Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo.

Piantadosi, Claude A.; Sylvia, Avis L.; Jöbsis, Frans F.

doi:10.1172/jci111078

Cited by 31 publications

(13 citation statements)

References 29 publications

(30 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The light was focused with a lens on a spot -2 mm wide just beneath the skull. The depth to which light penetrated into the brain was not known precisely; however, most of the signal was probably derived from the first millimeter of cerebral cortex using this optical configuration (13). Diffusely reflected light was collected from the ipsilateral hemisphere using an internally reflecting glass rod coupled to the parietal bone with an optical gel, and shielded from the source by an O-ring.…”

Section: Methodsmentioning

confidence: 99%

Recovery of energy metabolism in rat brain after carbon monoxide hypoxia.

Brown¹,

Piantadosi²

1992

J. Clin. Invest.

Self Cite

128

View full text Add to dashboard Cite

Carbon monoxide (CO) may inhibit mitochondrial electron transport in the brain and increase the toxic effects of the gas. This hypothesis was investigated in anesthetized rats during CO exposure and recovery at either normobaric or hyperbaric 02 concentrations. During exposure and recovery, we measured the oxidation level of cerebrocortical cytochrome c oxidase by differential spectroscopy and biochemical metabolites known to reflect aerobic energy provision in the brain. CO exposure (HbCO = 71±1%) significantly decreased blood pressure and cytochrome oxidation level. Cerebral ATP was maintained while lactate/pyruvate, glucose, and succinate rose, and phosphocreatine (PCr) fell, relative to control (P < 0.05). Intracellular pH (pHi) calculated from the PCr equilibrium also declined during the exposures. During recovery, HbCO fell more rapidly at hyperbaric than at normobaric 02 levels, but returned to 10% or less in both groups by 45 min. Cytochrome oxidation state improved to 80% ofcontrol after 90 min at normobaric 02, but recovered completely after hyperbaric 02 (P < 0.05). In normobaric 02, PCr and pHi continued to fall for 45 min after CO exposure and did not recover completely by 90 min. PCr and pHi in animals after hyperbaric 02 improved within 45 min, but also remained below control at 90 min. These data indicate that intracellular uptake of CO can impair cerebral energy metabolism, despite the elimination of HbCO from the blood. (J. Clin. Invest. 1992.89:666472.)

show abstract

Section: Methodsmentioning

confidence: 99%

Recovery of energy metabolism in rat brain after carbon monoxide hypoxia.

Brown¹,

Piantadosi²

1992

J. Clin. Invest.

Self Cite

128

View full text Add to dashboard Cite

show abstract

“…This is a direct result of CN binding and subsequent reduction of the active metal centers in CcO. 14,32,[34][35][36] Thus, during CN poisoning, the direction of change of cytochrome oxidation is opposite to that of hemoglobin oxygenation (unlike that seen during hemorrhage).…”

Section: Discussionmentioning

confidence: 99%

“…16 Absorption below 650 nm was excluded from data processing to avoid potential complications from the much stronger absorption changes due to cyt a and cyt a 3 in this region, which could confuse the interpretation of the NIR spectra which are predominantly from Cu A . 9,32 At the baseline, broadband reduced scattering coefficients are calculated as a function of wavelength throughout the NIR region (650 to 1000 nm) by fitting a power-law to five discrete frequency domain reduced scattering coefficients and are used throughout the entire data analysis to extract absorption spectra. At each subsequent measurement, the difference absorption spectra are calculated with respect to baseline values.…”

Section: Dos Measurements In Rabbit Animal Modelsmentioning

confidence: 99%

“…34 As a result, the CuA center, which accounts for the majority of the NIR absorption signal of CcO), becomes reduced. 32,35,36 Unfortunately, noninvasive spectroscopic monitoring of CcO redox information in vivo has been limited by (i) a lack of clearly valid gold standard cytochrome oxidase measures for comparison and (ii) major concerns regarding optical interference from "cross talk" from dominant hemoglobin and myoglobin absorption signals in tissues. 16,37 The objective of this study is to provide evidence for the validity of in vivo measurement of cytochrome oxidase redox state changes during CN poisoning with DOS in peripheral muscle.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Noninvasive optical cytochrome c oxidase redox state measurements using diffuse optical spectroscopy

et al. 2014

View full text Add to dashboard Cite

Abstract. A major need exists for methods to assess organ oxidative metabolic states in vivo. By contrasting the responses to cyanide (CN) poisoning versus hemorrhage in animal models, we demonstrate that diffuse optical spectroscopy (DOS) can detect cytochrome c oxidase (CcO) redox states. Intermittent decreases in inspired O 2 from 100% to 21% were applied before, during, and after CN poisoning, hemorrhage, and resuscitation in rabbits. Continuous DOS measurements of total hemoglobin, oxyhemoglobin, deoxyhemoglobin, and oxidized and reduced CcO from muscle were obtained. Rabbit hemorrhage was accomplished with stepwise removal of blood, followed by blood resuscitation. CN treated rabbits received 0.166 mg∕ min NaCN infusion. During hemorrhage, CcO redox state became reduced concurrently with decreases in oxyhemoglobin, resulting from reduced tissue oxygen delivery and hypoxia. In contrast, during CN infusion, CcO redox state decreased while oxyhemoglobin concentration increased due to CN binding and reduction of CcO with resultant inhibition of the electron transport chain. Spectral absorption similarities between hemoglobin and CcO make noninvasive spectroscopic distinction of CcO redox states difficult. By contrasting physiological perturbations of CN poisoning versus hemorrhage, we demonstrate that DOS measured CcO redox state changes are decoupled from hemoglobin concentration measurement changes.

show abstract

“…33 The reduced state of CcO has a strong absorption peak at 605 nm. 34,35 However, the key challenges for in vivo optical monitoring of CcO redox changes come from the fact that there is a significant overlap in the NIR spectra of hemoglobin and the respiratory chain. In order to overcome the spectral overlap and potential crosstalk from hemoglobin NIRS signal, it is imperative to utilize the unique absorption characteristics of CcO redox states.…”

Section: Discussionmentioning

confidence: 99%

Noninvasive monitoring of treatment response in a rabbit cyanide toxicity model reveals differences in brain and muscle metabolism

et al. 2012

View full text Add to dashboard Cite

Abstract. Noninvasive near infrared spectroscopy measurements were performed to monitor cyanide (CN) poisoning and recovery in the brain region and in foreleg muscle simultaneously, and the effects of a novel CN antidote, sulfanegen sodium, on tissue hemoglobin oxygenation changes were compared using a sub-lethal rabbit model. The results demonstrated that the brain region is more susceptible to CN poisoning and slower in endogenous CN detoxification following exposure than peripheral muscles. However, sulfanegen sodium rapidly reversed CN toxicity, with brain region effects reversing more quickly than muscle. In vivo monitoring of multiple organs may provide important clinical information regarding the extent of CN toxicity and subsequent recovery, and facilitate antidote drug development.

show abstract

Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo.

Cited by 31 publications

References 29 publications

Recovery of energy metabolism in rat brain after carbon monoxide hypoxia.

Recovery of energy metabolism in rat brain after carbon monoxide hypoxia.

Noninvasive optical cytochrome c oxidase redox state measurements using diffuse optical spectroscopy

Noninvasive monitoring of treatment response in a rabbit cyanide toxicity model reveals differences in brain and muscle metabolism

Contact Info

Product

Resources

About