Blood and cerebrospinal fluid lactate during hyperventilation

Plum, Fred; Jb, Posner

doi:10.1152/ajplegacy.1967.212.4.864

Cited by 182 publications

(38 citation statements)

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“…Cerebral venous oxygen tension was elevated in our experiments (Table III) and is usually related closely to cerebral blood flow as measured by xenon-133 clearance (13). Although Plum and Posner (15) and others (16)(17)(18) have found that passive hyperventilation may lead to decreased cerebral blood flow and increased CSF lactate, this association was not observed (17) at Pco2 values as high as those we observed in the presence of increased CSF lactate (Table I). Another possible source of increased lactic acid production is the phagocytosing inflammatory cells in the meninges (19).…”

Section: Respiration and Circulation In Meningitissupporting

confidence: 61%

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Sears¹,

O’Donoghue²,

Fisher³

et al. 1974

J. Clin. Invest.

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Section: Respiration and Circulation In Meningitissupporting

confidence: 61%

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Sears¹,

O’Donoghue²,

Fisher³

et al. 1974

J. Clin. Invest.

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“…27 In addition, infusion of bicarbonate into normal animals produces a lactacidemia similar to that seen in hyperventilated animals. 28 In conclusion: Continuous hyperventilation of normal, unanesthetized goats produced only transient reductions in CBF and CMR0 2 , which returned to normal within 6 hours. In addition, goats subjected to 12 hours of hyperventilation showed no ill effects for several days after treatment.…”

mentioning

confidence: 75%

Cerebral effects of extended hyperventilation in unanesthetized goats.

Albrecht¹,

Miletich²,

Ruttle³

1987

Stroke

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Thirty-six adult, male unanesthetized goats were hyperventilated to a Pacoj level of 16-18 nun Hg for 6 hours. Arterial and sagittal sinus blood and cerebrospinal fluid were analyzed for pH, blood gases, bicarbonate, lactate, and pymvate before hyperventilation, during hyperventilation, and after the termination of hyperventilation. Total cerebral blood flow, regional brain blood flows, and cerebral metabolic rate for oxygen were calculated from the distribution of radioactive microspheres. Intracranial pressure was measured in either the right or left cerebral ventricle. With the initiation of hyperventilation, cerebral blood flow and cerebral metabolic rate for oxygen fell significantly (64 ± 5 ml/100 g/min to 41 ± 3; 4.6 ± 0.3 ml O 2 /100 g/min to 3.6 ± 0.2), but both returned to prehyperventilation values within 6 hours of hyperventilation. With termination of hyperventilation, cerebral blood flow and cerebral metabolic rate for oxygen increased significantly above control levels (64 ± 5 vs. 105 ± 9; 4.6 ± 0.3 vs. 5.4 ± 0.4). Intracranial pressure was unaffected by hyperventilation or its termination. Arterial and sagittal sinus blood and cerebrospinal fluid pH increased with hyperventilation but returned to control values by 6 hours. However, pH was still significantly elevated at 6 hours. Lactate and pyruvate followed a similar pattern except in the cerebrospinal fluid, where both increased throughout the course of hyperventilation. There were no significant differences in the lactate: pyruvate ratio. On termination of hyperventilation, pH of the arterial and sagittal sinus blood and cerebrospinal fluid fell below control levels. Bicarbonate values decreased in all fluid compartments and were still below control values 2 hours after the cessation of hyperventilation. Blood flows to the cerebral cortex, thalamus, hypothalamus, medulla, and cerebellum fell significantly with hyperventilation and, with the exception of the thalamus, all recovered during hyperventilation. On termination of hyperventilation, blood flows to the cortex, thalamus, medulla, and cerebellum increased significantly above control values. Only the brainstem (except the medulla) appeared unresponsive to hyperventilation. Hyperventilation had little effect on mean arterial blood pressure and heart rate. Received December 4, 1985; accepted December 22, 1986. els, 34 but not all studies have shown a recovery of CBF during hyperventilation.5 -6 Because a sustained reduction in CBF is central to the theory of hyperventilation therapy, one would think that the behavior of CBF during extended hyperventilation would be understood and well documented. The absence of consensus on this crucial point clearly suggests a need for studies concerned with the physiologic effects of prolonged hyperventilation. The purpose of this study, therefore, was to conduct a comprehensive analysis of the effects of protracted hyperventilation on CBF, cerebral metabolic rate for oxygen (CMRO2), and other cerebral parameters in normal, unanesthetized goats. Hopeful...

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“…The disinhibition of the regulatory glycolytic enzyme phosphofructokinase would be expected to result in increases in: (a) glycolytic flux and hence respiratory quotient (RQ) (Scheuer & Berry, 1967); (b) blood [lactate] (Eichenholz et al 1962;Eldridge & Salzer, 1967;Plum & Posner, 1967); (c) ýOµ, although only by some 10% of the resting level for this degree of acute alkalosis (Cain, 1970;Karetzky & Cain, 1970); and (d) cardiac output (McGregor et al 1962). However, in all but the latter, these influences would not be expected to slow ýCOµ: in the latter, this would be contributory to reducing the tissue COµ stores (Farhi & Rahn, 1955).…”

Section: ------------------------------------------------------------mentioning

confidence: 99%

Effect of Altered Body CO₂ Stores on Pulmonary Gas Exchange Dynamics During Incremental Exercise in Humans

Özçelik

Ward

Whipp

1999

Experimental Physiology

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Blood and cerebrospinal fluid lactate during hyperventilation

Cited by 182 publications

References 0 publications

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Cerebral effects of extended hyperventilation in unanesthetized goats.

Effect of Altered Body CO₂ Stores on Pulmonary Gas Exchange Dynamics During Incremental Exercise in Humans

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Blood and cerebrospinal fluid lactate during hyperventilation

Cited by 182 publications

References 0 publications

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Effect of Experimental Pneumococcal Meningitis on Respiration and Circulation in the Rabbit

Cerebral effects of extended hyperventilation in unanesthetized goats.

Effect of Altered Body CO2 Stores on Pulmonary Gas Exchange Dynamics During Incremental Exercise in Humans

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Product

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Effect of Altered Body CO₂ Stores on Pulmonary Gas Exchange Dynamics During Incremental Exercise in Humans