Radiotherapy after hyperbaric oxygenation for malignant gliomas: a pilot study.

The results of radiotherapy combined with hyperbaric oxygen in 9 patients with malignant glioma were compared with those of radiotherapy without hyperbaric O2 in 12 patients. This is the first report of a pilot study of irradiation immediately after exposure to hyperbaric O2 in humans. All patients receiving this treatment showed more than 50% regression of the tumor, and in 4 of them, the tumors disappeared completely. Only 4 out of 12 patients without hyperbaric O2 showed decreases in tumor size, and all 12 patients died within 36 months. So far, this new regimen seems to be a useful form of radiotherapy for malignant gliomas.

Hyperbaric oxygen therapy adjunctive to mild hypertensive hypervolemia for symptomatic vasospasm.

The efficacy of hyperbaric oxygen (HBO) therapy was evaluated retrospectively in 43 patients who developed symptomatic vasospasm following acute aneurysm surgery. HBO therapy was given as an adjunct to mild hypertensive hypervolemia in 24 patients. Before HBO therapy, 17 patients had no infarct (Group 1), and seven had infarcts (Group 2) caused by vasospasm. A further 19 patients received mild hypertensive hypervolemia alone (Group 3). Cerebral infarcts developed in four Group 1 and 12 Group 3 patients. A good outcome 1 month after surgery was achieved by 13 Group 1 (76%), one Group 2, and seven Group 3 patients (37%). Fifteen of the 24 patients who received HBO therapy responded to HBO exposure, and 12 responding patients (80%) had a good outcome. During HBO exposure, electroencephalographic improvements were all accompanied by neurological improvements. There were no complications related to HBO therapy. HBO therapy adjunctive to mild hypertensive hypervolemia is helpful in preventing cerebral infarction associated with symptomatic vasospasm.

Intracranial pressure responses during hyperbaric oxygen therapy.

The responses of intracranial pressure (ICP) to hyperbaric oxygen (HBO) therapy and arterial gas pressures were investigated. ICP was measured through a ventricular or spinal drainage catheter in patients with brain tumor or cerebrovascular disease. Changes in ICP, heart rate (HR), arterial blood pressure (ABP), and transcutaneous partial pressure of carbon dioxide (PtcCO2) or oxygen (PtcO2) were recorded continuously during air or 100% O2 breathing at 1 and 2.5 atmospheres absolute (ATA). HR and PtcCO2 decreased and mean ABP was unchanged during HBO inhalation. ICP was reduced at the beginning and tended to increase gradually during HBO inhalation. The change from air to O2 without altering respiratory frequency and volume caused a gradual increase of ICP and PtcCO2 with a transient ICP reduction in an artificially respirated patient. Intentionally reduced respiration to maintain PtcCO2 at the value at 2.5 ATA with air caused the ICP to return to near the value at 2.5 ATA with air even during HBO inhalation. These findings suggest that reduced ICP is initially due to direct cerebral vasoconstriction caused by hyperoxia and is maintained mainly by induced hypocapnia during HBO inhalation. Care is required when giving HBO therapy to patients with a high ICP and/or who are respirated artificially.

Esophageal and tympanic temperature responses to core blood temperature changes during hyperthermia.

Esophageal, rectal, tympanic, and central blood temperature, i.e., pulmonary artery and aortic arch, were recorded in three patients during iatrogenic whole-body hyperthermia for the treatment of advanced malignant metastatic cancer. Aortic temperature closely followed changes in pulmonary arterial temperature, with an average delay time of 27 s. Esophageal temperature reflected quantitatively and more quickly (avg lag time, 80 s) the temperature changes in the pulmonary artery than tympanic membrane temperature. Tympanic temperature was consistently lower than the blood temperature of the heart during steady state. Therefore it is suggested that esophageal temperature is a preferable index of central blood temperature. Additionally, measurement of esophageal temperature can be made more easily and safely than tympanic membrane temperature.

Electrophysiology of olfacto-limbic-hypothalamic connections in the pig.

To analyse fibre connections between the olfactory bulb (OB) and limbic-hypothalamic structures, the lateral olfactory tract (LOT) was stimulated electrically and extracellular action potentials were recorded from single units in the OB, the cortico-medial portion of the amygdala (AMY) and the mediobasal hypothalamus (MBH). More than 29% of the antidromically identified mitral cells in the OB showed a spontaneous episodic firing pattern consisting of alternating periods of activity and inactivity. Nearly 14% of the orthodromically excited non-mitral cells showed the same phasic firing pattern. 2.9% of AMY neurons were antidromically activated by LOT stimulation, whereas more than 52% showed orthodromic responses. In contrast to the AMY no neuron in the MBH could be antidromically invaded by electrical stimulation. The incidence of orthodromic responses was much less in the MBH when compared to the AMY (13.5%). It is concluded that the firing pattern of OB cells in the pig is complex, often phasic and unrelated to respiration or sniffing. The main OB is more closely related to the AMY than to the MBH. It is suggested that olfactory information is probably transmitted to the MBH via the AMY. The AMY may play a role in the regulation of OB activity.

Data on the sites of stimulatory feedback action of gonadal steroids indispensable for luteinizing hormone release in the rat.

The sites of the stimulatory feedback action of gonadal steroids on LH release were investigated in estrogen-primed ovariectomized rats. Either estradiol benzoate (E2) or estrone (E1) injections 72 h after E2 priming induced a significant increase in serum LH 30 h later, whereas injections of progesterone (P) did so 6 h later. Horizontal sections placed above the medial preoptic area prevented the increase after E2 injections but not after E1 and P injections. Retrochiasmatic sections or bilateral lesions placed in the medial-basal part of the suprachiasmatic area prevented any increases in serum LH induced by steroid injections. Intracerebral implantations of E2 and P in E2-primed ovariectomized rats induced a similar significant increase in serum LH when E2 was implanted into the bed nucleus of stria terminalis (BST), the lateral septum (l-SEPT) and the preoptic suprachiasmatic area (POSC), and when P was implanted in to the medial amygdala, the diagonal band of Broca (DBB), the POSC, the l-SEPT and the anterior hypothalamic area (AHA). These results suggest that the stimulatory feedback effect of E2 is exerted on the limbic structures, especially the BST and the l-SEPT, while the main sites of the stimulatory feedback action of P are located in the DBB, the POSC, and the AHA.

[Electrophysiological studies of the forebrain-limbic inhibitory systems in relation to gonadotropin regulation (author's transl)].

By the earlier studies it has been shown that electrical stimulation of some brain areas such as the medial amygdala and the medial septum increased multiple unit activity (MUA) in the medial preoptic area (MPO) and the arcuate nucleus (ARC) and resulted in gonadotropin release and/or ovulation. On the basis of this evidence, the present study was made to elucidate the effects of stimulation of the forebrain-limbic inhibitory systems on MUA in the MPO and the ARC in relation to the control of gonadotropin release using Wistar female rats. 1) In proestrous rats, electrical stimulation of the basolateral complex of amygdala (1-AMYG), the anterior amygdala (AAA), the hippocampus (HPC), the anterior hippocampus (HIA) and the ventral and lateral part of the central gray matter at the caudal midbrain level (CG) depressed the MUA levels in both the MPO and the ARC in almost of all cases. In the same experiments using ovariectomized and no-primed rats, it was observed that electrical stimulation of the above-mentioned areas was also successful to depress the MUA levels in the MPO and the ARC. But the incidence of inhibition was somewhat lower than that of in proestrous rats. 2) Simultaneous stimulation of the HPC and the 1-AMYG decreased in their inhibitory effects on the MUA in the MPO and the ARC which were apparently observed through the separate stimulation. This was true in combined stimulation of the CG and the 1-AMYG or of the CG and the HPC. It seemed that inhibitory effect on gonadotropin release which was induced by the separate stimulation was cancelled by the combined stimulation. 3) The 1-AMYG and the HPC seemed to form an inhibitory feedback circuit, excitation of a site inhibiting the other. 4) In ovariectomized rats, electrical stimulation of the 1-AMYG or the HPC decreased the MUA levels in the MPO and the ARC after the estrogen injection even in the case that facilitatory effects were observed before estrogen administration. It seemed that inhibitory effects of these inhibitory areas on the hypothalamic activity were enhanced under the dominant influence of estrogen. 5) After an injection of atropine, electrical stimulation of the HPC increased the MUA levels in the MPO and the ARC, while the stimulation of the same sites decreased when no treatment. On the other hand, atropine did not alter the effects of 1-AMYG stimulation on the MUA in the MPO and the ARC. It seems that the forebrain-line inhibitory systems have more important roles in the control of gonadotropin release than it has been assumed, through inhibiting the electrical activity in the MPO and the ARC.