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Biomedical subjects

R Ferrari

Publications and source records attributed to R Ferrari.

At least 451 records · Page 25Linked to original sources
PubMed1980

[Effect and action mechanism of hypothermia to preserve the ischaemic myocardium (author's transl)].

The ability of hypothermia (34 degrees, 28 degrees) to preserve cardiac metabolism and performance during ischemia, was evaluated in the isolated Langendorff perfused rabbit heart. The hearts, isolated and perfused aerobically for 20', were made ischemic for 90' and their wall temperature maintained either at 37 degrees, 34 degrees and 28 degrees. The hearts were consequently reperfused at 37 degrees for 30'. Some of the hearts were frozen and assayed for ATP and CP. Others were homogenized and their mitochondria harvest, using either an EDTA free or an EDTA-containing extraction medium. The oxidative phosphorylating and ATP generating capacity of these mitochondria were established and their Ca++ content determined. The mechanical performance of the hearts, which were paced, was monitored by means of an intra-ventricular balloon filled with water and connected with a pressure transducer. The hearts that were made ischemic and maintained at 37 degrees were severely depleted in ATP and CP content, their mitochondria accumulated Ca++ and their oxidative phosphorylating activity was impaired. During reperfusion mitochondrial Ca++ was substantially increased, the capacity of the mitochondria to use O2 for state III respiration was further impaired and their ATP generating capacity reduced. Diastolic pressure increased and there was no recovery of the ability of the hearts to develop sistolic pressure. The hearts made ischemic and maintained at 28 degrees were protected. There was a less marked rise in mitochondrial Ca++ concentration after ischemia and during reperfusion; the mitochondria recovered the capacity of utilizing O2 and of generating ATP. That was coincident with and almost complete recovery of mechanical performance. Hypothermia at 34 degrees during ischemia provoked only a partial protection. These results are discussed in accordance with the hypothesis that hypothermia protects heart muscle against the deleterious effects of ischemia not only by reducing the metabolic requirement but also by maintaining intracellular homeostasis with respect to Ca++.

Adenosine Triphosphate↗
PubMed1980

Myocardial lactic acid balance after left ventriculography.

In order to study the effects of contrast media on myocardial metabolism the percentage of lactic acid extraction during left ventricular angiography has been determined in 16 normal patients (Group I), and in 29 patients with coronary artery disease (Group II). In addition, the lactic acid uptake was evaluated after atrial pacing (in 10 patients of Group I and in 13 patients of Group II) and after aortography (in 6 patients of Group I and in 9 patients of Group II). Normal patients usually did not show a myocardial lactic acid production after left ventriculography while the patients with coronary artery disease showed a net lactic acid production in the coronary sinus, which was similar to that obtained after atrial pacing stimulation and after aortography. These results indicate that ventriculography can be a useful technique to assess the kinetics of lactic acid uptake or release into the coronary sinus in patients with coronary artery disease and, in this respect could be useful for studying myocardial metabolism in aortic valve disease and to assess the toxicity of different contrast media.

Adult↗
PubMed1979

Cholesterol synthesis in isolated rat hepatocytes: effect of homologous and heterologous serum lipoproteins.

The present study investigated the effect of serum lipoproteins on sterol synthesis by isolated rat hepatocytes. These cells were maintained in culture medium for 24 hr and incubated for the same period of time with increasing concentrations of serum lipoproteins (5-150 microgram of lipoprotein-protein per ml) isolated from different animal species. The viability of the cells was ascertained by their ability to synthesize cholesterol and protein and to secrete serum proteins into the medium. Rat VLDL and LDL did not alter sterol synthesis, which was stimulated instead by HDL. Rat serum chylomicrons were also ineffective. Human LDL significantly reduced the synthesis of sterols from both acetate and tritiated water; this effect was also induced by human VLDL to a reduced extent. VLDL isolated from hypercholesterolemic rabbit (VLDLC) strongly inhibited sterol synthesis from acetate but not from mevalonate. Cholesteryl-ester-rich VLDL isolated from a patient with type III hyperlipidemia (type III VLDL) were more effective than normal VLDL in suppressing sterol synthesis from acetate. The implications of these findings are discussed with regard to the possible role of cholesteryl-ester-rich lipoproteins on the in vivo regulation of sterol synthesis in the liver.

Acetates↗
PubMed1979

[Creatine phosphokinase release from perfused cardiac muscle under hypoxic conditions. Effect of propranolol, verapamil, reserpine and deslanoside].

Experiments were undertaken to determine if some drugs (propranolol, reserpine, verapamil and deslanoside) have an effect on CPK release from hypoxic heart muscle. Hypoxia was induced in isolated Langerdorff perfused rabbit hearts by gassing the perfusate with 95% N2 + 5% CO2. Hypoxic induced damage of the rabbit heart muscle has been quantited in terms of the relase of the intracellular enzymes creatinephosphokinase (CPK) into the extracellular space. Propranolol was either added at the start of the hypoxic perfusion or the rabbit were pretreated with it. Verpamil, dl-propranolol and reserpine provided protection evidenced by a reduction of hypoxic induced CPK release, while lanatoside C and d-propranolol failed to prevent the hypoxic muscle from releasing CPK.

Animals↗