Hi OTDude, are you sure the inflammatory stage has high presence of vasodilation and not vasoconstriction? I was just thinking that vasoconstriction would be able to contribute to decrease loss of blood whereas vasodilation might do the opposite. just a thought. LMK if you have an answer pls.
I thought this chatgpt response was pretty accurate as a general explanation. Then I did one quick fact check below. "In burn injuries, the initial inflammatory response typically causes vasodilation (dilation of blood vessels). This is because the inflammatory mediators released during the initial stages of inflammation, such as histamine and prostaglandins, cause the blood vessels in the affected area to widen. This widening allows more blood to flow to the area, bringing immune cells and nutrients needed for healing. However, as the inflammation progresses, the affected blood vessels may begin to constrict (vasoconstriction) in an attempt to limit the extent of damage and prevent excessive swelling. This constriction may also occur as a result of the release of other inflammatory mediators, such as thromboxane A2 and leukotrienes, which can cause smooth muscle cells in the blood vessels to contract." Quick Google scholar search for "burn inflammatory vasodilation" yielded Pathophysiology of the burn wound. G Arturson Annales chirurgiae et gynaecologiae 69 (5), 178-190, 1980 The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid oedema formation, due to increased microvascular permeability, *vasodilation* and increased extravascular osmotic activity. This appears to be a human model and not animal as it mentioned patient. Edit: I followed up with chatgpt and had it cite it's sources and it returned: Arturson, G. (2004). Pathophysiology of the burn wound and pharmacological treatment. The Anaesthesia and intensive care medicine, 5(5), 162-165. doi: 10.1383/anes.5.5.162.52522 Berger, M. M., & Chioléro, R. L. (2012). Hypertonic saline in critical care: a review of the literature and guidelines for use in hypotensive states and raised intracranial pressure. Anaesthesiology intensive therapy, 44(4), 191-206. doi: 10.5603/AIT.2012.0036 Xu, X., & Liu, D. (2019). Endothelial dysfunction in burn injury. Microvascular research, 125, 103869. doi: 10.1016/j.mvr.2019.103869 In general, for us to maintain homeostasis, the answer is generally not one or the other. We often have an opposite response to counter the physio effects. Good question. Freaked me out with it though cause I hate making mistakes on my videos!
Hi OTDude, are you sure the inflammatory stage has high presence of vasodilation and not vasoconstriction? I was just thinking that vasoconstriction would be able to contribute to decrease loss of blood whereas vasodilation might do the opposite. just a thought. LMK if you have an answer pls.
I thought this chatgpt response was pretty accurate as a general explanation. Then I did one quick fact check below.
"In burn injuries, the initial inflammatory response typically causes vasodilation (dilation of blood vessels). This is because the inflammatory mediators released during the initial stages of inflammation, such as histamine and prostaglandins, cause the blood vessels in the affected area to widen. This widening allows more blood to flow to the area, bringing immune cells and nutrients needed for healing.
However, as the inflammation progresses, the affected blood vessels may begin to constrict (vasoconstriction) in an attempt to limit the extent of damage and prevent excessive swelling. This constriction may also occur as a result of the release of other inflammatory mediators, such as thromboxane A2 and leukotrienes, which can cause smooth muscle cells in the blood vessels to contract."
Quick Google scholar search for "burn inflammatory vasodilation" yielded
Pathophysiology of the burn wound.
G Arturson
Annales chirurgiae et gynaecologiae 69 (5), 178-190, 1980
The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid oedema formation, due to increased microvascular permeability, *vasodilation* and increased extravascular osmotic activity.
This appears to be a human model and not animal as it mentioned patient.
Edit: I followed up with chatgpt and had it cite it's sources and it returned:
Arturson, G. (2004). Pathophysiology of the burn wound and pharmacological treatment. The Anaesthesia and intensive care medicine, 5(5), 162-165. doi: 10.1383/anes.5.5.162.52522
Berger, M. M., & Chioléro, R. L. (2012). Hypertonic saline in critical care: a review of the literature and guidelines for use in hypotensive states and raised intracranial pressure. Anaesthesiology intensive therapy, 44(4), 191-206. doi: 10.5603/AIT.2012.0036
Xu, X., & Liu, D. (2019). Endothelial dysfunction in burn injury. Microvascular research, 125, 103869. doi: 10.1016/j.mvr.2019.103869
In general, for us to maintain homeostasis, the answer is generally not one or the other. We often have an opposite response to counter the physio effects. Good question. Freaked me out with it though cause I hate making mistakes on my videos!
1:55 Say that five times fast. /o/
👍🏻