Biomedical subjects

G Aya

Publications and source records attributed to G Aya.

6 recordsLinked to original sources

PubMed2000

Comparison of the diagnostic value of cardiac troponin I and T determinations for detecting early myocardial damage and the relationship with histological findings after isoprenaline-induced cardiac injury in rats.

Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. The purpose of this study was to investigate the diagnostic value of cTnI and cTnT with regard to creatine kinase (CK) and lactate dehydrogenase (LD) and to determine whether they can be used for early diagnosis of myocardial damage in rats, and to examine the relationship between cTnl and cTnT release with histological examinations, using isoprenaline-induced cardiac muscle damage as an experimental model in the rat. Eighteen Wistar rats per group were treated with a single dose of either isoprenaline (iso) or with normal saline as a control group. The anti-cTnI and cTnT monoclonal antibodies (mAbs) employed in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rat. A highly significant rise of cTnl or cTnT was found already 2 h after iso. The time-courses of cTnI and cTnT were monophasic in form. The highest cTnI (mean+/-S.D., 1.1+/-2.3 ng/ml) and cTnT (mean+/-S.D. 3.6+/-30 ng/ml) were found 4 h after iso. cTnI and cTnT significantly increased in iso-treated rats in comparison with controls whether the differences between 2-, 4- and 6-h levels and basal levels were considered or not. The areas under cTnl and cTnT curves (AUC) (0-6 h) and the maximal cTnI and cTnT (0-6 h) after iso were significantly different from the controls. For CK and LD, no elevation in comparison with controls could be detected (except a trend for LD whether or not the difference between 6-h levels and basal levels were considered (P=0.08) and for LD AUC (0-6 h) (P=0. 059)). Correlations between maximal cTnI and cTnT and AUC were 0.69 (P=0.0001) and 0.60 (P=0.0066), respectively. Histological examinations of iso-treated rats revealed acute focal or multifocal myofibrillar degeneration of the myocardial tissue in ten out of 14 rats and showed the earliest alterations 4 h after iso in one treated rat. Only four of the controls exhibited evidence of mild changes and slight mononuclear cell infiltration. cTnl and cTnT peak values to at least 0.35 and 1.3 ng/ml, respectively, were necessary to detect histological myocardial cell injury after iso. cTnI and cTnT were found to be early markers for diagnosing iso-induced myocardial damage in comparison with CK and LD. Elevations of cTnI and cTnT appeared to relate to the severity of histologic changes after myocardial injury. Although there was a difference in the absolute concentration of results between cTnI and cTnT assays, due to a lack of standardization and heterogeneity in the cross-reactivities of mAbs to various troponin I and T forms, cTnI and cTnT can be used as easily measurable target parameters for detection of cardiotoxic and/or cardiodegenerative effects in rats.

Animals↗

PubMed1999

Release kinetics of cardiac troponin I and cardiac troponin T in effluents from isolated perfused rabbit hearts after graded experimental myocardial contusion.

BACKGROUND: Few experimental studies report effects of direct contusion on cardiac enzyme release. Cardiac troponins I (cTnI) and T (cTnT) have been shown to be highly sensitive and specific markers of myocardial cell injury. This investigation was designed to determine and compare the acute effects of quantified magnitudes of blunt cardiac trauma upon release of cTnI and cTnT in comparison with creatine kinase (CK) and lactate dehydrogenase (LD). METHODS: In 24 rabbit hearts prepared on a standard Langendorff apparatus, myocardial contusion (MC) was produced by a single blow with a ball falling from a predefined height, delivered directly to the surface of the heart. Hearts were divided into control (n = 6) and various quantified impacts: 75 mJoules (mJ) (n = 6), 100 mJ (n = 6), 200 mJ (n = 6). Coronary effluent samples for cTnI, cTnT, CK, and LD were collected at baseline, immediately after MC and 5, 15, 30, 45, and 60 minutes after MC. At the end of experiment, histologic condition was evaluated. RESULTS: The anti-cTnI and cTnT MAbs used in the cTnI (Access) and cTnT (Elecsys) assays cross-react with cTnI and cTnT of the rabbit. The time-courses of cTnI, cTnT, CK, and LD were monophasic in form. After MC, all parameters rose significantly compared with baseline and with control group. The maximal release occurred immediately after MC. The area under the cTnI curve and the maximal cTnI concentration were linked to the contusion energy when increased at 200 mJ. Maximal concentrations and areas under cTnT, CK, LD time activity curve were not linked to the contusion energy level and showed no between-energy group differences. The correlation found between maximal cTnI and maximal cTnT concentrations was 0.70 (p = 0.0001). Histologic examination showed cellular disruption and after the more severe impact, the extent of pathologic changes was more extensive. CONCLUSION: After graded experimental MC, maximal cTnI concentration and area under cTnI curve increase with the power of impact kinetic energy. Levels of cTnI allow a much higher accuracy in detecting the extent of myocardial injury postMC in comparison with cTnT, CK, and LD in this experimental study. These results should be consistent with the more extensive cTnI release with more severe impact in patients with blunt chest trauma. Furthermore, because specificity and time-course of release, both cTnI and cTnT should have a role in the diagnosis and evaluation of such patients.

Animals↗

PubMed1997

Comparison of proarrhythmogenic effects of two potassium channel openers, levcromakalim (BRL 38227) and nicorandil (RP 46417): a high-resolution mapping study on rabbit heart.

This study was designed (a) to test and (b) to compare proarrhythmic effects of levcromakalim and nicorandil; and (c) determine the mechanism of arrhythmia initiation by using high-resolution ventricular epicardial mapping on 44 Langendorff-perfused rabbit hearts. Eighteen hearts were kept intact and received incremental doses (1-500 microM) of levcromakalim, nicorandil, and isosorbide dinitrate. In 26 hearts, a thin layer of epicardium was obtained after endocardial cryotechnique (frozen hearts). In intact hearts, isosorbide dinitrate did not produce any arrhythmia. In contrast, levcromakalim induced spontaneous ventricular fibrillation (VF) in all hearts at 50 microM, whereas only one VF occurred at 500 microM nicorandil. These three drugs produced a dose-dependent bradycardia in intact hearts. In frozen hearts, arrhythmias were induced by 5 microM levcromakalim and 50 microM nicorandil. Isosorbide dinitrate had no proarrhythmogenic effect. Epicardial mapping showed that most of induced ventricular tachycardias were based on reentry around an arc of functional conduction block. Ventricular conduction velocities did not change, but levcromakalim and nicorandil shortened ventricular effective refractory period. We conclude that (a) levcromakalim and nicorandil, used in toxic concentrations, have direct proarrhythmic effects; (b) nicorandil proarrhythmogenic effects are 10 times less marked than those of levcromakalim (arrhythmia is solely the result of the potassium channel opener property of nicorandil); and (c) most of ventricular tachycardias induced are based on reentry.

Animals↗

PubMed1995

Cardiac output measurement in critically ill patients: comparison of continuous and conventional thermodilution techniques.

The purpose of the study was to compare cardiac output (CO) measurement by continuous (CTD) with that by conventional thermodilution (TD) in critically ill patients. In 19 of 20 critically ill patients requiring a pulmonary artery catheterism, 105 paired CO measurements were performed by both CTD and TD. Regression analysis showed that: CTD CO = 1.18 TD CO - 0.47. Correlation coefficient was 0.96. Bias and limit of agreement were -0.8 and 2.4 L.min-1, respectively. When a Bland and Altman diagram was constructed according to cardiac index ranges, biases were -0.2 and -0.3 and -0.8 L.min-1.m-2 and limits of agreement were 0.3, 0.7 and 1.6 L.min-1.m-2 for low (< 2.5 L.min-1.m-2), normal (between 2.5 and 4.5 L.min-1.m-2) and high (> 4.5 L.min-1.m-2) cardiac indexes, respectively. It is concluded that CTD, compared with TD, is a reliable method of measuring CO, especially when cardiac index is < or = 4.5 L.min-1.m-2.

Bias↗

PubMed1993

[Postdural puncture headache].

PDPH are not the privilege of spinal anaesthesia, as they can occur in various circumstances including epidural anesthesia, surgical wound of the dura, spinal tap and/or myclography. Diagnosis PDPH can be discussed with four etiologies: cortical vein thrombosis, meningitis, intracranial haematomas (intracerebral, subdural) or migraine. PDPH result from the leakage of CSF via the dural hole, responsible of hypotension of CSF in the subarachnoid compartment. Several etiologies and predisposing factors are discussed. The incidence of PDPH varies with age, maximum from 15 to 50 years-old, the decreasing to reach a very low incidence over 65 PDPH seems to occur more frequently in women, especially during pregnancy. The diameter of the spinal needle is the main factor of PDPH. Using small diameters (25 G and less) allows to reduce the percentage of PDPH, as well as using specially designed needles with a "pinpoint bevel" (Sprîtte, Whitacre). When PDPH occur, no specific treatment is required before the fifth day, as they spontaneously resolve in 80% of the patients, without any intervention. After then, epidural blood patch allows 90% success rate. Other therapeutic proposals are discussed. Finally, prevention of PDPH appears to be the keypoint, paying particular attention to the choice of the needle and of the spinal puncture technique.

Anesthesia, Epidural↗

PubMed1991

[Opioids by the perimedullary route: mechanisms of opioid analgesia].

The identification of multiple opioid receptors and opioid peptides in the 1970 was the starting point of an increasing knowledge on opioid physiology and pharmacology. The mechanisms of action of spinally supraspinal levels. At the spinal level, opioids act by a modulation of specific supraspinal effect is the consequence of the migration of opioids, other in the bloodstream or in the cerebrospinal fluid, towards the encephalon. This action involve complex systems of inhibitory control on spinal structures. Opioids act on specific receptors which have a broad distribution in the central nervous system. the classification of opioid receptors is based on the activity of specific ligands: mu (morphine), kappa (ketocyclazocine), sigma (SKF 10047), delta (leu-enkephalin) and epsilon (beta-endorphin). Evidence for the existence of different isoreceptors for each type has been given by experimental studies. At the receptor level, opioid agonists act, hypothetically via the system of adenylcylase, more certainly via a modulation of membrane tonic channels. Thus, opioids modify sodium, calcium and potassium currents, and modify the successives phases of the membrane action potential. The result is an hyperpolarization which is responsible of an inhibition of the release of various neurotransmitters such as P substance.

Analgesia, Epidural↗