Mechanisms of myocardial hypercarbic acidosis during cardiac arrest

1995 ◽  
Vol 78 (4) ◽  
pp. 1579-1584 ◽  
Author(s):  
B. A. Johnson ◽  
M. H. Weil ◽  
W. Tang ◽  
M. Noc ◽  
D. McKee ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Myocardial Ischemia ◽  
Rat Model ◽  
Co2 Production ◽  
Co2 Removal ◽  
Rat Hearts ◽  
Regional Myocardial Ischemia

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.

Deep hypothermia in the cat

1959 ◽  
Vol 196 (2) ◽  
pp. 354-356 ◽  
Author(s):  
Arthur F. Battista
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Body Temperature ◽  
Deep Hypothermia ◽  
Critical Parameters ◽  
Large Animal ◽  
Carbon Dioxide Concentrations ◽  
Adult Cats ◽  
Body Cooling

Sixteen adult cats were cooled, using the method of hypercapnia and hypoxia. Seven cats died during the cooling or warming period due to irreversible ventricular fibrillation or cardiac arrest. Nine cats survived and the lowest body temperature obtained was 12.5°C. The rate of body cooling and the oxygen and carbon dioxide concentrations were critical parameters difficult to control in a large animal such as the cat.

scholarly journals Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jun Jiang ◽  
Xiangshao Fang ◽  
Yue Fu ◽  
Wen Xu ◽  
Longyuan Jiang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Cardiopulmonary Resuscitation ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Rat Model ◽  
Mitochondrial Function ◽  
High Energy ◽  
Mitochondrial Morphology ◽  
High Energy Phosphates

Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.

Dependence of ventricular fibrillation propensity on coronary blood flow without myocardial ischemia

1981 ◽  
Vol 101 (4) ◽  
pp. 440-449 ◽  
Author(s):  
Alexandros C. Kralios ◽  
William J. Bugni ◽  
Mary Ann McDonnell ◽  
Theofilos J. Tsagaris ◽  
Hiroshi Kuida
Keyword(s):  
Blood Flow ◽  
Ventricular Fibrillation ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow

Effects of atrial pacing on regional myocardial gas tensions with critical coronary stenosis

1977 ◽  
Vol 232 (1) ◽  
pp. H49-H53 ◽  
Author(s):  
J. B. O'Riordan ◽  
J. T. Flaherty ◽  
S. F. Khuri ◽  
R. K. Brawley ◽  
B. Pitt ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Stenosis ◽  
Oxygen Demand ◽  
Myocardial Oxygen Demand ◽  
Atrial Pacing ◽  
Myocardial Layers ◽  
Regional Myocardial Ischemia ◽  
Stenosed Vessel

Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a “critical stenosis” resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.

Cardiac microdialysis to estimate interstitial adenosine and coronary blood flow

1990 ◽  
Vol 258 (6) ◽  
pp. H1642-H1649 ◽  
Author(s):  
D. G. Van Wylen ◽  
J. Willis ◽  
J. Sodhi ◽  
R. J. Weiss ◽  
R. D. Lasley ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Fold Increase ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Simultaneous Estimation ◽  
Microdialysis Probe ◽  
Regional Myocardial Ischemia

The purpose of this study was twofold: 1) to investigate the feasibility and usefulness of cardiac microdialysis for the simultaneous estimation of regional cardiac interstitial fluid (ISF) adenosine (ADO) concentration and coronary blood flow (CBF); and 2) to determine the changes in the ISF levels of ADO and CBF during cardiac stimulation or regional myocardial ischemia. Cardiac microdialysis probes were implanted in the left ventricular myocardium of chloralose-urethan-anesthetized dogs and perfused with Krebs-Henseleit buffer. The concentration of ADO in the effluent dialysate was used as an index of intramyocardial ISF ADO concentration while local CBF was measured by H2 clearance via a platinum wire within the dialysis fiber. Dialysate ADO was elevated immediately after insertion of the microdialysis probe, declined rapidly in the first 20 min, stabilized by 60 min, and remained constant for 2 h. Based on the relationship in vitro and in vivo between microdialysis probe perfusion rate and dialysate ADO concentration, ISF ADO concentration within the left ventricular myocardium was estimated to be 0.9-1.3 microM. Dobutamine (10 micrograms.kg-1.min-1) infusion resulted in a 36% increase in CBF and a 2.5-fold increase in dialysate ADO (n = 9; P less than 0.05). Regional myocardial ischemia, induced by occlusion of the left anterior descending artery (LAD), caused a 13-fold increase in dialysate ADO in the LAD perfused myocardium (n = 9; P less than 0.05). These results are consistent with the ADO hypothesis and suggest that cardiac microdialysis provides a reliable technique for the sampling of regional intramyocardial ISF.

Adrenergic influences on cardiac function during ventricular fibrillation in isolated rat hearts

1991 ◽  
Vol 261 (5) ◽  
pp. H1452-H1456
Author(s):  
I. Derad ◽  
I. Funk ◽  
P. Pauschinger ◽  
J. Born
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Ventricular Fibrillation ◽  
Cardiac Function ◽  
Coronary Blood Flow ◽  
High Energy ◽  
High Energy Phosphates ◽  
Tissue Concentrations ◽  
Rat Hearts ◽  
Isolated Rat

Effects of norepinephrine (NE, 10(-6) M), epinephrine (E, 10(-6) M), and vehicle on coronary blood flow (CF), oxygen consumption, and lactate release were compared in 32 isolated rat hearts during 5 min of ventricular fibrillation (VF). After VF, tissue concentrations of ATP, AMP, creatinine phosphate (CP), and lactate were measured. Perfusion of treatments started 30 s after onset of VF and was maintained throughout VF. CF during VF was greater (P less than 0.005) during perfusion of E (mean +/- SE, 5.73 +/- 0.15 ml/min) than NE (5.06 +/- 0.32 ml/min) or vehicle (5.11 +/- 0.18 ml/min). Oxygen consumption during VF was higher during perfusion of E (29.5 +/- 0.9 microliters.min(-1).g wet heart wt(-1)) than vehicle (27.3 +/- 0.7 microliters.min(-1).g(-1); P less than 0.05); average oxygen consumption during NE (27.6 +/- 1.4 microliters.min(-1).g(-1)) and vehicle were comparable. After NE, but not E, tissue AMP concentrations were significantly increased, and CP concentrations were reduced compared with vehicle (P less than 0.05). Enhanced consumption of high-energy phosphates during NE suggests that there is also an enhanced demand for oxygen. However, unlike during E, during NE this demand is not met by an augmented CF. Thus, compared with E, NE treatment during VF may increase the risk of hypoxic damage.

Abstract 289: Relationship Between Myocardial Glycogen Concentrations and Amplitude Spectrum Area During Ventricular Fibrillation in a Rat Model of Cardiac Arrest and Resuscitation

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Qiaohua Hu ◽  
Xiangshao Fang ◽  
Zhengfei Yang ◽  
Wanchun Tang
Keyword(s):  
Cardiac Arrest ◽  
Energy Metabolism ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Glycogen Content ◽  
Amplitude Spectrum ◽  
High Energy ◽  
Myocardial Energy Metabolism ◽  
Spectrum Area ◽  
The Relationship

Introduction: Myocardial high-energy phosphate (ATP) levels has been demonstrated correlating with amplitude spectrum area (AMSA) during ventricular fibrillation (VF) in previous experimental studies. In the present study, we investigated the relationship between AMSA and myocardial glycogen content (MGC),which can be used to reflect the status of myocardial energy metabolism indirectly during VF. Hypothesis: AMSA has a significantly correlation with MGC during VF in a rat model of cardiac arrest and resuscitation. Methods: Twenty male Sprague-Dawley rats weighing 350 to 450 g were utilized and randomized into two groups: VF and cardiopulmonary resuscitation (CPR) (VF/CPR group) or untreated VF (VF group). 5 mins of CPR was performed after 10 mins of untreated VF in VF/CPR animals. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 mins were calculated from ECG signals. The rats’ hearts were quickly removed at the predetermined time of 15 min for determines the glycogen contents by the anthrone reagent method using a glycogen assay kit. Results: AMSA values significantly decreased during untreated VF in both VF and VF/CPR animals. However, much greater AMSA during CPR was achieved by the VF/CPR group in comparison with the VF group. There was a marked and negative relationship between AMSA at VF 15 min and MGC. (Figure). Conclusion: MGC was significantly and negatively correlated with AMSA during VF in this rat model of cardiac arrest and resuscitation. In clinical practice, we can use AMSA to reflect the state of myocardial energy metabolism indirectly. Figure The changes of AMSA and relationship between AMSA and glycogen content:(A) The change of AMSA between VF/CRP group and VF group;(B) The relationship between AMSA and glycogen content. AMSA, amplitude spectrum area; V, time of ventricular fibrillation; # p <0.05 vs. V4.

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