Lactate and Pyruvate Levels in Brain and Skeletal Muscle During Hyperthermia in Dogs

1971 ◽  
Vol 49 (6) ◽  
pp. 520-524 ◽  
Author(s):  
Robert B. Dunn ◽  
Franco Lioy
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Metabolism ◽  
Free Breathing ◽  
Respiratory Alkalosis ◽  
Tissue Hypoxia ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Lactate And Pyruvate

Tissue hypoxia, as shown by an increase of the arterial concentration of lactate and of the lactate–pyruvate (L/P) ratio, has been observed during hyperthermia in free-breathing animals with high arterial [Formula: see text]. The effect of raising body temperature to 41.9 °C for 2 h on lactate and pyruvate concentrations in arterial, muscle venous, and sagittal sinus blood and cerebrospinal fluid was studied in anesthetized dogs. The animals were paralyzed with gallamine, and arterial pH and [Formula: see text] maintained at normal levels by artificial ventilation with 50% O2[Formula: see text]. A slight increase in lactate and pyruvate took place in the arterial blood and parallel changes were observed both in the muscle venous and sagittal sinus blood. The L/P ratio did not change. Lactate and pyruvate increased markedly in the CSF, without a change in the L/P ratio. Therefore hyperthermia, in the absence of respiratory alkalosis, does not appear to induce tissue hypoxia associated with an increase in L/P ratio. The lack of correlation between lactate and pyruvate concentrations in sagittal sinus blood and cerebrospinal fluid confirms the fact that the A–V differences of these substrates across the brain are not a good index of cerebral metabolism.

Acid-base changes in blood and cerebrospinal fluid during altered ventilation

1961 ◽  
Vol 16 (6) ◽  
pp. 1016-1018 ◽  
Author(s):  
C. R. Merwarth ◽  
H. O. Sieker
Keyword(s):  
Carbon Dioxide ◽  
Cerebrospinal Fluid ◽  
Venous Blood ◽  
Clinical Importance ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Arterial Ph ◽  
The Central Nervous System

Functional abnormalities of the central nervous system are observed with hypo- and hyperventilation. This study correlates changes of pH, carbon dioxide tension and carbon dioxide content in arterial and cerebral venous blood and cerebrospinal fluid during altered ventilation. With the experimental design in which ventilation was controlled and the sagittal sinus, femoral artery, and cisterna magna were cannulated, a slight metabolic acidosis was found. With 10% CO2 inhalation acidosis occurred in both blood and spinal fluid and early in the period of inhalation, the usual cerebrospinal-arterial fluid pCO2 gradient was reversed. With hyperventilation, pH and pCO2 changes were more pronounced in the arterial blood but, as hyperventilation was continued, the arterial-cerebrospinal fluid difference decreased. It appeared likely that brain tissue acts as an important buffer, absorbing and releasing CO2 during states of altered ventilation. CO2 diffuses rapidly across cell boundaries, whereas bicarbonate crosses more slowly, thus providing an explanation for the differences noted between blood and cerebrospinal fluid. The particular clinical importance of these observations is that arterial pH, pCO2, and CO2 content may not accurately reflect changes within the cerebrospinal fluid or brain when ventilation is altered. Submitted on May 1, 1961

Changes in brain surface pH during acute isocapnic metabolic acidosis and alkalosis

1981 ◽  
Vol 51 (2) ◽  
pp. 276-281 ◽  
Author(s):  
S. Javaheri ◽  
A. Clendening ◽  
N. Papadakis ◽  
J. S. Brody
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Interstitial Fluid ◽  
Acid Base ◽  
Surface Ph ◽  
Brain Surface ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean ◽  
The Brain

It has been thought that the blood-brain barrier is relatively impermeable to changes in arterial blood H+ and OH- concentrations. We have measured the brain surface pH during 30 min of isocapnic metabolic acidosis or alkalosis induced by intravenous infusion of 0.2 N HCl or NaOH in anesthetized dogs. The mean brain surface pH fell significantly by 0.06 and rose by 0.04 pH units during HCl or NaOH infusion, respectively. Respective changes were also observed in the calculated cerebral interstitial fluid [HCO-3]. There were no significant changes in cisternal cerebrospinal fluid acid-base variables. It is concluded that changes in arterial blood H+ and OH- concentrations are reflected in brain surface pH relatively quickly. Such changes may contribute to acute respiratory adaptations in metabolic acidosis and alkalosis.

Central infusion of vasopressin decreased plasma vasopressin concentration in dogs

1982 ◽  
Vol 243 (5) ◽  
pp. E365-E369
Author(s):  
B. C. Wang ◽  
L. Share ◽  
J. T. Crofton
Keyword(s):  
Cerebrospinal Fluid ◽  
Physiological Role ◽  
The Other ◽  
Intracerebroventricular Infusion ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Severe Hemorrhage ◽  
Anesthetized Dogs ◽  
Vasopressin Secretion ◽  
Hypertonic Saline Infusion

The effects of increasing the cerebrospinal fluid (CSF) vasopressin concentration (CSFADH) by intracerebroventricular infusion of vasopressin on the plasma vasopressin concentration (PADH) were studied in four groups of anesthetized dogs. One group received an intracerebroventricular infusion of artificial CSF (ACSF) alone for 90 min; the other groups were infused intracerebroventricularly with vasopressin at rates of 10, 20, or 50 microunits/min for 90 min. Arterial blood and CSF samples were taken just before infusion and at 30-min intervals for 210 min. Vasopressin infused intracerebroventricularly at 10, 20, and 50 microunits/min resulted in peak CSFADH of 32.2 +/- 5.3, 82.6 +/- 4.5, and 131.4 +/- 12.5 microunits/ml and reductions in PADH of 32, 47, and 51%, respectively. Only the latter two responses were significant (P less than 0.5-0.01). Because the peak increases in CSFADH after intracerebroventricular infusion of vasopressin ranged from values that were similar to or five times higher than those seen after severe hemorrhage or intracerebroventricular hypertonic saline infusion, we suggest that centrally acting vasopressin may play a physiological role in control of vasopressin secretion.

Cerebrospinal fluid lactate and lactate/pyruvate ratios in hydrocephalus

1976 ◽  
Vol 44 (3) ◽  
pp. 337-341 ◽  
Author(s):  
James E. Raisis ◽  
Glenn W. Kindt ◽  
John E. McGillicuddy ◽  
Carole A. Miller
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Perfusion ◽  
Inverse Relationship ◽  
Redox State ◽  
Anaerobic Metabolism ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Lactate And Pyruvate ◽  
Fine Print

✓ Cerebral metabolism in 21 hydrocephalic patients was studied. Preoperative and postoperative specimens of cerebrospinal fluid (CSF) were obtained and the cerebral perfusion pressure (CPP) was calculated in each instance. The specimens of CSF were analyzed for lactate and pyruvate and the lactate/pyruvate (L/P) ratio was calculated for each sample. The L/P ratio, which reflects the redox state of the cell, was used to determine the extent of anaerobic metabolism. An inverse relationship was noted between CPP and lactate as well as the L/P ratio. In general, the level of anaerobic metabolism was decreased after insertion of a shunt.

Vasopressin in plasma and cerebrospinal fluid of dogs during hypoxia or acidosis

1984 ◽  
Vol 247 (4) ◽  
pp. E449-E455 ◽  
Author(s):  
B. C. Wang ◽  
W. D. Sundet ◽  
K. L. Goetz
Keyword(s):  
Mechanical Ventilation ◽  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Synergistic Effects ◽  
Muscle Paralysis ◽  
Arterial Ph ◽  
Anesthetized Dogs ◽  
Vasopressin Secretion ◽  
Slow Intravenous Infusion ◽  
Mild Hypoxia

Hypoxia and hypercapnia have been shown to cause an increase in the concentration of vasopressin in plasma, but their effects on vasopressin in cerebrospinal fluid (CSF) are not known. In addition, the effect of metabolic acidosis on plasma and CSF vasopressin has not been reported. In this study, plasma and CSF vasopressin levels were measured in anesthetized dogs subjected to either hypoxia, hypercapnia, or metabolic acidosis. Rate and depth of respiration were closely regulated with the aid of muscle paralysis and mechanical ventilation. Vasopressin increased markedly in both plasma and CSF during severe hypoxia (10% O2) and during hypercapnia (10% CO2) but did not change during either mild (15% O2) or moderate (12.5% O2) hypoxia. Although mild hypoxia by itself did not affect either plasma or CSF vasopressin, it did potentiate the increase in plasma and CSF vasopressin that was induced by severe hypercapnia, thus suggesting that hypoxia and hypercapnia may exert synergistic effects on vasopressin secretion. Metabolic acidosis produced by slow intravenous infusion of 1 N hydrochloric acid decreased arterial pH to values comparable to those induced by hypercapnia and increased vasopressin in plasma; CSF vasopressin was unchanged. These results are consistent with the concept that the source of vasopressin secreted into plasma may be different from that secreted into CSF.

Cerebrospinal fluid drainage as influenced by ventricular pressure in the rabbit

1982 ◽  
Vol 56 (6) ◽  
pp. 790-797 ◽  
Author(s):  
J. Gordon McComb ◽  
Hugh Davson ◽  
Shigeyo Hyman ◽  
Martin H. Weiss
Keyword(s):  
Cerebrospinal Fluid ◽  
Indigo Carmine ◽  
Normal Pressure ◽  
Cervical Lymph Nodes ◽  
Content Type ◽  
Cisterna Magna ◽  
Arterial Circulation ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion

✓ Artificial cerebrospinal fluid (CSF) containing radioisotope iodinated (125I) serum albumin (RISA) and either blue dextran or indigo carmine was given to white New Zealand rabbits over 4 hours. In one group it was given by ventriculocisternal perfusion, in one by ventricular infusion, and in one by cisterna magna infusion. Blood was sampled continuously from the superior sagittal sinus (SSS) or intermittently from the systemic arterial circulation. Removal of CSF from the cisterna magna during the ventriculocisternal perfusion kept the intracranial pressure (ICP) at 0 to 5 torr, whereas ventricular or cisterna magna infusion raised the ICP to 20 to 30 torr and 15 to 20 torr, respectively. In the two groups with raised ICP, an increased concentration of RISA was present in the optic nerves, olfactory bulbs, episcleral tissue, and deep cervical lymph nodes; but this was not found in the group with normal ICP. In all three groups, the concentration of RISA in the SSS blood was the same as in the systemic arterial blood. The concentration gradient of RISA across the cerebral cortex was similar in both the ventriculocisternal perfusion and the ventricular infusion groups. With cisterna magna infusion, the concentration of RISA was the same on the cortical surface and less in the ventricles compared with the ventricular infusion. It is concluded that, with elevated ICP, CSF drained via pathways that are less evident under normal pressure. Drainage of CSF was similar irrespective of whether the infusion site was the ventricles or cisterna magna. It did not appear that acute dilatation of the ventricles during ventricular infusion compromised the subarachnoid space over the surface of the hemisphere, as the concentration of RISA on the convexities and in the SSS blood did not significantly differ between the groups. Transcortical bulk transfer of CSF was not evident with raised ICP.

Ventilatory and Circulatory Responses to Hyperthermia in the Mute Swan (CYGNUS OLOR)

1980 ◽  
Vol 88 (1) ◽  
pp. 195-204
Author(s):  
C. BECH ◽  
K. JOHANSEN
Keyword(s):  
Tidal Volume ◽  
Peripheral Resistance ◽  
Respiratory Alkalosis ◽  
Deep Body Temperature ◽  
Cygnus Olor ◽  
Arterial Blood ◽  
Arterial Ph ◽  
End Tidal ◽  
Mute Swans ◽  
Hypocapnic Alkalosis

Ventilatory parameters of mute swans were measured at thermoneutral conditions and during heat stress. Deep body temperature increased from 39·5 to 41·1 °C. Breathing frequency increased 29 times, compared to the thermoneutral condition. Tidal volume decreased to 18 % of the pre-panting value, and the total ventilatory volume increased by 5·4 times. End-tidal PCOCO2 and POO2 values decreased and increased, respectively. The swans developed a slight respiratory alkalosis; arterial Pcoco2 decreased from an average of 27·1 to 25·7 mmHg and arterial pH increased from 7·501 to 7·559. Cardiac output, heart rate and stroke volume were 106%, 154%, and 70%, respectively, of the values at thermoneutrality. Mean arterial blood pressure and total peripheral resistance were slightly reduced. It is concluded that the increased ventilation during panting mainly constitutes dead space ventilation resulting from the great reduction in tidal volume. Parabronchial ventilation remains nearly unchanged, resulting in only a slight hypocapnic alkalosis.

Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

1975 ◽  
Vol 49 (2) ◽  
pp. 157-169
Author(s):  
N. N. Stanley ◽  
B. G. Salisbury ◽  
L. C. McHenry ◽  
N. S. Cherniack
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Liver Failure ◽  
Metabolic Rate ◽  
Ventilatory Response ◽  
Cerebral Metabolism ◽  
Experimental Production ◽  
Arterial Blood ◽  
Ventilatory Response To Co2

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial Pco2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased Pco2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated Pco2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the Pco2 is increased.

Effect of hypoglycemia on cerebral metabolism and carbon dioxide responsivity

1989 ◽  
Vol 256 (3) ◽  
pp. H697-H706 ◽  
Author(s):  
F. E. Sieber ◽  
S. A. Derrer ◽  
C. D. Saudek ◽  
R. J. Traystman
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Metabolism ◽  
Carbon Dioxide Tension ◽  
Cerebrovascular Reactivity ◽  
Cerebral Oxygen ◽  
Cerebral Vasoconstriction ◽  
Sagittal Sinus ◽  
Cerebral Metabolites ◽  
Anesthetized Dogs ◽  
Beta Hydroxybutyrate

This study examined the effects of hypoglycemia (HG) on cerebral metabolism and cerebrovascular reactivity to carbon dioxide. Cerebral blood flow (CBF) was determined using radiolabeled microspheres in pentobarbital-anesthetized dogs. Cerebral oxygen, glucose, lactate, pyruvate, acetoacetate, and beta-hydroxybutyrate uptakes were calculated using the respective concentrations measured in arterial and sagittal sinus blood samples. EEG was recorded throughout each experiment. HG was induced with insulin to obtain a blood glucose less than 30 mg/100 ml. Hypercapnia was studied in 10 animals (3 control, 7 HG) by increasing arterial carbon dioxide tension (PaCO2) from control (35 +/- 4; mean +/- SE) to 54 +/- 2 Torr during normoglycemia (NG) and HG. Hypocapnia was studied in 11 animals (3 control, 8 HG) by decreasing PaCO2 from control (39 +/- 1) to 14 +/- 1 Torr in NG and HG. Measurements were taken after reaching steady-state PaCO2 in both groups at each control and altered PaCO2 state. In the hypercapnic group, glucose decreased from 71 +/- 3 to 28 +/- 3 mg/100 ml. CBF increased with hypercapnia to 175% of control in both NG and HG. Cerebral metabolic rate of oxygen and electroencephalogram (EEG) did not change in the hypercapnic group. In the hypocapnic group glucose decreased from 71 +/- 3 to 19 +/- 2 mg/100 ml. CBF decreased with hypocapnia to 62 +/- 5% of control in NG but remained at control in HG. This was not accompanied by changes in cerebral oxygen consumption; however, a flat EEG occurred in all HG hypocapnic animals. No change occurred in uptake of the other cerebral metabolites measured in any group. This study shows that the CBF hypercapnic response remains intact during HG; however, hypocapnia causes severe EEG disturbances and impairs the cerebral vasoconstriction response.

Diuretic response to acute hypoxia in the conscious dog

1982 ◽  
Vol 243 (5) ◽  
pp. F440-F446 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Blood Pressure ◽  
Acute Hypoxia ◽  
Respiratory Alkalosis ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Hypoxic Exposure ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Prostaglandin Release ◽  
Diuretic Response

Experiments were performed to determine the renal effects of acute hypoxia in conscious normovolemic dogs. Dogs were made hypoxic and also became hypocapnic through increased ventilation. Hypocapnic hypoxia was associated with increased urine flow, arterial blood pressure, cardiac output, PAH and inulin clearance, and electrolyte excretion. Urinary excretion of prostaglandin E2 (PGE2) also increased during hypocapnic hypoxia. To test whether the respiratory alkalosis accompanying hypoxic exposure was important in mediating the observed response, experiments were conducted in which the dogs were hypoxic but remained isocapnic via addition of CO2 to the inspired gas. Urine flow increased and was associated with changes in renal function and hemodynamics similar to those during hypocapnic hypoxia. Experiments were also conducted to determine whether the increased PGE2 release in hypoxia was functionally significant. Dogs were pretreated with meclofenamate and then made hypoxic. Prostaglandin synthesis inhibition did not alter the renal response to hypocapnic hypoxia. Dogs were also treated chronically with propranolol in an attempt to blunt the rise in blood pressure during hypoxia. In dogs with only a small transient increase in blood pressure, the diuresis was blocked. It is concluded that systemic hypoxia results in a mild diuresis in the conscious normovolemic dog. This response occurs independent of changes in arterial pH or renal prostaglandin release. The diuretic effect of hypoxia is probably due to increased renal perfusion pressure and resultant increased filtration.

Sign in / Sign up

Export Citation Format

Share Document