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Biomedical subjects

G Bruschi

Publications and source records attributed to G Bruschi.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

[Acid-base modifications induced by treatment with concentration-reinfusion of ascitis fluid in cyrrhosis (author's transl)].

In 9 cyrrhotic patients with ascites we have studied the acid base status and the renal acidogenic capacity (urinary titrable acidity, ammonia) before, during and after reinfusion of concentrated ascitic fluid. Acid-base parameters have been evaluated also in the ascitic fluid and in the concentrated reinfusion fluid. The treatment does not determine any significant variation of acid base equilibrium in the cyrrhotic patients, while there is a remarkable loosing of CO2 with lowering of pCO2 in the concentrated ascitic fluid. We discuss the main physiopathological factors involved in such a type of treatment.

Ascitic Fluid↗
PubMedDate not supplied

[Cellular calcium, vasoconstriction, hypertension].

The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.

Animals↗