Ischemic Reperfusion Injury

The term, ischemia, denotes inadequate blood supply to tissues due to blockage of the arterial inflow, while, reperfusion injury is defined as the injury caused by the restitution of blood flow after an ischemic peroid, leading to death of cells that were only reversibly injured at the time of blood flow restitution. [63]. The final infarct size after an MI event is therefore the result of the ischemic and reperfusion damage. For this reason, the term that best describes this process of myocyte death in reperfused MI is myocardial ischemia/reperfusion (I/R) injury [64]. In the early hours post myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which activate the G

Because the PCO2 levels are too high the body is not getting the adequate amount of oxygen. This means the oxygen-carrying hemoglobin is not working properly do to the excessive amounts carbon dioxide causing respiratory acidosis.

When tissue injury occurs, a network of chemical signals activate a host response which is designed to protect and heal the damaged tissues (i.e. inflammation) (Coussens & Werb, 2002). This process involves the activation and migration of leukocytes (neutrophils, monocytes, and eosinophils) to the site of damage as well as recruitment of tissue mast cells (Coussens & Werb, 2002). Additionally, this inflammatory response involves migration of macrophage progenitors, which travel through the venous system to the site of injury. This migratory process is directed to the site of tissue damage by a host of chemotactic factors, among these are cytokines including interleukin-1β (IL-1β) and

Also Cytokines an be secreted by a variety of cells including neutrophils, activated macrophages, fibroblasts, endothelial cells and damaged muscle cells. The physiological response to tissue injury is inflammation, which involves the production of cytokines. .These soluble molecules will enhance the arrival of neutrophils, monocytes and lymphocytes to the damaged muscle tissue. Cytokine ruesponse depends on type of exercise, intensity, duration, recovery between exercise bouts and training status. cytokines is playing a significant role in both destruction and repair processes on damaged tissues. Some data reported that when IL-6 is secreted by muscle, it has been shown that it increases anti-inflammatory cytokines such as IL-10 and IL-1ra (Powers, 2012, Calle, M.,& Luz, F.,

The response to a SCI can be separated into three discrete, partially overlapping phases: acute (seconds to minutes after SCI), sub-acute (minutes to weeks after SCI), and chronic (months to years after SCI). The acute phase centers around the primary SCI damage resulting from the trauma, resulting in immediate physical and biochemical cellular changes. These include direct cell death, vasospasms (leads to vasoconstriction, ischemia, and tissue death), plasma membrane compromise, disruption of ionic homeostasis, and accumulation of neurotransmitters (26, 27). Many local immune cells such as microglia, neutrophils, and astrocytes respond instantly. While some acute events continue into the sub-acute phase (such as neurotransmitter and ionic dysregulation), the sub-acute and chronic phases are defined by the

In an in vitro model of cerebral ischemia, increase of miR-497 expression following oxygen-glucose deprivation, correlated with increased cell death and down regulation of its anti-apoptotic proteins, Bcl2 and Bclw [17]. Temporal regulation of miRNA expression has been shown in the brain of rat models subjected to middle cerebral artery occlusion (MCAo) [20]. An up regulation of the anti-apoptotic miR-21 has been shown to protect neurons from death in cerebral ischemic model. The temporal and biphasic regulation of these miRNAs have been proposed to play a crucial role either in the acute injury phase or the late recovery phase [16]. In addition, biphasic expression of miRNAs has also been demonstrated in the same animal models. Cerebral ischemia

Local cardiac preconditioning or postconditioning has been shown to have direct cardioprotective effects against myocardial ischemia and reperfusion (I/R) injury. Likewise, remote ischemic pre- or post-conditioning is a phenomenon whereby brief episodes of short periods of ischemia/reperfusion stimuli executed in distant tissues or organs may exert protective effects in the heart and render the myocardium more tolerant to a subsequent sustained episode of ischemia or reperfusion injury. Studies have shown that this remote cardioprotective trigger can be used in distant vascular beds (lower and upper limbs, cerebral, renal, mesenteric, intestinal, renal and abdominal arteries)1. However, it is unclear whether brief ischemic conditioning of visceral organs such as the liver, the largest metabolic organ in the body, can produce cardioprotection. A few reports have shown that liver

Adenosine is probably the main mediator of local IPC-mediated renoprotection and exerts its beneficial effect via activation of the adenosine receptor (AR) subtypes A2A and A2B.8, 9 Subsequent activation of the PI3K/Akt pathway is essential for IPC-mediated early renoprotection.4 In analogy to what has been extensively studied in the heart, this pathway improves cell survival by enhancing GSK-3ß phosphorylation, activating the mitochondrial K(ATP) channel and protecting against opening of mitochondrial permeability transition

Critical events in ischemic cascade. Adapted from Midori et al. (2012) (17). Following ischaemia, the deprivation of oxygen and glucose to the brain lead to loss of ATP (energy loss) and ion pump failure. The loss of ion concentration gradients causing to cytotoxic oedema and releasing of excitatory amino acids (EAAs). Following glucose lessening cell aerobic metabolism switch to anaerobic, which resulting to metabolic acidosis. All of these events lead to cell death, or necrosis. Ischaemia also caused to the upregulation and activation of many immediate early genes and stress signals, which lead to inflammatory responses, cell apoptosis and, subsequently, activation of matrix metalloproteinases (MMPs) as a damaging protease which can lead

As blood pressure rises and “the blood moves with enough force, [it] increases the chances of tearing that plaque loose” and rupturing it (Sapolsky, 2004, p. 45). When a rupture occurs, the material that has become loose, a blood clot known as a thrombus, can pose as much more of a threat to a person’s life than the initial build up of plaque. If the thrombus blocks a coronary vessel then the heart muscle is unable to receive blood that is full of needed oxygen and other essential nutrients, this is known as cardiac ischemia (Steffen, Lecture 11). Ischemia can cause angina and discomfort. Another possible result of a blocked coronary artery is a heart attack, which can lead to death, and if a blood vessel in the brain is clogged then a stoke will occur.

* The type of proteins in the cell membrane that was involved in homeostatic imbalance of his heart cells were ATP. There was no ATP, so it affected the pumps in the membrane. The calcium levels rose, and it caused proteases to spill into the interior of the cell, attacking the cytoskeleton. This caused the lysosome enzymes to digest the plasma membranes and membranes of the organelles.

This paper will discuss the effects perfusion has on the body as well as the multiple body systems that are effected from poor perfusion. We will be looking at the relationships between profusion as it relates to ischemic stroke, myocardial infarction, and tuberculosis. This paper will use online journal entries from EPSCO as well as off line entries from Lewis to help us find a better understanding into the related topics at hand. Lastly I will discuss stroke in depth as it pertains to my clinical experience and explain the strong link profusion has on ischemic stroke and the measures used to retain brain tissue. We will look at research done by Agarwal, Smriti (2015) that looks at the effectiveness and time saving procedures researched by his team when detecting stroke as well as research done by Dong, Hongli (2015) that shows a strong correlation between vitamin b12 and folic acid and the prevention of an ischemic event.

Ren et al. studied the effects of dexmedetomidine on seven-day old Sprague Dawley rats with left brain HI [3]. Various times after brain hypoxic ischemia, Sprague Dawley rats were given intraperetoneal Dex and were evaluated 7, 28 and 43 days after the brain hypoxia-ischemia. Intaperetoneal Dexmedetomidine dereased the brain cell and tissue loss as well as neurological and cognitive dysfunction when records were examined from 28 days after brain HI. This result has proved that post treatment by Dex confers neuroprotection against hypoxia-ischemia brain injury in neonatal rats which was possible because of inhibition of inflammation in the ischemic brain tissues through the activation of α2-adrenergic

We acknowledge several limitations of this study. First, we used only one liver ischemic intervention protocol, i.e. three cycles of 5 min ischemia/5 min reperfusion; thus, it remains unknown whether other liver stimuli strategies can produce cardioprotection. Second, we did not use all three liver ischemic conditioned hearts for immunohistochemical analysis. Rather, we used only RPre+RPost treated hearts, to prove the concept that liver conditioning can inhibit apoptosis in the myocardium. Thus, it remains unknown whether RPre or RPost alone can affect apoptotic protein expression after I/R injury. In addition, the mechanisms by which remote liver conditioning enhance cytoprotective actions seem to be related to MAPK signaling pathways, since

The major effect of acidosis is depression of the central nervous system. When the pH of the blood falls below 7.35, the central nervous system malfunctions, and the individual becomes disoriented and possibly comatose as the condition worsens. Causes for acidosis include things such as; obesity, disease of the airway and diseases involving the chest. (Hadjiliadis, 2014)