at sea Level Mechanism Fall of PI02 (and thus of Pa 02) causes stimulation of 'peripheral chimoreceptors'(PC')' neural impulses

respiretoary stimulation 3 However, if the P CQ2 of the brain capitary blood remains persistenly high (- exite of excessCQ2 from the blood to CSF or brain tissue fluid is persistenlyy high), same compenatory changes occur liding to regaining of the anginal ph of the CSF thus CSF is no longer acid and it no longer stimulates the CC in l practice. a drammatice example is very advanced case of emphiysema In such case, blood PC02 rremember persistently high but the pH of C5f (and presumably of the bram tissue fluid) remains alkalin Therefort these fluids cannot and do not stimulate the CC cell In short. these patints have high Pa CO2 (and also PA CO2). but the high PaC02 deos not stimulated the respiration yet, for his survivai.the patient requires increased respiratory drive (otherwise he will die of CO2 narcosis) This increased drive cornes from the concomitantl hypxia presenet in such casses. The ultimate conclusion is. inspite of the presented hy poxia in sush cases over enthusiatic correction of hypoxia (by O2 therapy) can kill the patientas as it extingushes the only respiretory stimulus available in this patent Recent wotks indicate that theCC cells are present. in the ventral surfaca of the in three areas. termed tostral, intermidiate and caudal areas. They are also known by their alternate names, viz. areas Mitchell (M). Schlafeke (S) and Loeuhke (L) respectively C02 can also stimulate the respiratory center (RC) via the peripheral chemoreceptares. see bellow. Role ofOxygen What happens in 02 lack (hypoxia) and 02 excess? Between them 02 lack ib much much important and will be described frist . Effects of 02 lack A moderate fall of PI02 (02 tension of inspised air) or PI02 (02 tension ofarterial blood) unlike those with C02, has no appreciable effec evenslight rise of PIC02 or PaC02 causes sharp rise ofE However gross fall ofPl 02 (or concenitration of 02 in the inspired air)leads to sharp rise of Vg which thut Causes correction of the hypoxia. E rises when the concentration of 02, (02). in the inspired air becomes 12% Or lessi. at sea Level Mechanism Fall of PI02 (and thus of Pa 02) causes stimulation of 'peripheral chimoreceptors'(PC')' neural impulses arising fromthese PCa cells go to the RC stimulation of -respiration What causes stimulation of PC? Low Pa O2 is the most important example. Fall of blood pH is another. Rise of Pa C02 also stimulates. Some anatomical (and histological details) of PC can now be discusseld there are two sets of PCs, (l) the caotided body chemreeeptors (fig. 4.3.6) and (ii) The aortic body chemoreceptores. Between them, the carolid body chemoreceptors havt between studied much more extentsively,, no doubt, because of thir easy accessibility But it is safe to presume that the behaviores of and functions of the carotid body (CB) are more or lass same as those of aortic body chemoreceptores. CB At bffurcation of each common carotid artery (fig 4. 3.5), withen the vascular andothelium, in direct contact with the blood, lise the CB. The CB can analyze the Pa 02 f Pa Co2 / H+ concentration if there is )ow Pa 02 or high Pa C02 or low blood pH the CB cells an stimulated nauiral impulses art art up medulary RC stimulated increased repiration homeostasis regained the aortic bodies also behave similar ways (i.e. they also analyze the above mentained chemicals send signals achive homeostasis). The neural from the CB also called glomus caroticum ) travel via nerve Of Hering (a branch Of glossophryngeall or the IXh nerve) the IXlh nerve (fig. 4. 3. 5) 4 medullary RC. Whereas, from the aortic bodies, impulses travel up via (afferent) vagal fiberes medullary R.C There are altogether two CB. one On each side (fig 4.3.5.) There are two types Of Cells in the CB.' type 1 and (ii) Type II cells. Type I cells contain large vesicles and sensory nerve fibers (which eventually constitute the nerve ofHering) emerge from the type I cell Probably the type I cells themsellves or the begining of these nnerves are the detectlores (= receptors ) of the chemical sensation (e.q. anoxial). Three neurotransmitter chemicals are involved in the above mention detection of chemical senses as well as their' tranimiision. They are, (i) dopamine (DA), (ii) subttance P, and (iii) acetyl choline Ach) Of them DA and substance P are present in the vesicles of type I cells Proba- bly DA causes blunting of the sensivity of the chemoresepter cells. whereas substance P increases it. ACh might probably be the neurotransmitter involved in the transmission between the type I cell and the emeging nerve fiber. Thai it, stimutation of lypt I call releaser (locally) ofACh stimulation of the afferent nerves. Molecular level mechanism(s) of action of tha CB (glomius caraticum)
is uncertain and contraversial. Some very popular (and mutually comphmentary) ideas are given below .Any one or all of them may be correct. I
. The CB cells (glomus cells) are metabolically axtremely active Therefore, inspite oft the fact that the CB it tremendously vascular. there.are normally. areas. where there is some hypoxia Of these
-,„-