Experimental carbon monoxide encephalopathy in the primate. I. Physiologic and metabolic aspects

Myron Ginsberg, R. E. Myers

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Nineteen rhesus monkeys received single exposures to carbon monoxide (CO) sufficient to produce consistent neuropathologic lesions. Inhalation of 0.2% CO led to stable plateau levels of blood carboxyhemoglobin, which averaged 76%. The mean arterial blood oxygen content of these animals declined to 4.2 ml/100 ml. The arterial oxygen pressure remained normal. The jugular venous oxygen content exceeded that of the central venous blood during and following the intoxication. Arterial hypotension and metabolic acidosis evolved consistently though to a variable extent. The central venous pressure remained unaltered. Severe respiratory depression occurred only rarely, whereas cardiac arrhythmias constituted a major risk to life during the actual exposure. Ventricular fibrillation occurred in 4 animals and was fatal in 2 but could be largely prevented by the use of lidocaine prophylactically. Arterial hypotension led to the death of 2 animals.

Original languageEnglish
Pages (from-to)202-208
Number of pages7
JournalArchives of Neurology
Volume30
Issue number3
StatePublished - Dec 1 1974
Externally publishedYes

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Brain Diseases
Carbon Monoxide
Primates
Oxygen
Hypotension
Carboxyhemoglobin
Central Venous Pressure
Ventricular Fibrillation
Lidocaine
Acidosis
Macaca mulatta
Respiratory Insufficiency
Inhalation
Cardiac Arrhythmias
Arterial Pressure
Neck
Carbon
Blood
Animals

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Experimental carbon monoxide encephalopathy in the primate. I. Physiologic and metabolic aspects. / Ginsberg, Myron; Myers, R. E.

In: Archives of Neurology, Vol. 30, No. 3, 01.12.1974, p. 202-208.

Research output: Contribution to journalArticle

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