. Endotoxin plus 95% O2 had no consistent effect on the antioxidant enzyme profile in pulmonary artery or aortic endothelial cells. These results indicate that (1) hyperoxia injures both pulmonary artery and aortic endothelial cells in culture and causes changes in the antioxidant enzyme profile that are similar in the two cell types; (2) hyperoxia-induced decreases in CAT activity and increases in SOD activity may be responsible for increased sensitivity of endothelial cells to O2 toxicity; and (3) endotoxin protects against hyperoxic injury to endothelial cells in vitro, but increases in antioxidant enzyme activities are not the mechanism for this protection.

Animals↗
PubMed1985

Cyclophosphamide-induced depression of the antioxidant defense mechanisms of the lung.

Cyclophosphamide causes lung toxicity in a wide variety of animals, including humans. Recent evidence suggests that oxygen (O2) potentiates cyclophosphamide-induced pulmonary injury. We hypothesized that cyclophosphamide or one of its toxic metabolites, acrolein, may potentiate O2 toxicity by depressing lung antioxidant defense mechanisms. To test this, we gave rats cyclophosphamide (100 mg/kg), acrolein (5 mg/kg), or a vehicle (control) in a single intraperitoneal injection and then killed them during a 5-day study period. Excised lungs were analyzed for reduced glutathione (GSH) content, glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GSH-R), glutathione peroxidase (GSH-P), and superoxide dismutase (SOD) activities. In the lungs of cyclophosphamide-treated rats, GSH content was increased 48% (P less than 0.001) on day 2 but progressively decreased to 50% of control values (P less than 0.001) on day 5. Significant reductions (P less than 0.005) in G6PD, GSH-R, and GSH-P activities occurred on days 1-5, and SOD activity was significantly decreased (P less than 0.005) on days 4 and 5 by cyclophosphamide. In acrolein-treated rats, GSH content and GSH-R, GSH-P, and SOD activities were indistinguishable from those in controls. However, G6PD was increased (35-38%) on days 2 and 3 but returned to control values thereafter. To assess whether the cyclophosphamide-induced reduction in lung antioxidant defenses increased susceptibility to acute O2 toxicity, we gave a separate group of rats cyclophosphamide, acrolein, or vehicle, and 4 days later exposed them to 100% O2 or air at 1 atmosphere absolute. All cyclophosphamide-, acrolein-, and vehicle-treated rats survived 60 h air exposure, and all vehicle-treated rats exposed to 100% O2 survived. In contrast, all of the cyclophosphamide-treated rats exposed to 100% O2 died (P less than 0.05) within 40 h. Acrolein had no effect on survival in 100% O2. These results indicate that cyclophosphamide, but not acrolein, depresses lung antioxidant defense mechanisms, which may be responsible for increased mortality from O2 toxicity in cyclophosphamide-treated animals.

Acrolein↗
PubMed1984

Biochemical indices of cyclophosphamide-induced lung toxicity.

Cyclophosphamide (CP) requires metabolic activation for its therapeutic action, and this metabolism results in the formation of two toxic metabolites, acrolein (ACR) and phosphoramide mustard (PM). To determine which metabolite is responsible for CP-induced lung injury, biochemical indices of toxicity and histopathologic changes in the lungs of CP-, ACR-, or PM-treated rats were evaluated. Experimental rats were given 200 mg kg-1 day-1 CP, 5 mg kg-1 day-1 ACR, or 50 mg kg-1 day-1 PM for 1 to 3 days, or were given 100 mg/kg CP for 1 day; control rats received vehicle alone for 1 to 3 days. Twenty-four hr after the last treatment the lungs were analyzed for (a) microsomal NADPH cytochrome c reductase and aniline hydroxylase activities; (b) microsomal lipid peroxide formation; and (c) glutathione content. In rats given 200 mg/kg CP, NADPH cytochrome c reductase and aniline hydroxylase activities decreased 66% (p less than 0.001) and 40% (p less than 0.001), respectively. Lipid peroxidation was increased 100 to 200% (p less than 0.001), and glutathione content was increased 60 to 70% (p less than 0.001). Similar but smaller changes were observed in the lungs of rats given 100 mg/kg CP. In rats given ACR, NADPH cytochrome c reductase and aniline hydroxylase activities decreased 66% (p less than 0.001) and 45% (p less than 0.001), and glutathione content increased 38% (p less than 0.05). In rats given PM, none of the biochemical variables examined were significantly altered. Phenobarbital and SKF 525-A prevented CP-induced biochemical alterations. Despite CP-induced biochemical alterations, no significant light microscopic changes were observed in the lungs. Alterations in lung mixed-function oxidase activity, GSH content, and microsomal lipid peroxide formation are early biochemical indices of CP-induced lung toxicity, and are due at least in part to the reactive metabolite ACR.

Aniline Hydroxylase↗
PubMed1983

The effect of incisional infiltration of bupivacaine hydrochloride upon pulmonary functions, atelectasis and narcotic need following elective cholecystectomy.

Forty randomly selected patients admitted for elective cholecystectomy were entered into the study after they have given informed consent. Arterial blood gas analysis, FVC and FEV1 were measured preoperatively and on the second postoperative day. Preoperatively and on the third postoperative day, roentgenograms of the chest were obtained. The frequency of administration of narcotics was recorded through day 3. The double-blind method selected 17 patients for infiltration of 50 milliliters of 0.25 per cent bupivacaine hydrochloride into the wound and 23 patients for infiltration of 50 milliliters of normal saline solution at the time of closure of the incision. In the saline solution group, postoperative FVC and FEV1 values were only 50 per cent of the preoperative levels (p less than 0.005), while in the bupivacaine hydrochloride group, the FEV1 value was 72 per cent of the preoperative values (p less than 0.05) and the FVC, 78 per cent (p less than 0.05). Roentgenographic evidence of atelectasis occurred postoperatively in four patients of the saline solution group and in only nine patients of the bupivacaine hydrochloride group (p less than 0.001). The saline solution group required 10.8 doses of narcotic through day 3 in contrast with 6.5 doses for the bupivacaine hydrochloride group (p less than 0.05). The hospital stay was 6.6 days for those in the saline solution group and 5.9 days for those in the bupivacaine hydrochloride group (p value, not significant). No complications occurred. Intraoperative infiltration of bupivacaine hydrochloride into the wound improves pulmonary function, reduces the incidence of atelectases and lessens the use of narcotics following cholecystectomy.

Adult↗