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Biomedical subjects

J Pincemail

Publications and source records attributed to J Pincemail.

65 records · Page 4Linked to original sources
PubMed1986

Trypsin-like activity and thromboxane release in adult respiratory distress syndrome.

Plasmatic immunoreactive trypsin (IRT), thromboxane and trypsin-like enzymatic activity were measured in 117 patients at risk of developing adult respiratory distress syndrome (ARDS) (53 multiple injury, 30 abdominal surgery, 17 acute pancreatitis, 12 burnt and 5 disseminated intravascular coagulation patients). 69 of these patients developed ARDS. Immunoreactive trypsin and thromboxane were measured by radio-immuno-assay and trypsin-like enzymatic activity by spectrophotometry, using a specific chromogenic substrate. Mean IRT value was 675 ng/ml in ARDS and 265 ng/ml in non ARDS patients (p less than 0.05). Mean IRT value was 685 ng/ml in septic and 170 ng/ml in non septic patients (p less than 0.01). An abnormal trypsin-like enzymatic activity was measured in 26 ARDS patients. In 60 patients (37 ARDS and 23 non ARDS), thromboxane appeared in plasma simultaneously or about 24 hours after the beginning of IRT release. The importance of thromboxane release parallels the intensity of IRT. Originating from pancreas, trypsin can appear in plasma either by absorption from gastrointestinal tract or after pancreatic ischemia.

Clinical Enzyme Tests↗
PubMed1986

Consumption of pentane by hepatic microsomes and consequences on pentane measurement in exhaled gases.

Pentane measurement in exhaled gases was proposed as a safe method to evaluate the importance of lipoperoxidation in vivo, in man and in animals. However we have observed that pentane, which arises from lipoperoxide decomposition, is significantly consumed by cytochrome P-450-rich liver microsomes. This pentane consumption is completely inhibited after heating the microsomes at 100 degrees C, and is considerably reduced by metyrapone, a cytochrome P-450 inhibitor. Hepatic metabolism of pentane, particularly after cytochrome P-450 induction, constitutes a risk of error, when pentane exhalation is taken as an index of lipoperoxidation in vivo.

Animals↗
PubMed1984

Immunoreactive trypsin in the adult respiratory distress syndrome.

With the purpose of studying the role of proteinases in the development of ARDS, plasma levels of immunoreactive trypsin (IRT) and amylase were measured in 43 intensive care patients at risk of developing ARDS (22 polytrauma, seven abdominal surgery, four burns, two DIC and eight pancreatitis). Twenty four of these 43 patients developed ARDS and 31 presented abnormal IRT values (above 70 micrograms/L). Twenty-one of these 31 patients had ARDS; a significant correlation thus appeared between ARDS and abnormal IRT values. In nine patients, IRT values were higher than 800 micrograms/L and remained high for 3 to 4 days. A statistically significant correlation also appeared between abnormal IRT and septic phenomena: 20 patients with high IRT values presented septic problems. When IRT values were high, amylase values were often also abnormal: 12 of 23 patients with high IRT had abnormal amylase levels (the eight patients with documented pancreatitis were excluded); no other clinical signs or symptoms of pancreatitis were present in these patients. IRT could be one of the mediators of ARDS in septic patients. It is not clear that the pancreas is the origin of IRT in all cases.

Abdomen↗
PubMed1983

Stimulation of cyclo-oxygenase by lidocaine, a pro-lipoperoxidant.

Lidocaine, which was recently demonstrated to be a good pro-lipoperoxidant, was tested on in vitro PGs biosynthesis, and on arachidonate-induced arterial hypotension, in the rabbit. In the in vitro experiments, lidocaine alone was a poor stimulant of cyclo-oxygenase, but it enhanced significantly the cyclo-oxygenase activation of uric acid. In the rabbit, lidocaine lowered the i.v. arachidonate dose necessary to obtain a significant drop of blood pressure.

Animals↗
PubMedDate not supplied

Oxidative stress in the liver and the brain of rats in fulminant hepatic failure.

The etiological mechanisms of brain edema in fulminant hepatic failure are incompletely understood. In a surgical model of fulminant hepatic failure in the rat, we tested whether oxidative stress may be involved in the early steps of brain edema. Moreover, we took advantage of this model to determine if oxidative stress may be involved in the hepatocyte dysfunction observed in the setting of fulminant hepatic failure. Oxidative stress was evaluated by measurement of tissue ascorbic acid in the brain and liver of rats at 6 hours after induction of fulminant hepatic failure versus in control or partially hepatectomized rats. After 6 hours, the level of ascorbic acid was not different in the brain tissue of the various groups, indicating no oxidative stress. The liver showed a significant decrease in ascorbic acid levels, both in ischemic and nonischemic liver tissue, suggesting that oxidative stress might be involved in the failure of liver regeneration in fulminant hepatic failure. In this rat model no oxidative stress was demonstrated in the brain during the early phase of fulminant liver failure.

Animals↗
PubMedDate not supplied

Platelets mediate the action of diethylcarbamazine on microfilariae.

More than 400 million people in the world are infected by filarial parasites leading to a wide range of pathologies. Although introduced in 1947, the mainstay of the therapy and control of the filariases is diethylcarbamazine (N,N-diethyl-4-methyl-1-piperazine carboxamide; DEC), the mode of action of which still remains unknown despite widespread use and intensive laboratory investigations. The marked contrast between an extremely rapid action in vivo and the absence of any significant activity on microfilariae in vitro is unique among chemotherapeutic agents. DEC has been thought to modify the surface layer of the microfilariae and expose them to immunological cell-mediated lysis. This report provides the first evidence that the effect of DEC is mediated by blood platelets with the additional triggering of a filarial excretory antigen (FEA). The killing mechanism is antibody-independent and involves the participation of free radicals.

Animals↗
PubMedDate not supplied

Blood levels of reduced/oxidized glutathione and plasma concentration of ascorbic acid during eccentric and concentric exercises of similar energy cost.

In an attempt to assess the possible oxidative stress associated with the transient exercise-induced activation of polymorphonuclear neutrophils (PMN), we compared the effects of eccentric and concentric exercises (downhill run: DR and uphill walk: UW, respectively) of equal duration (35 min) and similar energy cost (60% VO2max) on plasma levels of ascorbic acid ([AA]) and blood concentration of reduced ([GSH]) and oxidized ([GSSG]) glutathione. Eight healthy male subjects took part in this study. Plasma concentration of myeloperoxidase ([MPO]) was used as a specific marker of PMN activation. While there were no significant changes in [MPO] and [AA] in UW experiments, [MPO] increased (+80%) and [AA] decreased significantly during DR tests (P < 0.01 and P < 0.05, respectively). A significant negative relationship was observed between [AA] and [MPO] in DR experiments only (r = -0.49; P < 0.01). Mean (+/- SEM) basal GSH and GSSG concentrations, calculated by pooling the values measured before both tests, were 0.54 +/- 0.02 and 0.12 +/- 0.007 mM, respectively. The blood concentration of these compounds remained practically unchanged in both exercise tests. These results confirm the role played by the eccentric component of muscle contraction in transient exercise-induced PMN activation and suggest that this activation was partly involved in the decrease in [AA] observed in DR experiments. The oxidant stress associated with the exercise protocol used in this study was insufficient to alter blood levels of reduced and oxidized glutathione.

Adult↗
PubMedDate not supplied

[Determination of plasma concentrations of antioxidants, antibodies against oxidized LDL, and homocysteine in a population sample from Liège].

A large number of epidemiological and clinical studies suggest that oxidative stress plays an important role in the development of cardiovascular diseases. In this way, following reference values in plasmatic antioxidants have been determined in a group of 123 blood donors (94 males, 29 females; age: 21-64 years) living in the surroundings of Liege, Belgium: vitamin A (1.5-3.62 mmol/l), vitamin C (3.68-75.21 mmol/l), vitamin E (16.98-46.46 mmol/l), ratio vitamin E/cholesterol (3.92-8.32 mmol/mmol), selenium (0.66-1.26 mmol/l), sulphydryl proteins (216-556 mmol/l), uric acid (174-477 mmol/l), superoxide dismutase (542-852 IU/g hemoglobine), glutathion peroxidase (39.55-91.83 IU/g hemoglobine). Only a few number of subjects were found with values corresponding to high risk of deficiency in antioxidants although low values in vitamin C (< 11.35 mmol/l) and in selenium (< 0.75 mmol/l) were respectively observed in 5.69 and 10.5% of our subjects. Autoantibodies against oxidized LDL, as marker of oxidative stress, and homocysteine, as a risk factor of atherosclerosis involved in the development of oxidative stress, have also been investigated. Approximatively 40% of the population presented values higher than the superior limit mean value (20.3% > 650 IU/l in autoantibodies and 19.5% > 15.2 mmol/l in homocysteine) that are, however, not correlated with age or low levels in antioxidants. The effect of smoking (25% of the population) contributed to significantly decrease vitamin C, selenium and glutathion peroxidase concentrations by 31.9 and 13% when compared to nonsmokers. Intake of 1 to 4 fruits per day resulted in a significant increase of 56.9% in vitamin C when compared to nonconsumers (26.8% of the population). In contrast, homocysteine concentrations were significantly decreased by 21.4% in fruits consumers. Thank to the development of methods allowing the routine dosage of all these parameters, general practitioners can now easily establish the oxidative stress status of their patients and, as fonction of getting patterns, detect populations at risk of developing cardiovascular diseases.

Adult↗
PubMedDate not supplied

[Oxygen metabolism and toxicity in the phenomenon of ischemia-reperfusion].

One of the major cause of human disease results from the compromise of blood flow and oxygen delivery to tissues. Ischemia phenomenon is defined as blood flow that is inadequate to maintain normal tissue function. Prolonged ischemia ultimately results in irreversible changes in cell metabolism and cell death. Historically, it was felt that if ischemia results in altered cell function and injury, then reoxygenation or reperfusion leading to a restoration of a normal blood flow was expected to have a beneficial effect and promote salvage of tissue depending on the extent of ischemia. Recent studies have, however, revealed that reoxygenation leads to an oxygen metabolism resulting in the generation of active and toxic oxygen intermediates (free radicals) which play an important role in the pathophysiology of reperfusion injury.

Antioxidants↗
PubMedDate not supplied

Biochemical pathways of acute lung injury.

Complement fragments (C3, C3d, C5a), thromboxane B2 (TxB2), 6-keto-PGF1 alpha and immunoreactive trypsin (IRT) were measured in 98 patients at risk of developing the adult respiratory distress syndrome (ARDS): 53 multiple trauma, 28 abdominal surgery and 17 acute pancreatitis. Sixty-five of these patients developed ARDS: 30 multiple trauma, 19 abdominal surgery and 16 acute pancreatitis patients. Forty of the 65 ARDS patients and 9 out of the 33 non-ARDS patients died. Mean value of the C3d to C3 ratio was abnormal in both ARDS and non-ARDS patients. C5a-like activity was detected in 70 out of the 98 patients (49 ARDS and 22 non-ARDS patients). TxB2 abnormal values (greater than 100 pg . ml-1) were found in 70% of the patients, especially when sepsis occurred. No correlation could be made between abnormal 6-keto PGF1 alpha values and ARDS or sepsis. The mean peak IRT value was 675 micrograms . 1(-1) for ARDS patients and 274 micrograms . 1(-1) for non-ARDS patients (p less than 0.05). A firm correlation was also measured between IRT and sepsis (p less than 0.01). C5a-like activity was regularly detected soon after injury, while TxB2 and IRT tend to appear later in patients developing ARDS. Neither C3d/C3, nor C5a-like activity, nor TxB2, nor IRT are specific markers of ARDS, since they also appeared in severely ill patients who did not develop ARDS.

6-Ketoprostaglandin F1 alpha↗