EFFECT OF CARBON DIOXIDE (HYPOCAPNIA AND HYPERCAPNIA) ON REGIONAL MYOCARDIAL TISSUE OXYGEN TENSION IN THE DOG

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A486
Author(s):  
K. Okazaki ◽  
K. Hashimoto ◽  
Y. Okutsu ◽  
A. F. Fukunaga
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Tension ◽  
Tissue Oxygen Tension ◽  
Myocardial Tissue ◽  
Tissue Oxygen

A549 EFFECT OF CARBON DIOXIDE (HYPOCAPNIA AND HYPEPXAPNIA) ON REGIONAL MYOCARDIAL TISSUE OXYGEN TENSION IN DOGES WITH CORONARY STENOSIS

1990 ◽  
Vol 73 (3A) ◽  
pp. NA-NA
Author(s):  
K. Okazaki ◽  
K. Hashimoto ◽  
Y. Okutsu ◽  
F. Okumura ◽  
A. F. Fukunaga
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Tension ◽  
Coronary Stenosis ◽  
Tissue Oxygen Tension ◽  
Myocardial Tissue ◽  
Tissue Oxygen

scholarly journals Adenosine and amrinone reverse felypressin-induced depression of myocardial tissue oxygen tension in dogs

2000 ◽  
Vol 47 (11) ◽  
pp. 1107-1113 ◽  
Author(s):  
Masataka Kasahara ◽  
Tatsuya Ichinohe ◽  
Yuzuru Kaneko
Keyword(s):  
Oxygen Tension ◽  
Tissue Oxygen Tension ◽  
Myocardial Tissue ◽  
Tissue Oxygen

scholarly journals Peritoneal tissue-oxygen tension during a carbon dioxide pneumoperitoneum in a mouse laparoscopic model with controlled respiratory support

2007 ◽  
Vol 22 (4) ◽  
pp. 1149-1155 ◽  
Author(s):  
Nicolas Bourdel ◽  
Sachiko Matsuzaki ◽  
Jean-Etienne Bazin ◽  
Jean-Luc Pouly ◽  
Gérard Mage ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Tension ◽  
Tissue Oxygen Tension ◽  
Respiratory Support ◽  
Tissue Oxygen ◽  
Carbon Dioxide Pneumoperitoneum ◽  
Peritoneal Tissue

Effects of Profound Anemia on Brain Tissue Oxygen Tension, Carbon Dioxide Tension, and pH in Rabbits

2001 ◽  
Vol 13 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Yasuhiro Morimoto ◽  
Mali Mathru ◽  
Julian F. Martinez-Tica ◽  
Mark H. Zornow
Keyword(s):  
Carbon Dioxide ◽  
Brain Tissue ◽  
Oxygen Tension ◽  
Carbon Dioxide Tension ◽  
Tissue Oxygen Tension ◽  
Tissue Oxygen ◽  
Brain Tissue Oxygen ◽  
Brain Tissue Oxygen Tension

Measurement of Nitric Oxide and Brain Tissue Oxygen Tension in Patients after Severe Subarachnoid Hemorrhage

Neurosurgery ◽  
2001 ◽  
Vol 49 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Ahmad Khaldi ◽  
Alois Zauner ◽  
Michael Reinert ◽  
John J. Woodward ◽  
M. Ross Bullock
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Oxygen Tension ◽  
Carbon Dioxide Tension ◽  
Tissue Oxygen Tension ◽  
Tissue Oxygen ◽  
Brain Tissue Oxygen ◽  
Brain Tissue Oxygen Tension

Abstract OBJECTIVE Nitric oxide (NO), one of the most powerful endogenous vasodilators, is thought to play a major role in the development of delayed vasospasm in patients with subarachnoid hemorrhage (SAH). However, the role of the production of cerebral NO in patients with SAH is not known. In other SAH studies, NO metabolites such as nitrite and nitrate have been demonstrated to be decreased in cerebrospinal fluid and in plasma. METHODS In this study, a microdialysis probe was used, along with a multiparameter sensor, to measure NO metabolites, brain tissue oxygen tension, brain tissue carbon dioxide tension, and pH in the cortex of patients with severe SAH who were at risk for developing secondary brain damage and vasospasm. NO metabolites, glucose, and lactate were analyzed in the dialysates to determine the time course of NO metabolite changes and to test the interrelationship between the analytes and clinical variables. RESULTS Brain tissue oxygen tension was strongly correlated to dialysate nitrate and nitrite (r2 = 0.326;P < 0.001); however, no correlation was noted between brain tissue oxygen tension and NO metabolites in cerebrospinal fluid (r2 = 0.018;P = 0.734). No significant correlation between NO production, brain tissue carbon dioxide tension, and dialysate glucose and lactate was observed. CONCLUSION Cerebral ischemia and compromised substrate delivery are often responsible for high morbidity rates and poor outcomes after SAH. The relationship between brain tissue oxygen and cerebral NO metabolites that we demonstrate suggests that substrate delivery and NO are linked in the pathophysiology of vasospasm after SAH.

Effects of Temperature on Cerebral Tissue Oxygen Tension, Carbon Dioxide Tension, and pH during Transient Global Ischemia in Rabbits 

1998 ◽  
Vol 88 (2) ◽  
pp. 403-409 ◽  
Author(s):  
Andreas Bacher ◽  
Jae Young Kwon ◽  
Mark H. Zornow
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Ischemia ◽  
Oxygen Tension ◽  
Random Sequence ◽  
Carbon Dioxide Tension ◽  
Tissue Oxygen Tension ◽  
Global Cerebral Ischemia ◽  
Moderate Hypothermia ◽  
Tissue Oxygen ◽  
Cerebral Tissue

Background A decrease in brain temperature (Tbrain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (PO2 brain), carbon dioxide tension (PCO2 brain), and pH (pHbrain) were monitored during short episodes of global cerebral ischemia. Methods After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (alpha-stat). A sensor to measure PO2 brain, PCO2 brain, pHbrain, and Tbrain was inserted into the brain through a burr hole in the skull. Tbrain was adjusted to 38 degrees C, 34.4 degrees C, and 29.4 degrees C in a random sequence in each animal. PO2 brain, PCO2brain, and pHbrain (all variables are reported at the actual Tbrain) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of Tbrain. Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means +/- SD. Results During ischemia, PO2 brain decreased from 56 +/- 3 to 33 +/- 2 mmHg at 38 degrees C, from 58 +/- 3 to 32 +/- 3 mmHg at 34.4 degrees C, and from 51 +/- 2 to 32 +/- 2 mmHg at 29.4 degrees C (p = NS). PCO2 brain increased by 6.7 +/- 2 mmHg at 38 degrees C, by 5.1 +/- 1.4 mmHg at 34.4 degrees C, and by 2.3 +/- 0.8 mmHg at 29.4 degrees C. pHbrain inversely followed the trend of PCO2 brain. Conclusions The attenuated increase in PCO2 brain during hypothermic ischemia results from the reduced CMRO2. The similar decrease in PO2 brain at all temperature levels indicates that despite the reduction in CMRO2, PO2 brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.

scholarly journals Felypressin-induced reduction in coronary blood flow and myocardial tissue oxygen tension during anesthesia in dogs

1999 ◽  
Vol 46 (11) ◽  
pp. 1070-1075 ◽  
Author(s):  
Hideharu Agata ◽  
Tatsuya Ichinohe ◽  
Yuzuru Kaneko
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Tissue Oxygen Tension ◽  
Myocardial Tissue ◽  
Tissue Oxygen
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