A system for investigating oesophageal photoplethysmographic signals in anaesthetised patients

The monitoring of arterial blood oxygen saturation in patients with compromised peripheral perfusion is often difficult, because conventional non-invasive techniques such as pulse oximetry (SpO2) can fail. Poor peripheral circulation commonly occurs after major surgery including cardiopulmonary bypass. The difficulties in these clinical situations might be overcome if the sensor were to monitor a better perfused central part of the body such as the oesophagus. A new oesophageal photoplethysmographic (PPG) probe and an isolated processing system have been developed to investigate the pulsatile signals of anaesthetised adult patients undergoing routine surgery. Measurements were made in the middle third of the oesophagus, 25 cm to 30 cm from the upper incisors. The AC PPG signals are sampled by a data acquisition system connected to a laptop computer. The signals recorded correspond to infrared and red AC PPGs from the middle third oesophagus and the finger. Preliminary results from 20 patients show that good quality AC PPG signals can be measured in the human oesophagus. The ratio of the oesophageal to finger AC PPG amplitudes was calculated for the infrared and red wavelengths for each patient. The mean (+/- standard deviation) of this ratio was 2.9 +/- 2.1 (n = 19) for the infrared wavelength and 3.1 +/- 2.4 (n = 16) for the red wavelength. The red and infrared wavelengths used are appropriate for pulse oximetry and this investigation indicates that the mid-oesophagus may be a suitable site for the reliable monitoring of SpO2 in patients with poor peripheral perfusion

Fatty acid oxidation in the myocardium: Effects of parathyroid hormone and CRF

Fatty acids constitute an important substrate utilized by the myocardium as a major fuel for energy production; certain data suggest that oxidation of long chain fatty acids (LCFA) may be impaired in uremia, and such a derangement could, in part, contribute to the myocardiopathy of uremia. The latter is associated with secondary hyperparathyroidism and PTH has been shown to affect myocardial metabolism. The present study evaluated in rats the effects of four days administration of PTH and 21 days of chronic renal failure (CRF) with and without excess PTH on oxidation of α-ketoglutarate, β-hydroxybutyric acid, LCFA and short chain fatty acids (SCFA). PTH impaired oxidation of α-ketoglutarate, LCFA, SCFA, but not of β-hydroxybutyric acid and reduced the activity of carnitine palmitoyl transferase (CPT). Inactivation of the PTH abolished its effects. CRF rats with intact parathyroid glands also had impaired oxidation of LCFA and CTP activity. Carnitine contents of myocardium were not altered. The data show that PTH excess in normal rats is associated with impaired oxidation of LCFA and SCFA, and secondary hyperparathyroidism in CRF animals impairs oxidation of LCFA. This effect is due to: 1) reduction in the activity of CPT, a key enzyme for the transport of LCFA to mitochondrial matrix for β-oxidation; and 2) impairment in β-oxidation. The data provide for new and additional pathway through which excess PTH and CRF can affect myocardial metabolism

Deficiência muscular de carnitina: relato de 8 casos com estudo clínico, eletromiográfico, histoquímico e bioquímico muscular

São relatados os casos de 8 pacientes, sendo 7 do sexo masculino, cuja idade variou entre 5 dias e 64 anos. Sete pacientes apresentavam diminuição da força muscular e todos apresentavam, nas biópsias musculares, acúmulo de lipídios. Os sintomas iniciaram nos primeiros dias de vida em três pacientes, na infância em dois, na idade adulta em dois; um dos casos apresentava-se assinto-mático aos 64 anos de idade (heterozigoto?). Em graus variáveis os pacientes apresentavam dificuldades na deglutição, hipotonia, atrofia muscular, dificuldades na mastigação, parestesias em membros inferiores, hepatomegalia e esplenome-galia. Cinco casos tinham história familiar e um relatava recorrências dos sintomas. Todos apresentavam aumento dos enzimas séricos, principalmente da creatinoquinase. A eletromiografia foi compatível a envolvimento muscular primário em um caso, desenervação em dois e neuromiopático em dois, não tendo sido realizada em três casos. Na biópsia muscular, em todos os casos, além do acúmulo de lipídios, ocorriam: componente de desenervação em 4, miopa-tia crônica em 4, atrofia de fibras do tipo II em um. Em dois casos, as alterações histológicas eram sugestivas de atrofia espinhal infantil. Um dos casos, possivelmente pertencente à forma sistêmica de deficiência de carnitina, possuía importante envolvimento miocárdico, vindo a falecer. São discutidos aspectos clínicos, metabólicos e terapêuticos das deficiências musculares de carnitina