Interdependence Between Cardiac Function, Oxygen Demand, and Supply

Author(s):  
Joseph S. Janicki ◽  
Karl T. Weber ◽  
Ponnambalam Sundram
2007 ◽  
Vol 103 (4) ◽  
pp. 1352-1358 ◽  
Author(s):  
Kazuto Masamoto ◽  
Jeff Kershaw ◽  
Masakatsu Ureshi ◽  
Naosada Takizawa ◽  
Hirosuke Kobayashi ◽  
...  

To investigate the dynamics of tissue oxygen demand and supply during brain functions, we simultaneously recorded Po2 and local cerebral blood flow (LCBF) with an oxygen microelectrode and laser Doppler flowmetry, respectively, in rat somatosensory cortex. Electrical hindlimb stimuli were applied for 1, 2, and 5 s to vary the duration of evoked cerebral metabolic rate of oxygen (CMRO2). The electrical stimulation induced a robust increase in Po2 (4–9 Torr at peak) after an increase in LCBF (14–26% at peak). A consistent lag of ∼1.2 s (0.6–2.3 s for individual animals) in the Po2 relative to LCBF was found, irrespective of stimulus length. It is argued that the lag in Po2 was predominantly caused by the time required for oxygen to diffuse through tissue. During brain functions, the supply of fresh oxygen further lagged because of the latency of LCBF onset (∼0.4 s). The results indicate that the tissue oxygen supports excess demand until the arrival of fresh oxygen. However, a large drop in Po2 was not observed, indicating that the evoked neural activity demands little extra oxygen or that the time course of excess demand is as slow as the increase in supply. Thus the dynamics of Po2 during brain functions predominantly depend on the time course of LCBF. Possible factors influencing the lag between demand and supply are discussed, including vascular spacing, reactivity of the vessels, and diffusivity of oxygen.


2021 ◽  
Vol 8 (5) ◽  
pp. 835
Author(s):  
Jhansi Rani Kotha ◽  
Hari Krishna Kothapally ◽  
Sai Chand Pinnoju ◽  
Sudheer Kumar

Background: Shock is a state of impaired tissue perfusion which result in an imbalance between oxygen demand and supply. This reduction in effective tissue perfusion causes insufficient or improper delivery and distribution of oxygen and nutrients. There is sparse date regarding epidemiology of shock in paediatrics. In this study we were aimed to assess the types of shock and treatment of shock with Inotropes.Methods: Children of age 1 month to 12 years with a clinical diagnosis of shock were included.Results: Out of 155 children admitted with shock 72.2% had septic shock, 25.8% had hypovolemic shock, 1.2% had cardiogenic shock, 0.6% had dengue shock. In this study the mortality rate was 8.39% of total patients. The mortality rate of septic shock, hypovolemic shock, cardiogenic shock was 84%, 7.69%, 7.69% respectively. 74.33% of patients were treated with two Inotropes, 5.3% were treated with more than two Inotropes, 11.5% were treated with single Inotropes and 0.88% was treated with no inotrope.Conclusions: In the present study, among all types of shock the prevalence and mortality rate was more with Septic shock. As shock has high mortality rate in children the early recognition and patient education is required.


2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Ramon Diaz Trelles ◽  
Maria Cecilia Scimia ◽  
Pilar Ruiz Lozano ◽  
Mark Mercola

Cardiac microvasculature density is critical for a correct cardiac function under normal and stress conditions. We found that the transcription factor RBPJ, downstream of the Notch signalling, can regulate angiogenic factors gene expression by repression (normal homeostasis) or activation (stress) and also by modulating the hypoxia induced angiogenic response. Accordingly, in normal conditions cardiomyocyte specific RBPJ KO adult mice hearts show a denser microvasculature. Isolated mouse adult cardiomyocytes show increased gene expression and promoter hyperacetylation and hypermethylation of angiogenic factors and Notch target genes (like HES1). Stress induced by myocardial infarction (MI) or cardiac overload (TAC) activate an angiogenic response to compensate the increased oxygen demand. Notch pathway is activated and RBPJ accumulated in the nucleus after MI and TAC. After TAC, deletion of RBPJ did not block hypertrophy induction, but prevented the increase in angiogenic factor production and microvessel density that normally occurs in response to increased workload. Remarkably, the KO preserved cardiac function and reduced cell death and fibrosis after myocardial infarction. Thus, RBPJ acts in cardiomyocytes as a master factor orchestrating homeostatic and disease-induced angiogenesis, and modulating RBPJ protects against ischemic injury.


1981 ◽  
Vol 12 (4) ◽  
pp. 193-197 ◽  
Author(s):  
Robert J. Fleischaker ◽  
Anthony J. Sinskey

2018 ◽  
Vol 44 (08) ◽  
pp. 780-786 ◽  
Author(s):  
Emmanuel Favaloro ◽  
Fabian Sanchis-Gomar ◽  
Giuseppe Lippi

AbstractAlthough few doubts remain that physical exercise should be widely promoted for maintenance of health and fitness, the risk of adverse events such as sudden death (especially due to cardiac causes, i.e., sudden cardiac death [SCD]) during exercise remains tangible. The overall risk of sudden death in athletes is relatively low (i.e., usually comprised between 0.1 and 38/100,000 person-years), and globally comparable to that of the general population. However, up to 20% of all sudden death cases are still recorded while exercising. The most frequent underlying disorders encountered in SCD are hypertrophic cardiomyopathy and coronary artery disease (CAD), representing three quarters of all conditions. The risk related to CAD increases with aging (>35 years old), while that attributable to cardiomyopathies or fatal arrhythmias is especially frequent among young people (<35 years old). Taken together, these findings would lead to the conclusion that physical exercise may be seen as an acute trigger of myocardial ischemia or arrhythmias in some predisposed individuals. Nonetheless, the prevalence of coronary atherosclerosis seems to be higher in athletes than in sedentary subjects with comparable risk profile. On the contrary, coronary plaques in physically active subjects appear more stable, thereby attenuating the risk of rupture and subsequent myocardial ischemia. These findings, along with evidence of a considerable increase of peak coronary blood flow during exercise, make it very likely that an imbalance between oxygen demand and supply may be the most frequent cause of myocardial ischemia in athletes suffering SCD and/or cardiac arrest. Therefore, all subjects who wish to practice moderate- to high-intensity exercise are recommended to undergo preparticipation screening and annual follow-up.


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