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Biomedical subjects

B Riou

Publications and source records attributed to B Riou.

At least 91 records · Page 5Linked to original sources
PubMed1997

Interaction of halothane with alpha- and beta-adrenoceptor stimulations in rat myocardium.

BACKGROUND: Halothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta-adrenoceptor stimulation. However, its effects on the inotropic response to alpha-adrenoceptor stimulation and its effects on the lusitropic effects of alpha- and beta-adrenoceptor stimulation are unknown. METHODS: The effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) and isoproterenol (10(-8) to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (in Krebs-Henseleit solution at 29 degrees C, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions. RESULTS: One MAC halothane induced a negative inotropic effect (54 +/- 3%, P < 0.05), increased R1 (109 +/- 3%, P < 0.05), and decreased R2 (88 +/- 2%, P < 0.05). In control groups, phenylephrine (137 +/- 7%, P > 0.05) and isoproterenol (162 +/- 6%, P < 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/- 19%, P < 0.05) and isoproterenol (205 +/- 11%, P < 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P < 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load. CONCLUSIONS: At clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha- and beta-adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic-effect of beta-adrenoceptor stimulation under low load.

Anesthetics, Inhalation↗
PubMed1997

In vitro effects of dantrolene on rat myocardium.

BACKGROUND: Dantrolene is the only known effective treatment for malignant hyperthermia. However, its effects on myocardial contraction and relaxation remain debatable. METHODS: The effects of dantrolene (10(-5)-10(-3) M) on the contractility of rat left ventricular papillary muscles were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, 2.5 and 0.5 mM Ca2+, stimulation frequency 12 pulses/min). The authors studied contraction, relaxation, contraction-relaxation coupling under high and low load, energetics, and postrest potentiation. The effects of dantrolene after depletion of catecholamine stores with reserpine also were studied. RESULTS: Dantrolene induced a moderate concentration-dependent negative inotropic effect at a low calcium concentration (active force at 10(-4) M: 86 +/- 14% of control values, P < 0.05), but not at a high calcium concentration. Dantrolene did not significantly modify the curvature of the force-velocity relation, suggesting that it did not modify myocardial energetics. Dantrolene induced no significant lusitropic effect under low load, suggesting that it did not modify calcium uptake by the sarcoplasmic reticulum. Dantrolene did not significantly modify postrest potentiation and postrest potentiation recovery, suggesting that it did not modify maximum capacity of calcium release by the sarcoplasmic reticulum nor its postrest resetting capacity. Reserpine did not modify the myocardial effects of dantrolene. CONCLUSIONS: In rat myocardium, dantrolene did not modify any of the sarcoplasmic reticulum functions tested (uptake, release, postrest recovery). Dantrolene induced a moderate negative inotropic effect, probably mediated by a decrease in transarcolemmal calcium entry, and this negative inotropic effect was blunted by an increase in calcium concentration.

Animals↗
PubMed1997

Effects of desflurane in rat myocardium: comparison with isoflurane and halothane.

BACKGROUND: The cardiovascular effects of desflurane have been investigated in several in vivo animal and human studies. To determine the possible contributions of myocardial depression, the effects of desflurane on various contractile parameters in isolated cardiac papillary muscles were compared with those of isoflurane and halothane. METHODS: The effects of desflurane, isoflurane, and halothane (0.5-2.5 minimum alveolar concentration [MAC]) were studied in rat left ventricular papillary muscles (29 degrees C; pH 7.40; stimulation frequency, 12 pulses/min). The inotropic effects were compared under low (isotony) and high (isometry) loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions. RESULTS: Desflurane has no significant inotropic effect (AF at 2.5 MAC: 95 +/- 11% of control values; NS) in contrast with halothane and isoflurane (AF at 2.5 MAC: 37 +/- 14 vs. 65 +/- 10%, respectively; P < 0.05). After alpha- and beta-adrenoceptor blockade or pretreatment with reserpine, desflurane induced a negative inotropic effect (AF at 2.5 MAC: 83 +/- 11 vs. 89 +/- 8%, respectively) that was not significantly different from that of isoflurane (AF at 2.5 MAC: 80 +/- 12%). Halothane induced a negative lusitropic effect under low load, which was significantly greater than those of isoflurane and desflurane. In contrast to halothane, isoflurane and desflurane induced no significant lusitropic effect under high load and did not modify postrest potentiation. These results suggest that desflurane did not impair sarcoplasmic reticulum function. CONCLUSIONS: When compared with isoflurane, desflurane induced a moderate positive inotropic effect related to intramyocardial catecholamine release. After adrenoceptor blockade, desflurane induced a negative inotropic effect comparable with that induced by isoflurane.

Anesthetics, Inhalation↗
PubMed1997

Myocardial effects of halothane and isoflurane in hamsters with hypertrophic cardiomyopathy.

BACKGROUND: The effects of halothane and isoflurane on myocardial contraction and relaxation in diseased myocardium are not completely understood. METHODS: The effects of equianesthetic concentrations of halothane and isoflurane on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C; pH 7.40; Ca2+ 2.5 mM; stimulation frequency, 3/min) in isotonic and isometric conditions. RESULTS: Halothane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (1.5 vol%, active isometric force (AF): 19 +/- 8% vs. 28 +/- 11% of control values; P < 0.05). Isoflurane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (2.0 vol%, AF: 64 +/- 13% vs. 75 +/- 11% of control values; P < 0.01). However, the negative inotropic effects of halothane and isoflurane were not different for cardiomyopathic or healthy hamsters when their concentrations were corrected for minimum alveolar concentration (MAC) values in each strain. Halothane induced a negative lusitropic effect under low load, which was more important in cardiomyopathic hamsters, suggesting a greater impairment in calcium uptake by the sarcoplasmic reticulum. In contrast, isoflurane induced a moderate positive lusitropic effect under low load in healthy but not in cardiomyopathic hamsters. Halothane and isoflurane induced no significant lusitropic effect under high load. CONCLUSIONS: Halothane and isoflurane had greater negative inotropic effects in cardiomyopathic than in healthy hamsters. Nevertheless, no significant differences in their inotropic effects were noted when concentrations were correlated as a multiple of MAC in each strain.

Anesthetics, Inhalation↗
PubMed1997

Relaxation is impaired in the diaphragm muscle of the cardiomyopathic Syrian hamster.

Relaxation was examined in diaphragm muscle strips of cardiomyopathic Syrian hamsters and control hamsters. Isotonic lengthening velocity and isometric tension decay were analyzed over the load continuum in response to twitch. For each load level (P), we measured the maximum extent of shortening (deltaL), the peak lengthening velocity (VL), and the peak rate of tension decline (-dP/dtmax). The kinetics of sarcomere length (SL) were simultaneously measured by laser diffraction. In an attempt to account for the influence of shortening and/or load on relaxation, we calculated the slopes of the VL - deltaL and -dP/dtmax - P relationships. In both groups, there was a direct relationship between (1) VL and deltaL and (2) -dP/dtmax and P. In myopathic hamsters, we observed a decrease in the slope of the VL - deltaL relationship (p < 0.05), a decrease in VL at any common value of both muscle and sarcomere extent of shortening, and an increase in the duration of overall lengthening. Isometric tension decay was significantly prolonged in myopathic muscle strips, while the -dP/dtmax - P relationship was not significantly different than in controls. At low-to-medium loads, SLs at the onset of tension decline were greater in myopathy. These data indicate that relaxation of the diaphragm was both slowed and prolonged in myopathic Syrian hamsters.

Animals↗
PubMed1997

Circulating cardiac troponin T in myocardial contusion.

STUDY OBJECTIVE: Myocardial contusion may induce life-threatening complications, but its diagnosis is difficult. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. We investigate the value of cardiac troponin T measurement in the diagnosis of myocardial contusion. DESIGN: Prospective study. SETTING: Level 1 trauma center. METHODS: We prospectively measured circulating cardiac troponin T and performed echocardiography and continuous Holter monitoring in patients who had suffered blunt trauma. Myocardial contusion was diagnosed in patients who fulfilled one of the following criteria: (1) an abnormal echocardiography compatible with myocardial contusion; (2) severe cardiac rhythm abnormalities; (3) severe cardiac conduction abnormalities; and (4) hemopericardium. MEASUREMENTS AND RESULTS: One hundred twenty-eight patients were included and myocardial contusion was diagnosed in 29 patients. Patients with myocardial contusion had more severe trauma, experienced more frequently associated thoracic lesions, and had a lower left ventricular ejection fraction area (48 +/- 15 vs 61 +/- 10%; p < 0.001). Elevated circulating cardiac troponin T concentrations were significantly more frequent in patients with a myocardial contusion (31 vs 9%; p < 0.007). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L) was more accurate than MB fraction of creatine kinase (CK) (CK-MB) and CK-MB/CK ratio in the diagnosis of myocardial contusion, as shown by an area under the receiver operating characteristic (ROC) curve (AROC), which was significantly different from 0.50 (AROC = 0.69; 95% confidence interval, 0.56 to 0.80). However, this improvement was not clinically acceptable (sensitivity, 0.31; specificity, 0.91). CONCLUSIONS: Circulating cardiac troponin T measurement had a slightly greater diagnostic value than usual biological parameters (CK-MB, CK-MB/CK) in myocardial contusion. Nevertheless, it was concluded that an elevated circulating cardiac troponin T concentration has no important clinical value in the diagnosis of myocardial contusion.

Adolescent↗
PubMed1997

Use of transesophageal echocardiography for diagnosis of traumatic aortic injury.

This prospective study was conducted to describe the signs on transesophageal echocardiography (TEE) associated with traumatic aortic injury (TAI). Twenty-eight patients with TAI underwent TEE, and they were compared with a control group of 30 thoracic trauma patients without aortic injury. The TEE signs were classified as direct or indirect signs, and the quality of imaging was assessed. Patients' TEE images were compared with their anatomic lesions. The direct signs were thick stripes (n=19), false aneurysm (n=7), aortic dissection (n=6), free-edge intimal flap (n=15), aortic wall hematoma (n=2), fusiform aneurysm (n=13), and complete aortic obstruction (n=2). The indirect signs included minor increases in aortic diameter (n=7), impairment of the aortic Doppler color flow (n= 18), and an increase of aorta-probe distance, indicating hemomediastinum (n=23). TEE allowed diagnosis of recently described limited intimal lesions frequently missed by other conventional methods, and permitted rapid diagnosis of complete rupture in which fast degeneration means that more time-consuming methods are not practicable. Significant blurring of the aortic outline was noted in 20% of cases and intraluminal artifacts were observed in 36% of cases, but neither sign impaired accurate diagnosis of TAI. The echocardiographic signs of aortic injury are complex and may be confined to a short section of the aorta. Therefore, examination by a physician highly trained in echocardiography is necessary in such cases.

Adult↗
PubMed1996

Effect of hydroxyethylstarch in brain-dead kidney donors on renal function in kidney-transplant recipients.

BACKGROUND: Hydroxyethylstarch used as a plasma-volume expander in brain-dead kidney donors has been suggested to induce osmotic-nephrosis-like lesions. We have studied its effect on kidney-transplant function. METHODS: 52 patients who had received hydroxyethylstarch of iodinated contrast-media before brain death were excluded. 69 other brain-dead patients were prospectively included over 18 months and randomised into two groups. In the hydroxyethylstarch-gelatin group, patients received hydroxyethylstarch up to 33 mL/kg for colloid plasma-volume expansion, and afterwards received modified fluid gelatin. In the gelatin-only group, patients received only modified fluid gelatin as colloid plasma-volume expander. Multiple organs were procured in 29 cases, which included the kidneys in 27 cases (hydroxyethylstarch-gelatin 15, gelatin-only 12). FINDINGS: There were no significant differences in the characteristics of patients between the two groups of kidney donors or of recipients (except for a small imbalance in sex in the recipients). During the first 8 days after transplantation, nine of 27 (33%) patients required extrarenal haemodialysis or haemodiafiltration in the hydroxyethylstarch-gelatin group compared with one of 20 (5%) in the gelatin-only group (p = 0.029). Serum creatinine concentrations were significantly lower in the gelatin-only group than in the other group (p = 0.009). 10 days after transplantation, mean (SD) serum creatinine was, respectively, 145 (70) and 312 (259) mumol/L. INTERPRETATION: These data suggest that hydroxyethylstarch used as a plasma-volume expander in brain-dead donors impairs immediate renal function in kidney-transplant recipients.

Adult↗
PubMed1996

Hydroxocobalamin vs cobalt toxicity on rat cardiac and diaphragmatic muscles.

BACKGROUND: Hydroxocobalamin has been shown to be a rapid and powerful antidote in acute cyanide poisoning and to prevent cyanide poisoning during sodium nitroprusside administration. This cobalt-containing compound has been shown to be devoid of significant immediate side effects during acute administration. However, its potential delayed toxicity related to cobalt accumulation in tissue remains unknown. Therefore, we evaluated the toxicity of hydroxocobalamin as compared with that of cobalt salts on rat cardiac and diaphragmatic muscles. METHODS: For a 21-day period, rats were treated intraperitoneally with either hydroxocobalamin (70 mg kg-1 per day, n = 14), cobalt chloride hexahydrate (12 mg kg-1 per day, n = 14) or saline (n = 10). Hydroxocobalamin and cobalt chloride groups received equimolar doses of cobalt. We studied: (1) the mechanical properties of isolated left ventricular papillary muscles and diaphragmatic strips, (2) the cardiac and diaphragmatic cobalt tissue concentrations, and (3) the myocardial histological aspect. RESULTS: During the study period, no significant increase in body weight was noted in the cobalt-treated group (-4 +/- 1%), which was in contrast to the hydroxocobalamin-treated group (+21 +/- 2%) and the saline-treated group (22 +/- 2%). Compared with controls, the mechanical properties of cardiac and diaphragmatic muscles were unchanged after either hydroxocobalamin or cobalt salt treatments, and myocardial histological characteristics were similar in all groups. Conversely, large amounts of cobalt deposit were observed in the cobalt-treated group in both the diaphragm (41.90 +/- 16.30 vs 0.70 +/- 0.40 mu mol mu g-1 in the control group, P < 0.001) and the myocardium (16.90 +/- 6.40 vs 0.14 +/- 0.01 mu mol mu g-1 in the control group, P < 0.001). After hydroxocobalamin administration, cobalt concentrations were significantly lower in the diaphragm (25.10 +/- 16.50 mu mol mu g-1, P < 0.001 vs cobalt-treated group) and the myocardium (4.50 +/- 1.20 mu mol mu g, P < 0.001 vs cobalt-treated group). CONCLUSION: These results indicate that repeated administration of hydroxocobalamin was devoid of significant diaphragmatic and cardiac muscle toxicity and therefore remains a safe antidote for acute cyanide poisoning.

Analysis of Variance↗
PubMed1996

Oxygen consumption and delivery relationship in brain-dead organ donors.

The oxygen delivery (DO2) and consumption (VO2) relationship in brain-dead organ donors is unknown. Therefore, in a prospective study, we determined the DO2/VO2 relationship in 21 consecutive brain-dead patients. Patients were allocated to one of two groups, according to plasma lactate concentration: normal (group NL, n = 11) or high (> 2.5 mmol litre-1) (group HL, n = 10). VO2 was measured independently, using indirect calorimetry, under control conditions, during low DO2 challenge with PEEP administration, and high DO2 challenge with inflation of medical antishock trousers and volume expansion or blood transfusion, as required. Under control conditions, there were no significant differences between groups NL and HL in haemodynamic or oxygenation variables, both groups having a low VO2 (mean 114 (SD 21) ml min-1 m-2). In group HL there was a different DO2/VO2 relationship pattern, with a dependent VO2 only. The mean slope of the DO2/VO2 relationship was significantly higher in group HL than in group NL (0.12 (0.09) vs 0.04 (0.07), P < 0.05). We conclude that brain death was associated with a low VO2, and patients in group HL exhibited DO2/VO2 dependency which was not observed in patients in group NL.

Adolescent↗
PubMed1996

Myocardial effects of eltanolone in hamsters with hypertrophic cardiomyopathy.

Eltanolone is a new short-acting i.v. induction agent that induces less cardiovascular depression than propofol or thiopentone and has no significant effect on intrinsic contractility in normal myocardium. However, its effects on diseased myocardium are unknown. We have studied in vitro the effects of eltanolone 0.1, 1, and 10 micrograms ml-1 on the intrinsic contractility of left ventricular papillary muscles from normal hamsters and those with hypertrophic cardiomyopathy (strain BIO 14.6, 6-month-old) (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca2+ 2.5 mmol litre-1, stimulation frequency 3 min-1). Cardiac hypertrophy (mean 134 (SD 9)%, P < 0.001) was observed in cardiomyopathic hamsters. Contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the lower active isometric force (8 (3) vs 35 (14) mN mm-2, P < 0.001). Eltanolone did not induce any significant inotropic or lusitropic effects in normal hamsters, and the effects of eltanolone were not significantly different between normal hamsters and those with cardiomyopathy.

Anesthetics, Intravenous↗
PubMed1996

The effects of triiodothyronine on hemodynamic status and cardiac function in potential heart donors.

Brain death is associated with altered cardiac function and low concentrations of circulating triiodothryronine (T3). However, the effects of T3 administration on hemodynamic status and cardiac function in potential heart donors remain controversial. Thirty-seven brain-dead patients were randomly and blindly allocated to receive an intravenous bolus of either 0.2 microgram/kg T3 (n = 19) or saline placebo (n = 18). Measurements included conventional hemodynamic and echocardiographic variables of cardiac volume conditions and systolic function of the left ventricle (fractional area change [FAC], velocity of myocardial fiber shortening) using a transesophageal probe, arterial and mixed venous blood gas parameters, and serum thyroid hormone concentrations. The mean concentration of T3 was 1.86 +/- 1.55 pmol/L, and only six patients (16%) had normal values of T3 in control conditions. There was no significant correlation between T3 concentration and FAC (R = 0.17, not significant). All patients receiving T3 had normalized serum T3 concentration (7.55 +/- 2.56 pmol/L) in contrast to patients receiving saline (1.48 +/- 1.26 pmol/L). No significant differences in hemodynamic and echocardiographic parameters were observed between the placebo and T3 groups. Indeed, FAC remained unchanged after T3 (44% +/- 17% vs 46% +/- 22%) or placebo (47% +/- 18% vs 50% +/- 14%) administration. In 20 patients with impaired left ventricular function (FAC < 50%), FAC remained unchanged after T3 (n = 10; 34% +/- 12% vs 30% +/- 10%) or placebo (n = 10; 38% +/- 12% vs 35% +/- 13%) administration. In 17 patients in whom organ harvesting was delayed, transesophageal echocardiography was performed 6 h later and no significant changes in FAC were noted in the T3 group (n = 8; 49% +/- 17% vs 44% +/- 17%) and the placebo group (n = 9; 51% +/- 18% vs 47% +/- 18%). In conclusion, T3 administration did not improve hemodynamic status and myocardial function in brain-dead patients, suggesting that the euthyroid sick syndrome is not the main determinant of myocardial dysfunction in these patients.

Adolescent↗
PubMed1995

Circulating cardiac troponin T in potential heart transplant donors.

BACKGROUND: Brain death may induce myocardial dysfunction, the mechanisms of which are not yet fully understood. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. METHODS AND RESULTS: We prospectively measured circulating cardiac troponin T in 100 brain-dead patients and measured the left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. Sixty-one patients had normal LVEFa, 25 had moderate decrease in LVEFa (30% to 50%), and 14 had severe decrease in LVEFa (< or = 30%). Circulating cardiac troponin T concentrations were significantly higher (1.68 +/- 1.03 micrograms/L-1, P < .01) in patients with a severe decrease in LVEFa than in the two other groups (0.42 +/- 0.43 and 0.12 +/- 0.16 microgram/L-1, respectively), and there was a significant correlation between LVEFa and cardiac troponin T concentration (p = -0.59, P < .0001). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L-1) was more accurate (sensitivity, 1.00; specificity, 0.84) in predicting a severe decrease in LVEFa than an elevated CKMB value or an increased CKMB/CK ratio. CONCLUSIONS: An elevated circulating cardiac troponin T was associated with a severe decrease in LVEFa in brain-dead patients, suggesting that severe and potentially irreversible myocardial cell damage occurred. In contrast, CKMB determination was not useful. Since the quality of the donor's heart is considered an important prognosis factor in heart transplantation, the determination of circulating cardiac troponin T concentration could be useful to the heart transplantation team.

Adult↗
PubMed1995

Plasma ionized calcium in brain-dead patients.

BACKGROUND: The mechanism of brain death-induced myocardial dysfunction remains debatable. Hypocalcemia is known to induce reversible myocardial dysfunction. However, the incidence of hypocalcemia and its effect on myocardial function during brain death is unknown. METHODS: In 54 consecutive brain-dead patients, we measured plasma total and ionized calcium concentrations, QT and corrected QT intervals, and left ventricular ejection fraction area (LVEFa), using transesophageal echocardiography. RESULTS: 49 (91%) of brain-dead patients had a decrease in total plasma total calcium concentration but only 19 (35%) had a decrease in plasma ionized calcium. Corrected total plasma calcium failed to predict ionized calcium concentration and QT intervals were not significantly different in normo and hypocalcemic patients. The LVEFa was not significantly different between normo and hypocalcemic patients (53 +/- 13 versus 50 +/- 20%), and no correlation was found between LVEFa and ionized calcium (R = 0.02, NS). Hypocalcemic patients required greater doses of dopamine (8.2 +/- 5.2 versus 5.0 +/- 3.4 micrograms.kg-.min-1, p < 0.02) to maintain arterial pressure. Hypocalcemia was associated with a higher volume loading and a lower plasma protide concentration which reflected hemodilution. CONCLUSION: A decrease in plasma ionized calcium is not frequent, rarely severe, and probably not the main mechanism of myocardial dysfunction in brain-dead patients. Hypocalcemic patients required higher doses of dopamine, suggesting a decrease in systemic resistance. Only direct measurement of ionized calcium can assess plasma calcium ion status in brain-dead patients.

Adult↗
PubMed1995

[Comparison of the effects of ketorolac and aspirin on hemostasis in the rabbit].

OBJECTIVE: Comparison of ketorolac with aspirin and placebo for the antithrombotic activity using the Folts' model of experimental arterial thrombosis and the perioperative blood loss. STUDY DESIGN: Experimental randomized blinded study anaesthetized, tracheotomized and mechanically ventilated. Carotid blood flow variations were detected by a probe directly inserted around the artery and monitored by an electromagnetic flowmeter. A segment of the exposed carotid artery was de-endothelialized by gently squeezing the artery with a needle holder forceps, and an external constrictor was placed around it (stenosis 60%), to induce cyclic flow reductions (CFR). During 20 min, CFR rate was assessed. Animals were then randomized in 3 groups of 9: ketorolac (K) 1 mg.kg-1, aspirin (A) 10 mg.kg-1 or saline (S), injected intravenously (peripheral ear vein). After drug administration, CFR rate was assessed over 20 min, to determine the potential antithrombotic activity of the drug (curative phase). Thereafter, the opposite carotid artery was injured and stenosed and the occurrence of CFR was assessed over 20 min (preventive phase). The amount of blood loss of a xipho-pubic laparotomy with a spleen section was also measured 30 min after drug administration. RESULTS: In all untreated animals, CFRs developed with a mean rate of 4 cycles/20 min. Aspirin completely abolished CFR during the curative phase in all rabbits, except in one. No effect was observed during this phase with ketorolac or saline. During the preventive phase, a partial inhibition of CFRs was induced by ketorolac and aspirin. Peri-operative bleeding was not increased significantly by ketorolac or aspirin. Postinjection bleeding-time did not differ between the three groups. CONCLUSIONS: Ketorolac (1mg.kg-1) has not a strong antithrombotic activity. Ketorolac and aspirin do not increase peri-operative blood loss, and therefore do not seem to strongly interfere with haemostasis in the rabbit.

Animals↗