{"title":"Evolutionary Changes of the Cardiovascular System Initiated by Reduced Atmospheric O2 Gave Rise to Mammalian and Avian Endothermy","authors":"G. Soslau","doi":"10.33696/haematology.2.036","DOIUrl":null,"url":null,"abstract":"This commentary will address the salient points explored in a previous publication on the role of the red blood cell and platelet in the evolution of mammalian and avian endothermy [1], include additional concepts associated with the evolution of endothermy, and finally address future directions that may be followed in this area of research. The most simplistic definition of the terms endothermic and ectothermic is the former refers to warmblooded animals that maintain their body temperature by endogenous mechanisms while the latter refers to coldblooded animals that require external sources of heat to warm their bodies. In actuality the ability to maintain body heat is more complex for many animals categorized by these terms since some large-bodied ectotherms can maintain body temperatures by internal mechanisms and some endotherms do not maintain body temperature at selective times, such as when hibernating [2-7]. It was hypothesized that environmental pressures during the Permian/Triassic period when there was a dramatic drop in atmospheric O2 selected for vertebrates with genetic mutations that afforded the animal more efficient pathways to transport O2 to their tissues. Over millennia multiple mutations resulted in genetic and structural changes in the cardiovascular system and the cells within their blood. Structural changes included: the transition to a fourchamber heart that permitted the formation of high-pressure systemic and low-pressure pulmonary circulation [8]; greatly increased density of capillary networks and arterioles to allow for more efficient gas exchange [9]; a pulmonary/systemic differential of blood flow/pressure to enhance gas exchange in lungs; reduced red blood cell size with greater cell surface area/cell to enhance gas exchange at the tissue level, and in the case of mammals the enucleation of both red blood cells and platelets. The initial changes would have been directed by genetic mutations of genes in an ancestor common to Abstract","PeriodicalId":87297,"journal":{"name":"Journal of clinical haematology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of clinical haematology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.33696/haematology.2.036","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
This commentary will address the salient points explored in a previous publication on the role of the red blood cell and platelet in the evolution of mammalian and avian endothermy [1], include additional concepts associated with the evolution of endothermy, and finally address future directions that may be followed in this area of research. The most simplistic definition of the terms endothermic and ectothermic is the former refers to warmblooded animals that maintain their body temperature by endogenous mechanisms while the latter refers to coldblooded animals that require external sources of heat to warm their bodies. In actuality the ability to maintain body heat is more complex for many animals categorized by these terms since some large-bodied ectotherms can maintain body temperatures by internal mechanisms and some endotherms do not maintain body temperature at selective times, such as when hibernating [2-7]. It was hypothesized that environmental pressures during the Permian/Triassic period when there was a dramatic drop in atmospheric O2 selected for vertebrates with genetic mutations that afforded the animal more efficient pathways to transport O2 to their tissues. Over millennia multiple mutations resulted in genetic and structural changes in the cardiovascular system and the cells within their blood. Structural changes included: the transition to a fourchamber heart that permitted the formation of high-pressure systemic and low-pressure pulmonary circulation [8]; greatly increased density of capillary networks and arterioles to allow for more efficient gas exchange [9]; a pulmonary/systemic differential of blood flow/pressure to enhance gas exchange in lungs; reduced red blood cell size with greater cell surface area/cell to enhance gas exchange at the tissue level, and in the case of mammals the enucleation of both red blood cells and platelets. The initial changes would have been directed by genetic mutations of genes in an ancestor common to Abstract