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F B Pallavicini

Publications and source records attributed to F B Pallavicini.

3 recordsLinked to original sources

Pulsatile electrical impedance response from cerebrally dead adult patients is not a reliable tool for detecting cerebral perfusion changes.

The original objective of this work was to verify the possibility of using electrical pulsatile cerebral impedance measurements as a diagnostic aid for assessing the brain-death condition in adults; a subordinate target was to validate a simple method for detecting perfusional changes in the brain. To this end, impedance signals were recorded, for a comparative study, from both live subjects and brain-dead patients, using a simple four-electrode arrangement. Rather unexpectedly, pulsatile transcephalic impedance waveforms exhibiting a temporal dependance similar to those of live subjects were detected in artificially ventilated, cerebrally dead, adult subjects; distributions of the time delays between impedance peaks and ECG peaks were also recorded for the two groups (dead and live subjects). These data provided no evidence, at the 1% significance level, against the hypothesis that the two sample groups are drawn from identical populations. The detection of impedance variations from brain-dead patients can be explained by the residual persistence of blood flow through the scalp, by mechanical variations synchronous with the heart beat and by the presence of the oscillating flow and the systolic spikes that precede the final blood flow arrest. The fact that impedance variations can be traced back to a multiplicity of causes, unrelated to the normal unidirectional flow, renders the transcephalic impedance method inappropriate for detecting cerebral perfusion changes in adults. This conclusion is also strengthened by some theoretical results recently derived from a multilayer model of the head.

Adult↗

Restoration of blood 2,3-diphosphoglycerate levels in multi-transfused patients: effect of organic and inorganic phosphate.

Blood stored in acid-citrate-dextrose (ACD) shows a progressive decrease in 2,3-diphosphoglycerate (DPG) content. Since the decrease in DPG increases hemoglobin oxygen affinity, which in turn may reduce tissue and venous PO2 and peripheral oxygen delivery, many efforts have been made to preserve or restore DPG levels in stored blood. An in vivo rejuvenating technique, employing fructose-1,6-diphosphate (FDP) at a mean dosage of 1 mmol kg-1 day-1 of phosphate, to increase the DPG circulating level in multi-transfused patients is proposed. Eighteen patients, who received at least one-third of their estimated blood volume (3990 +/- 480 (SEM) ml of ACD stored blood) in blood transfusion, were treated: nine with inorganic phosphate, and nine with FDP. Basal DPG was very low in both groups: 12.61 +/- 1.34 (SEM) and 10.42 +/- 0.98 (SEM) mumol g-1, respectively (normal value is 14.5 mumol g-1, at pH 7.40). However, DPG values increased significantly and promptly in patients receiving FDP, whereas in cases of inorganic phosphate administration, it was not significantly raised over the basal value until the third day. Phosphatemia remained normal and constant with FDP, but it rose significantly on the third day of treatment with inorganic phosphate. FDP appears to consistently and rapidly increase DPG levels after transfusion with blood stored in ACD, and to be particularly safe.

2,3-Diphosphoglycerate↗