Focal Hypoxia Research Articles

Protection cérébrale : apport des agents anesthésiques intraveineux

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO 2) and abolish electrophysiological activity. This reflects a discontinuation of the functionnal neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO 2, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted. This allows proper application of protective measures, such as administration of intravenous anaesthetic agents. Not surprisingly, the only clinical documentation of a protective effect of barbiturates in man was achieved in patients undergoing cardiac surgery under extracorporeal circulation. The concept of pharmacological cerebral protection in case of cerebral ischaemia was investigated with other agents than barbiturates, such as etomidate, gamma-OH and propofol. Anaesthetic agents with their properties of reducing CMRO 2 might be of benefit if applied early, by « buying timein the very first phase of the ischaemic insult.

Adjunctive hyperbaric oxygen therapy in the treatment of the diabetic foot.

The use of hyperbaric oxygen therapy for the treatment of conditions of local or focal hypoxia is not new. The author discusses the potential benefits of hyperbaric oxygen in the treatment of chronic wounds when used as a part of a multidisciplinary wound care program. Rationale and mechanism of action are discussed along with possible adverse effects. Costs of care and limb salvage rates are considered.

Migraine and cerebral hypoxia: a hypothesis with pharmacotherapeutic implications.

It is postulated that a migraine attack is a specific reaction pattern to an episode of focal cerebral hypoxia. This hypothesis holds that any type of focal brain hypoxia (and thus not only a vasospasm) may provoke a migraine attack. Indeed, as hypoxia is a result of an imbalance between energy supply and energy use, the former can be decreased and/or the latter be increased. Spreading cortical depression, leading to the aura, is believed to be another consequence of brain hypoxia occurring in classical migraine. There are no other genuine differences between classical and common migraine, according to the cerebral hypoxia theory. The latter theory may improve our understanding of the mode of action of antimigraine drugs. Certain calcium entry blockers have a direct protective effect on brain hypoxia, but some other pharmacotherapeutic approaches may also prevent cerebral hypoxia via an effect on brain metabolism, vasomotion or platelet behavior.

Concluding Remarks

One of the most well-known pathophysiological phenomena in migraine is cerebral ischemia, possibly induced by vasospasm with consequent prodromic focal symptoms, followed by a reactive vasodilation associated with the pain. From a neuropharmacological point of view, the role of serotonin as a mediator of vasospasm has long dominated the scientific field, and antiserotonin drugs have, for almost as long, governed the therapeutic field. More recent approaches have implicated platelet aggregability, focal cerebral hypoxia and opioid neuropeptides in the genesis of migraine. Here I shall attempt to review the different aspects that, even though controversial, summarize the situation as it stands at the end of 1984.

Tissue ubiquinone and vitamin E levels in rats with experimental focal myocarditis and hypoxic hypoxia

Tissue ubiquinone and vitamin E levels in rats with experimental focal myocarditis and hypoxic hypoxia

Brain hypoxia: the turning-point in the genesis of the migraine attack?

The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack of migraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be provoked by different mechanisms in different patients; the potential role of decreased oxygen supply and of increased oxygen need are reviewed and excess sympathetic drive is considered a potential key mechanism in a majority of patients. Whether or not focal hypoxia leads to a genuine migraine attack, depends largely upon the quality of the whirlpool of biochemical, vascular and hematological changes that follow the hypoxic episode. These changes are discussed and it is concluded that those which have been reported to occur during migraine attacks could be due to a preceding hypoxic event. Finally, the hypoxia viewpoint is confronted with some popular theories about the pathogenesis of migraine. It is found that the other points of view are compatible with the hypoxia hypothesis.

Effects of hyperbaric oxygen therapy on long-tract neuronal conduction in the acute phase of spinal cord injury.

To study the acute effects of hyperbaric oxygen ventilation (HBO) on long-tract function following spinal cord trauma, the authors employed a technique for monitoring spinal cord evoked potentials (SCEP) as an objective measure of translesion neuronal conduction in cats subjected to transdural impact injuries of the spinal cord. Control animals subjected to injuries of a magnitude of 400 or 500 gm-cm occasionally demonstrated spontaneous return of translesion SCEP within 2 hours of injury when maintained by pentobarbital anesthesia and by ventilation with ambient room air at 1 atmosphere absolute pressure (1 ATA). Animals sustaining corresponding injuries but receiving immediate treatment with HBO at 2 ATA for a period of 3 hours following impact demonstrated variable responses to this treatment modality. Animals sustaining injuries of 400 gm-cm magnitude showed recovery of translesion SCEP in four of five cases, while animals sustaining injuries of 500 gm-cm magnitude responded to HBO treatment by recovery of SCEP no more frequently than did control animals. When the onset of HBO therapy was delayed by 2 hours following impact, there appeared to be no demonstrable protective effect on long-tract neuronal conduction mediated by HBO alone. The observations suggest that HBO treatments can mediate preservation of marginally injured neuronal elements of the spinal cord long tracts during the early phases of traumatic spinal cord injury. These protective effects may be based upon the reversal of focal tissue hypoxia, or by reduction of tissue edema. HBO treatment markedly diminished the protective effects of HBO on long-tract neuronal conduction following traumatic spinal cord injury.

Old subependymal necrosis and hemorrhage in the prematurely born infants

Old subependymal hemorrhage (SEH) and old subependymal necrosis (SEN) were found in 18 (23%) and 14 (19%) cases respectively out of a total of 78 prematurely born infants who survived more than 3 weeks. Most of the lesions were recognized in the region of th stria terminalis. A nonhemorrhagic infarct (SEN) might occur at the stria terminalis in the perinatal period of the premature infant, following focal ischemia or hypoxia, and on occasion predispose to the production of subependymal hemorrhage in impaired cerebral vascular autoregulation.

Aspirin, Hyperventilation, and Cerebellar Infarction in Sickle Cell Disease

Aspirin ingestion was followed by hyperventilation, cerebellar signs, and fatal brain stem dysfunction in a patient with sickle cell disease. Autopsy showed a swollen, recently infarcted cerebellum with tonsillar herniation compressing the medulla. We propose that hypocapnea from aspirin-induced hyperventilation caused carotid artery constriction and focal cerebral hypoxia, resulting in cerebellar sickling nad infarction. Hypocapnea should be treated promptly to prevent brain damage in patients with sickle cell disease.

Focal retinal hypoxia

Focal retinal hypoxia