Pulmonary vascular effects of furosemide on gas exchange in pulmonary edema

1984 ◽  
Vol 57 (1) ◽  
pp. 160-167 ◽  
Author(s):  
J. Ali ◽  
L. D. Wood
Keyword(s):  
Body Weight ◽  
Oleic Acid ◽  
Gas Exchange ◽  
Pulmonary Edema ◽  
Venous Blood ◽  
Control Group ◽  
Pulmonary Perfusion ◽  
Vascular Effects

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.

Factors affecting perfusion distribution in canine oleic acid pulmonary edema

1986 ◽  
Vol 60 (5) ◽  
pp. 1498-1503 ◽  
Author(s):  
J. Ali ◽  
L. D. Wood
Keyword(s):  
Oleic Acid ◽  
Pulmonary Edema ◽  
Venous Blood ◽  
Lower Lobe ◽  
Acid Group ◽  
Left Lower Lobe ◽  
Base Line ◽  
Positive End Expiratory Pressure ◽  
Vascular Effects ◽  
Factors Affecting

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.

Physiologic and histologic determinants of gas exchange during induction of oleic acid pulmonary edema

1988 ◽  
Vol 2 (4) ◽  
pp. 472-480
Author(s):  
John Y. Tsang ◽  
David C. Walker ◽  
H. Thomas Robertson
Keyword(s):  
Oleic Acid ◽  
Gas Exchange ◽  
Pulmonary Edema

Acid-base status affects gas exchange in canine oleic acid pulmonary edema

1991 ◽  
Vol 260 (4) ◽  
pp. H1080-H1086 ◽  
Author(s):  
S. Brimioulle ◽  
J. L. Vachiery ◽  
P. Lejeune ◽  
M. Leeman ◽  
C. Melot ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Metabolic Acidosis ◽  
Gas Exchange ◽  
Pulmonary Edema ◽  
Sulfur Hexafluoride ◽  
Respiratory Acidosis ◽  
Pulmonary Gas Exchange ◽  
Intrapulmonary Shunt ◽  
Pulmonary Hemodynamics ◽  
Acid Base Status

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.

Blunted hypoxic vasoconstriction in oleic acid lung injury: effect of cyclooxygenase inhibitors

1992 ◽  
Vol 72 (1) ◽  
pp. 251-258 ◽  
Author(s):  
M. Leeman ◽  
M. Delcroix ◽  
J. L. Vachiery ◽  
C. Melot ◽  
R. Naeije
Keyword(s):  
Oleic Acid ◽  
Gas Exchange ◽  
Lung Injury ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Balloon Catheter ◽  
Vena Cava ◽  
Cyclooxygenase Inhibitors ◽  
Control Group ◽  
Intrapulmonary Shunt ◽  
Time Control

Cyclooxygenase inhibitors have been reported to accentuate pulmonary hypertension and to improve gas exchange in oleic acid (OA) lung injury (Leeman et al. J. Appl. Physiol. 65: 662–668, 1988), suggesting inhibition of hypoxic pulmonary vasoconstriction by a vasodilating prostaglandin. To test this hypothesis, the hypoxic pulmonary vasoreactivity was examined at constant flow (Q; with an arteriovenous femoral bypass or a balloon catheter placed in the inferior vena cava) before and after OA in three groups of anesthetized and ventilated [inspired O2 fraction (FIO2) 0.4] dogs. Intrapulmonary shunt was measured using a SF6 infusion. A time control group (n = 7) had two consecutive hypoxic challenges after OA and received no drug. A treatment group (n = 6) received indomethacin (2 mg/kg iv) before the second hypoxic challenge after OA. A pretreatment group received indomethacin (2 mg/kg iv, n = 7) or aspirin (30 mg/kg iv, n = 6) before OA. In control and treated dogs, the hypoxic pulmonary vasopressor response was attenuated after OA. It was restored after indomethacin but also during the second hypoxic stimulus in the control dogs. After OA, gas exchange at FIO2 0.4 improved with indomethacin but not in controls. In pretreated dogs the hypoxic vasopressor response to hypoxia was preserved after OA, and gas exchange at FIO2 0.4 was less deteriorated compared with nonpretreated dogs (arterial O2 pressure 139 +/- 7 vs. 76 +/- 6 Torr, P less than 0.01, and intrapulmonary shunt 14 +/- 2 vs. 41 +/- 5%, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen radicals participate in alloxan-induced pulmonary EDEMA

1990 ◽  
Vol 48 (3) ◽  
pp. 298-299
Author(s):  
Tomoo Kawada ◽  
Michio Arakawa ◽  
Kenjiro Kambara ◽  
Takashi Segawa ◽  
Fumio Ando ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Oxygen Radicals ◽  
Bolus Injection ◽  
Physiological Saline ◽  
Baseline Period ◽  
Alveolar Epithelial Cells ◽  
Control Group ◽  
Intervention Period ◽  
Lung Water ◽  
Electron Microscopic

We know that alloxan causes increased-permeability pulmonary edema and that alloxan generates oxygen radicals (H2O2, O2−, ·OH) in blood. Therefore, we hypothesize that alloxan-generated oxygen radicals damage pulmonary capillary endothelial cells, and, possibly, alveolar epithelial cells as well. We examined whether oxygen radical scavengers, such as catalase or dimethylsulfoxide (DMSO), protected against alloxaninduced pulmonary edema.Five dogs in each following group were anesthetized: control group: physiological saline (20ml/kg/h); alloxan group: physiological saline + alloxan (75mg/kg) bolus injection at the beginning of the experiment; catalase group: physiological saline + catalase (150,000u/kg) bolus injection before injection of alloxan; DMSO group: physiological saline + DMSO (0.4mg/kg) bolus injection before alloxan. All dogs had 30-min baseline period and 3-h intervention period. Hemodynamics and circulating substances were measured at the specific points of time. At the end of intervention period, the dogs were killed and had the lungs removed for electron microscopic study and lung water measurement with direct destructive method.

L-Ascorbic Acid Addition to Chitosan Reduces Body Weight in Overweight Women

2014 ◽  
Vol 84 (1-2) ◽  
pp. 5-11 ◽  
Author(s):  
Eun Y. Jung ◽  
Sung C. Jun ◽  
Un J. Chang ◽  
Hyung J. Suh
Keyword(s):  
Ascorbic Acid ◽  
Body Weight ◽  
Fat Body ◽  
Body Weight Gain ◽  
Skinfold Thickness ◽  
The Body ◽  
Control Group ◽  
Percentage Body Fat ◽  
Overweight Women ◽  
Body Weights

Previously, we have found that the addition of L-ascorbic acid to chitosan enhanced the reduction in body weight gain in guinea pigs fed a high-fat diet. We hypothesized that the addition of L-ascorbic acid to chitosan would accelerate the reduction of body weight in humans, similar to the animal model. Overweight subjects administered chitosan with or without L-ascorbic acid for 8 weeks, were assigned to three groups: Control group (N = 26, placebo, vehicle only), Chito group (N = 27, 3 g/day chitosan), and Chito-vita group (N = 27, 3 g/day chitosan plus 2 g/day L-ascorbic acid). The body weights and body mass index (BMI) of the Chito and Chito-vita groups decreased significantly (p < 0.05) compared to the Control group. The BMI of the Chito-vita group decreased significantly compared to the Chito group (Chito: -1.0 kg/m2 vs. Chito-vita: -1.6 kg/m2, p < 0.05). The results showed that the chitosan enhanced reduction of body weight and BMI was accentuated by the addition of L-ascorbic acid. The fat mass, percentage body fat, body circumference, and skinfold thickness in the Chito and Chito-vita groups decreased more than the Control group; however, these parameters were not significantly different between the three groups. Chitosan combined with L-ascorbic acid may be useful for controlling body weight.

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

Systemic Thrombin Generation and Activity Resistant to Low Molecular Weight Heparin Administered Prior to Streptokinase in Patients with Acute Myocardial Infarction

1997 ◽  
Vol 77 (01) ◽  
pp. 057-061 ◽  
Author(s):  
Dennis W T Nilsen ◽  
Lasse Gøransson ◽  
Alf-Inge Larsen ◽  
Øyvind Hetland ◽  
Peter Kierulf
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Molecular Weight ◽  
Body Weight ◽  
Low Molecular Weight Heparin ◽  
Troponin T ◽  
Bleeding Complications ◽  
Control Group ◽  
Low Molecular Weight ◽  
Creatine Kinase Mb

SummaryOne hundred patients were included in a randomized open trial to assess the systemic factor Xa (FXa) and thrombin inhibitory effect as well as the safety profile of low molecular weight heparin (LMWH) given subcutaneously in conjunction with streptokinase (SK) in patients with acute myocardial infarction (MI). The treatment was initiated prior to SK, followed by repeated injections every 12 h for 7 days, using a dose of 150 anti-Xa units per kg body weight. The control group received unfractionated heparin (UFH) 12,500 IU subcutaneously every 12 h for 7 days, initiated 4 h after start of SK infusion. All patients received acetylsalicylic acid (ASA) initiated prior to SK.Serial blood samples were collected prior to and during the first 24 h after initiation of SK infusion for determination of prothrombin fragment 1+2 (Fl+2), thrombin-antithrombin III (TAT) complexes, fibrinopeptide A (FPA) and cardiac enzymes. Bleeding complications and adverse events were carefully accounted for.Infarct characteristics, as judged by creatine kinase MB isoenzyme (CK-MB) and cardiac troponin T (cTnT), were similar in both groups of patients.A comparable transient increase in Fl+2, TAT and FPA was noted irrespective of heparin regimen. Increased anti-Xa activity in patients given LMWH prior to thrombolytic treatment had no impact on indices of systemic thrombin activation.The incidence of major bleedings was significantly higher in patients receiving LMWH as compared to patients receiving UFH. However, the occurrence of bleedings was modified after reduction of the initial LMWH dose to 100 anti-Xa units per kg body weight.In conclusion, systemic FXa- and thrombin activity following SK-infusion in patients with acute MI was uninfluenced by conjunctive LMWH treatment.

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