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Biomedical subjects

A Trouwborst

Publications and source records attributed to A Trouwborst.

47 records · Page 3Linked to original sources
PubMed1986

Endotoxin protection against oxygen toxicity and its reversal by acetylsalicylic acid.

This study investigated the involvement of substances derived from arachidonic acid in the mechanism of endotoxin's protective action against pulmonary oxygen toxicity. Eighty-three percent of rats treated with a small dose of endotoxin (1 mg/kg) survived exposure to over 95% oxygen for 7 days. In contrast, all control rats exposed to the same oxygen concentration died within 3 days. When the endotoxin-treated rats were also treated with the soluble lysine salt of acetylsalicylic acid (100 mg/kg), 7-day survival decreased to 25%. This suggests that prostaglandin metabolism may play an important role in the protective action of endotoxin during hyperoxia.

Animals↗
PubMed1986

Transperitoneal oxygenation with fluorocarbons.

This work investigated the improvement of arterial oxygenation in hypoxic rats during peritoneal perfusion with the oxygen-carrying perfluorocarbon blood substitute FC43. Three groups of six Wistar rats were ventilated with hypoxic gas mixtures to obtain an arterial oxygen tension (PaO2) of approximately 55 mm Hg. Two groups were subjected to peritoneal perfusion at 20 ml/min with oxygenated FC43 or the gelatine solution Haemaccel. A third group was sham operated but not perfused. In both perfused groups PaO2 increased significantly, more so in the FC43 group. Carbon dioxide tensions significantly decreased only in the FC43 group. Significant increases in arterial oxyhemoglobin saturation were seen after 15 min in the FC43 group and after 60 min in the Haemaccel group. More than 15% of oxygen consumption could be delivered by peritoneal perfusion with FC43.

Animals↗
PubMed1985

The pituitary inhibitory system: its role in pain perception.

The present study was designed to investigate the pain relief mechanism of electrical stimulation to the pituitary and the relationship between hypothalamic and pituitary analgesic mechanism through the observation of monkey behavior and characteristics of tooth pulp-evoked potentials. The results suggest that pituitary-stimulating analgesia should be differentiated from hypothalamic-stimulating effect. In view of the facts, the theory of the Pituitary Inhibitory System is proposed.

Analgesia↗
PubMed1985

Electrophysiologic evidence for involvement of the pituitary region in opiate analgesia.

In the past, various reports have discussed the relationship between the pituitary and analgesia. The purpose of the present study was to explore the possible role of the pituitary region in the mediation of pain by opioids. Tooth pulp evoked potentials recorded from primary somatosensory cortex and from the pituitary region of rabbits were recorded before and after an injection of opiates. Tooth pulp evoked potentials recorded from the primary somatosensory cortex were markedly inhibited after admission of fentanyl, while the tooth pulp evoked potentials recorded from the pituitary region were facilitated. It is concluded that the pituitary region plays a role in the mediation of pain and that this area is involved in the mechanism of opiate analgesia.

Analgesics, Opioid↗
PubMed1984

Relief of cancer pain in man: alcohol-induced neuroadenolysis vs. electrical stimulation of the pituitary gland.

To explore new methods for the control of intractable pain caused by advanced cancer, the analgesic effect of electrical stimulation of the pituitary gland was investigated in 25 patients. The results were compared with a control study and with the effects of alcohol-induced pituitary neuroadenolysis (NALP) in the same patients. The pain score (0: no pain at all, 4: extreme pain) in the control study was 3.88 +/- 0.33. After electrical stimulation of the pituitary gland it was 1.24 +/- 1.61; and after NALP it was 1.0 +/- 1.60. The pain scores after electrical stimulation and NALP were significantly lower (P less than 0.01) than those in the control study; but there was no significant difference when the two were compared with each other. The duration of pain relief following NALP (59.65 +/- 68.72 days) was significantly longer compared with that recorded following electrical stimulation (2.97 +/- 2.58 days). Autopsy examinations of 3 patients who expired from their malignancies revealed that the pain relief was unrelated to the degree of necrosis induced in the pituitary by alcohol. Naloxone administration did not inhibit the analgesic effect of either NALP or electrical stimulation. The advantages and disadvantages of electrical stimulation, the pain relief mechanism activated by this method, and potential clinical applications are also discussed.

Adult↗
PubMed1984

Mechanism of neuroadenolysis of the pituitary for cancer pain control.

Several theories have been advanced to explain how neuroadenolysis of the pituitary (NALP) relieves cancer pain. Interference with hormonal regulation, interruption of pain pathways and a compensatory overproduction of brain endorphins have been proposed. The purpose of the present experimental study is to determine whether neuronal activity of the pituitary gland, as related to the primary somatosensory cortex (PSC), may be involved in the pain perception pathway influenced by NALP, using EEG and tooth pulp evoked potentials (TPEPs). Pituitary activity showed a high voltage slow activity which slowed after alcohol injection into the sella turcica. When naloxone was injected after NALP, a rhythmic high voltage activity appeared in the pituitary gland. After NALP, the TPEP recorded from the PSC disappeared, while NALP induced an increase in the amplitude of the TPEP in the pituitary gland. An injection of naloxone severely decreased this response in the pituitary gland, in contrast to changes in the PSC where the original response reappeared after an injection of naloxone. Our hypothesis is that an increase of TPEPs (hyperactivity) in the pituitary gland is produced after alcohol wounding (wounding effect), leading to a decrease of pain response in the sensory cortex (decrease of TPEPs). This wound effect may be influenced by endorphins, because naloxone, a specific antagonist of opiate receptors, reversed the changes in TPEPs in both places.

Analgesia↗