Browsing by Subject "Hyperbaric Oxygenation"

Now showing 1 - 8 of 8

Open Access
Baroreceptor afferents modulate brain excitation and influence susceptibility to toxic effects of hyperbaric oxygen.
(Journal of applied physiology (Bethesda, Md. : 1985), 2014-09) Demchenko, Ivan T; Gasier, Heath G; Zhilyaev, Sergei Yu; Moskvin, Alexander N; Krivchenko, Alexander I; Piantadosi, Claude A; Allen, Barry W
Unexplained adjustments in baroreflex sensitivity occur in conjunction with exposures to potentially toxic levels of hyperbaric oxygen. To investigate this, we monitored central nervous system, autonomic and cardiovascular responses in conscious and anesthetized rats exposed to hyperbaric oxygen at 5 and 6 atmospheres absolute, respectively. We observed two contrasting phases associated with time-dependent alterations in the functional state of the arterial baroreflex. The first phase, which conferred protection against potentially neurotoxic doses of oxygen, was concurrent with an increase in baroreflex sensitivity and included decreases in cerebral blood flow, heart rate, cardiac output, and sympathetic drive. The second phase was characterized by baroreflex impairment, cerebral hyperemia, spiking on the electroencephalogram, increased sympathetic drive, parasympatholysis, and pulmonary injury. Complete arterial baroreceptor deafferentation abolished the initial protective response, whereas electrical stimulation of intact arterial baroreceptor afferents prolonged it. We concluded that increased afferent traffic attributable to arterial baroreflex activation delays the development of excessive central excitation and seizures. Baroreflex inactivation or impairment removes this protection, and seizures may follow. Finally, electrical stimulation of intact baroreceptor afferents extends the normal delay in seizure development. These findings reveal that the autonomic nervous system is a powerful determinant of susceptibility to sympathetic hyperactivation and seizures in hyperbaric oxygen and the ensuing neurogenic pulmonary injury.
Open Access
Effects of striatal nitric oxide production on regional cerebral blood flow and seizure development in rats exposed to extreme hyperoxia.
(Journal of applied physiology (Bethesda, Md. : 1985), 2015-12) Gasier, Heath G; Demchenko, Ivan T; Allen, Barry W; Piantadosi, Claude A
The endogenous vasodilator and signaling molecule nitric oxide has been implicated in cerebral hyperemia, sympathoexcitation, and seizures induced by hyperbaric oxygen (HBO2) at or above 3 atmospheres absolute (ATA). It is unknown whether these events in the onset of central nervous system oxygen toxicity originate within specific brain structures and whether blood flow is diverted to the brain from peripheral organs with high basal flow, such as the kidney. To explore these questions, total and regional cerebral blood flow (CBF) were measured in brain structures of the central autonomic network in anesthetized rats in HBO2 at 6 ATA. Electroencephalogram (EEG) recordings, cardiovascular hemodynamics, and renal blood flow (RBF) were also monitored. As expected, mean arterial blood pressure and total and regional CBF increased preceding EEG spikes while RBF was unaltered. Of the brain structures examined, the earliest rise in CBF occurred in the striatum, suggesting increased neuronal activation. Continuous unilateral or bilateral striatal infusion of the nitric oxide synthase inhibitor N(ω)-nitro-L-arginine methyl ester attenuated CBF responses in that structure, but global EEG discharges persisted and did not differ from controls. Our novel findings indicate that: 1) cerebral hyperemia in extreme HBO2 in rats does not occur at the expense of renal perfusion, highlighting the remarkable autoregulatory capability of the kidney, and 2) in spite of a sentinel increase in striatal blood flow, additional brain structure(s) likely govern the pathogenesis of HBO2-induced seizures because EEG discharge latency was unchanged by local blockade of striatal nitric oxide production and concomitant hyperemia.
Open Access
Hyperbaric oxygen as a treatment for COVID-19 infection?
(Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc, 2020-01) Moon, Richard E; Weaver, Lindell K
Recently the internet has been abuzz with new ideas to treat COVID-19, including hyperbaric oxygen (HBO2) therapy, undoubtedly driven by the fact that until recently there have been few therapeutic options for this highly contagious and often lethal infection. . . . Refractory hypoxemia is certainly treatable with hyperbaric oxygen due to the obvious effect of increasing inspired oxygen partial pressure (PO2), the major reason for using HBO2 for its established indications. However, the length of time during which patients can safely be administered HBO2 inside a chamber is limited, due to practical issues of confinement and isolation from other necessary medical interventions, but also because of oxygen toxicity.
Open Access
Hyperbaric oxygen for decompression sickness.
(Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc, 2021-01) Moon, Richard E; Mitchell, Simon J
Decompression sickness (DCS, "bends") is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation). This may occur when ambient pressure is reduced during any of the following: ascent from a dive; depressurization of a hyperbaric chamber; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft; and during space walks.
Open Access
Ice storm-related carbon monoxide poisonings in North Carolina: a reminder.
(Southern medical journal, 2004-11) Ghim, Michael; Severance, Harry W
Severe winter weather, such as ice storms, that results in loss of electrical power, is frequently mentioned as a contributing factor in acute carbon monoxide (CO) poisoning. However, in our literature review, such events are infrequently reported. This article reports on such an event in which more than 200 patients were evaluated and treated at a single facility because of the crippling effects of an ice storm leading to prolonged loss of power and subsequent catastrophes with alternative heating and cooking sources. One hundred seventy-six patients were treated and subsequently released after Emergency Department-based treatment for CO exposure, and three patients were admitted. Eighteen patients were treated with hyperbaric treatments and discharged. Three others left before treatment was completed. Three cases representing varying levels of severity at presentation leading to differing treatment algorithms are discussed to demonstrate a suggested clinical decision pathway in the treatment of unintentional CO poisoning.
Open Access
Increased Antiseizure Effectiveness with Tiagabine Combined with Sodium Channel Antagonists in Mice Exposed to Hyperbaric Oxygen.
(Neurotoxicity research, 2019-11) Demchenko, Ivan T; Zhilyaev, Sergei Yu; Alekseeva, Olga S; Krivchenko, Alexander I; Piantadosi, Claude A; Gasier, Heath G
Hyperbaric oxygen (HBO₂) is acutely toxic to the central nervous system, culminating in EEG spikes and tonic-clonic convulsions. GABA enhancers and sodium channel antagonists improve seizure latencies in HBO₂ when administered individually, while combining antiepileptic drugs from different functional classes can provide greater seizure latency. We examined the combined effectiveness of GABA enhancers (tiagabine and gabapentin) with sodium channel antagonists (carbamazepine and lamotrigine) in delaying HBO₂-induced seizures. A series of experiments in C57BL/6 mice exposed to 100% oxygen at 5 atmospheres absolute (ATA) were performed. We predicted equally effective doses from individual drug-dose response curves, and the combinations of tiagabine + carbamazepine or lamotrigine were tested to determine the maximally effective combined doses to be used in subsequent experiments designed to identify the type of pharmacodynamic interaction for three fixed-ratio combinations (1:3, 1:1, and 3:1) using isobolographic analysis. For both combinations, the maximally effective combined doses increased seizure latency over controls > 5-fold and were determined to interact synergistically for fixed ratios 1:1 and 3:1, additive for 1:3. These results led us to explore whether the benefits of these drug combinations could be extended to the lungs, since a centrally mediated mechanism is believed to mediate hyperoxic-induced cardiogenic lung injury. Indeed, both combinations attenuated bronchoalveolar lavage protein content by ~ 50%. Combining tiagabine with carbamazepine or lamotrigine not only affords greater antiseizure protection in HBO₂ but also allows for lower doses to be used, minimizing side effects, and attenuating acute lung injury.
Open Access
S-nitrosylation of GAD65 is implicated in decreased GAD activity and oxygen-induced seizures.
(Neuroscience letters, 2017-07) Gasier, Heath G; Demchenko, Ivan T; Tatro, Lynn G; Piantadosi, Claude A
Breathing oxygen at partial pressures ≥2.5 atmospheres absolute, which can occur in diving and hyperbaric oxygen (HBO₂) therapy, can rapidly become toxic to the central nervous system (CNS). This neurotoxicity culminates in generalized EEG epileptiform discharges, tonic-clonic convulsions and ultimately death. Increased production of neuronal nitric oxide (NO) has been implicated in eliciting hyperoxic seizures by altering the equilibrium between glutamatergic and GABAergic synaptic transmission. Inhibition of glutamic acid decarboxylase (GAD) activity in HBO₂ promotes this imbalance; however, the mechanisms by which this occurs is unknown. Therefore, we conducted a series of experiments using mice, a species that is highly susceptible to CNS oxygen toxicity, to explore the possibility that NO modulates GABA metabolism. Mice were exposed to 100% oxygen at 4 ATA for various durations, and brain GAD and GABA transaminase (GABA-T) activity, as well as S-nitrosylation of GAD65 and GAD67 were determined. HBO₂ inhibited GAD activity by 50% and this was negatively correlated with S-nitrosylation of GAD65, whereas GABA-T activity and S-nitrosylation of GAD67 were unaltered. These results suggest a new mechanism by which NO alters GABA metabolism, leading to neuroexcitation and seizures in HBO₂.
Open Access
Successful treatment of pneumatosis intestinalis with associated pneumoperitoneum and ileus with hyperbaric oxygen therapy.
(BMJ case reports, 2017-05-30) Calabrese, Evan; Ceponis, Peter Jm; Derrick, Bruce J; Moon, Richard E
Pneumatosis intestinalis (PI), or the presence of air in the bowel wall, is a rare disorder that is associated with a variety of underlying diseases, including connective tissue disorders. PI presents on a spectrum from asymptomatic to bowel obstruction and acute abdomen. In general, treatment of PI consists of treating the underlying disease. Both normobaric and hyperbaric oxygen have been used to treat PI directly. Here we report a symptomatic scleroderma-related case of PI that responded clinically to hyperbaric oxygen therapy. This report adds to a growing body of literature supporting a role for hyperbaric oxygen therapy in symptomatic PI.