[Traumatic interventricular defect].
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Biomedical subjects
Publications and source records attributed to C Cattani.
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The effect of fructose-1,6-diphosphate (FDP) on the recovery of post-arrest cardiac performance was assessed in isolated rabbit heart preparations subjected to cold ischemic cardioplegic arrest (CICA). Twenty-eight hearts were perfused with Krebs-Henseleit (KHBS) solution followed by 40 minutes of CICA. After CICA normothermic reperfusion with KHBS was restarted. The experimental preparations were divided in four groups of seven hearts each: one group served as control and the other three were perfused with KHBS supplemented with FDP (500 mg/l) given before CICA, after CICA or at both study points. Left ventricular end-diastolic pressure, left ventricular systolic pressure, dP/dt and perfusion pressure were measured at different pre- and post-arrest phases. Time analysis of recovery was also performed. The results demonstrated that FDP supplied prior to and after CICA: prevents the ventricular wall rigidity induced by the ischemic arrest, improves cardiac contractile force both in the basal condition and after cardioplegia, reduces the perfusion pressure, reduces the time to recovery of cardiac contractility. Our findings in the isolated rabbit heart are consistent with published data suggesting FDP may limit the impairment of cardiac dynamics induced by ischemia and improve the recovery after cardiac arrest.
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During biventricular assistance as a bridge to cardiac transplantation, the flow data provided by the pumping systems were compared with flow data obtained with the Fick method. There was a difference between the data sets only in the first 20 hr of observation, with the Fick method giving higher values. During the same period, analysis of the arterial and pulmonary pressure traces showed pulsatile activity to be related with the electrocardiogram's T waves. In the long run, the flow data provided by both methods were no different and the T wave-related pulsatile activity disappeared. The authors concluded that the Fick method represents a useful tool when measuring total flow during biventricular support.
The effects of propofol on cardiovascular dynamics were studied, by means of SO2 Swan-Ganz catheter, in 12 patients scheduled for elective pulmonary resection and in 10 patients undergoing closed heart mitral valve commissurotomy. Myocardial contractility was also investigated in 10 patients (5 pulmonary and 5 mitral valve patients) by means of transthoracic echocardiography. The patients were premedicated with morphine (0.1 mg/kg i.m.), scopolamine (0.005 mg/kg i.m.) and diazepam (0.1 mg/kg p.o.). Anaesthesia was induced with propofol (2 mg/kg i.v.) and fentanyl (0.005 mg/kg i.v.) and maintained with propofol (6 mg/kg/h) plus fentanyl (0.005 mg/kg/h) infusion. Muscle relaxation was assured by pancuronium bromide (0.1 mg/kg). Ventilation (O2-N2O 50%) was controlled to maintain ETCO2 between 30 and 40 mmHg. All the patients undergoing pulmonary resection were intubated with double lumen endotracheal tube. Measurements were performed with the patients awake, after induction, during steady state anaesthesia, before and after thoracotomy. Propofol together with fentanyl significantly decreased arterial pressure (more than 35%) and cardiac index (more than 40%) in both groups of patients; heart rate showed no significant changes even after intubation. Right atrial pressure didn't change meanwhile wedge pressure showed a reduction, with statistical significance only in pulmonary patients. Total systemic resistances didn't show any variation in both groups of patients. The echocardiographic data revealed an important impairment of myocardial contractility after bolus of propofol, mainly in cardiac patients, as evidenced by decrease of ejection fraction values (20%) and by increase of left ventricle end systolic volume index (10%) from baseline. SVO2 and DO2/VO2 ratio values were stable, according with deep anaesthesia level and adequate metabolic balance. In pulmonary patients, during one lung ventilation, the intrapulmonary shunt values did not differed either during or without propofol infusion, thus suggesting that propofol doesn't interfere with pulmonary hypoxic vasoconstrictor response. In conclusion an aware use of propofol and a careful haemodynamic monitoring would be advisable primarily in patients with a well known or supposed cardiovascular disease.
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