Teams that affect microcirculation and tissue perfusion with microsurgical techniques must think at the cell level. Teams that lack such a perspective and cannot understand the event as just "cutting it down" or "putting it to sleep and waking it up" and not reducing it to the cell level will be doomed to failure.
Why do I insist on the cell level?
Let's talk about it briefly?
The issue lies in energy sharing, which is the main point of everything. It transports the oxygen and sugar in the air to the cell mitochondria, where it passes through the Krebs cycle and extracts 38 ATP to use it for the survival of the cell. Of course, it is not enough to ensure a hemodynamically balanced condition
during this procedure. At the same time, it is necessary to avoid agents that will damage the complex of five enzymes involved in energy production in mitochondria. We can explain these two facts with the following examples
. When cardiac output decreases, the biggest example is the decrease in systolic blood pressure.
The mitochondrial complex1 is damaged and sufficient ATP cannot be produced. Or if you use nitrous oxide
the same system cannot produce enough ATP and the DNA sequence changes. In that case, we will not reduce cardiac output
we will ensure blood fluidity and we will not use agents that will damage the mitochondrial enzyme system
We need to make an intervention that will prevent the free oxygen
radicals that occur as a result of ischemia-reperfusion injury.
In the meantime, the surgeon should avoid unnecessary surgical trauma. Because the vascular endothelium is the same
Acts like an endocrine organ. Mediators such as EDRF, endothelin, and thromboxane released from the endothelium will negatively affect blood fluidity. Particularly in a traumatized patient, factors such as hypovolemia, pain, and heat loss will activate the sympathetic system and cause deterioration in tissue oxygenation over time. Although we prevent all these negativities
we sometimes fail in cases of transplantation, replantation or major trauma.
Our research on this subject shows that the event occurs as a result of negative interactions at the cellular level
we thought. Our Chinese colleagues who researched this issue before us
They have moved the extent of pathological developments beyond mitochondria. Free radicals arising after ischemia-reperfusion injury increased the release of stochrome c from mitochondria and caused apoptosis by causing activation of the caspase family through stimulation of APAF 1. Apoptosis
means the cleaning of the leaves in the autumn. It is removed from the body by an autonomous mechanism
unwanted cells that are aging or infected with viruses and bacteria in a certain harmony
energy-consuming and time-indexed.
Genetic, drug, environmental factors, ionizing radiation and ischemia reperfusion damage are the most important factors that affect apoptosis.
In situations that create stress in the cell. It is stimulated in the endoplasmic reticulum just like the mitochondrial pathway
and activates mediators such as caspase 8 and 10, resulting in apoptosis. While a part of the caspase family plays a role in cell death, another part plays a role in cell repair. As examples of caspases that play a role in cell death, it is possible to group them as caspase 8-10 (DAD) and those that are effective in cell repair as caspase 2-
9 (CARD).
These responses given by the cellular organelles of the patient who is exposed to stress as a result of trauma
must be taken into consideration. One of the enzyme family that prevents the activation of caspases is the apoptosis
inhibitory factor. This is called the neuronal apoptosis inhibition program (NAIP) in the nerve tissue.
Its names are survivin and lıvin. Bcl family proteins have effects in both directions. While those collected under group B, called bad, bak and blk
, cause apoptosis, bcl, 2bcl
in group A are effective in antiapoptosis. Most of them sit on the outer mitochondrial membrane through the apoptotic program. For example
Caspase 12 is triggered by the endoplasmic reticulum and initiates apoptosis
during stress. It plays a major role in diseases affecting the nervous system such as Alzheimer's.
Cisplatin, calcium, endoplasmic reticulum. plays a role in stress. The protein called poly (ADP-ribose) polymerase
causes apoptosis in high amounts, while it causes inhibition
in low concentrations. Neurodegenerative diseases, aids and ischemia also have an important share.
In short, this work starts from the beginning. It should be carried out from beginning to end with the cooperation of “teams that think at the cellular level”. Teams should apply anesthesia according to the duration, location and nature of the surgery. For example
General anesthesia should be avoided in long-lasting surgery. While agents such as nitrous oxide, which have a negative
effect on the mitochondria, cause problems, the decrease in cardiac output caused by agents that have a depressive effect on the myocardium
also has a negative effect on the enzyme system in the mitochondria.
It prevents ATP release. If extremity microsurgery is to be performed, regional anesthesia will be applied.
Regional anesthesia will ensure blood fluidity, eliminate pain in the shortest time, and increase the oxygenation of mitochondria by providing vasodilatation in the vessels. In short, The pathological condition, which manifests itself with clinical changes, progresses to the organ and cell level
.
It is not just about performing the vascular anastomosis properly and putting the patient to sleep.
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