CARDIOVASCULAR RESPONSES TO HYPERCAPNIA AND VARYING LEVELS OF ARTERIAL ph IN THE ANESTHETIZED CAT

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1 Medical JOllrnal f the slamic Republic f ran Vlume 9 Nllmber4 Winter 374 February 996 CARDOVASCULAR RSPONSS TO HYPRCAPNA AND VARYNG LVLS OF ARTRAL ph N TH ANSTHTZD CAT GHOLAM A. DHGHAN, Ph.D. AND AL KHOSHBATN, Ph.D. Frm the Dept. f Physilgy, Shiraz Medical Schl, Shiraz University f Medical Sciences, Shiraz, and the Department f Physilgy, Faculty f Medical Sciences, mam Hssein University, Tehran, slamic Republic f ran. ABSTRACT ffects f acute hypercapnia n the cardivascular system (CYS) ere studied in the anesthetized cat. After surgery the animal as expsed t a gas mixture f 2% CO2 and 25% O2 in nitrgen, and hypercapnia ith l levels f arterial ph (pha) as prduced fr 2 minutes. n the secnd run the same level f hypercapnia as induced by ventilating the same cat frm the abve gas mixture but pha as kept nrmal by a sl and cntinuus infusin f HAM (.5 mm/ kg/min). Results f this study shed that hypercapnia increased artic fl and induced peripheral vasdilatin. Hypercapnia prduced tachycardia in the presence f arterial acidsis hereas in its absence this respnse reversed t bradycardia. Hypercapnia increased mean arterial bld pressure (Pa) by 2% during l pha, hereas this increase as nly % in the absence f arterial acidsis. Therefre, it is cncluded that hypercapnia in cnjunctin ith arterial acidsis has a much strnger stimulatry influence n the CYS via different arterial chemreceptrs. Keyrds: Hypercapnia; acidsis; cardivascular system; arterial chemreceptrs. M.TfRf, Vl. 9, N.4, ,996. NTRODUCTON Hypercapnia is the elevatin f arterial CO2 tensin hich, in acute cnditins, is usually accmpanied ith l arterial bld ph. Hypercapnia is shn t induce arterilar vasdilatin and elevatin f cardiac perfrmance.!,4 Despite vluminus literature devted t the influences f hypercapnia n the CVS, results are cntradictry and cnfusing.l,4,l t has been shn that hypercapnia in the cat increases the sensitivity f cartid bdies (cb) t hypxia, but this nly has a transient effect n artic bdies (ab).5" Arterial acidsis, n the ther hand, stimulates ab mre strngly.' Direct stimulatin f these chemreceptrs has been shn t have an intense influence n the CVS,7,3 Althugh the influence f cmbined hypxia and varying levels f hypercapnia n the CVS and endcrine secretin have been studied in the dg,,4,d the CVS respnses t acute hypercapnia during nrmxia in the presence r ab sence f arterial acidsis have as yet nt been evalu ated. S far, the arterial chemreceptr neural respnses t hypxia, hypercapnia and acidsis have been studied in the cat,5,' but there is n infrmatin cncerning the CVS respnses f this animal t hypercapnia. Since ur knledge abut the influences f hypercapnia and acidsis n neural activity f arterial chemreceptrs are btained frm experiments perfrmed in the cat, e cntinued ur research in the cat and tried t study the influences f hypercapnia and acidsis n the CVS. 34

2 Cardivascular Respnse t Hypercapnia and ph in Cat Table. Arterial bld ph, PaCOz and PaOz during hypercapnia ith arterial acidsis and recvery.+ Tbn. c"diii'n :,' Cntrl xpt min 3 xpt min xpt min 2 Recv min 3, Recv min Recv min 2 'J" ± ± ±. 7.4 ± ± ± ±. xpt = experiment; Recv = recvery. + Values are expressed as mean ± S. 35.±.9 55.± ± ± ± ± ±.8 2±8 2±9 6±6 5±6 4±9 5±8 2±9 Sign ificantly different frm that f nrmal cats at P 5:.5. Results f this study uld hpefully clear the cntrversies that exist beteen the reprted influences f hypercapnia n the CVS and the rle f arterial chemreceptrs in regulating this system. :::;; V)!!! : - : 2 9.L l ' ----.L.L t OFF CO2 2 " 24 3 TM (MNUT) Fig.!. Heart rate during H-A () and H-N (A). ( = significantly different frm cntrl. = sinificantly different frm each ther, P <.5). 52 MATRALS AND MTHODS xperiments ere carried ut n cats anesthetized ith 3 mg/kg intraperitneal injectins f sdium pentbarbital as a rutine prcedure.3,5.6 The right femral vein as cannulated in rder t infuse dextrse saline, tris hydrxymethyl amin methane (THAM) and the anesthetic agent. The right femral artery as cannulated in rder t measure arterial bld pressure and fr intermittent cllectins f bld samples. Trachestmy as dne fr artificial ventilatin. Arterial P2, PC2 (Pa2, PaC2) and pha ere measured ith a micr bld gas analyzer (Radimeter ph M 72 Mk2). A left lateral thractmy as perfrmed at the fifth interspace and the pericardium as cut t expse the heart. The ascending arta as dissected carefully frm the pulmnary artery. An electrmagnetic prbe (N. 5) as placed abut the rt f the arta. A third cannula as placed int the right atrium in rder t measure its pressure. The heart rate as cunted frm arterial pressure traces. A thermistr prbe as placed rectally t measure and maintain the cre temperature at 37±'C by using a heating plate. At the end f surgery the animal as left t rest fr three hurs in rder t eliminate the effects f surgical stress n the CVS as much as pssible. xperimental prcedure xperiments ere perfrmed n 22 cats. Three hurs after surgery hypercapnia ith a l arterial ph (hypercapneic acidsis; H-A) as induced fr 2 minutes by artificially ventilating the cat frm a gas Z ::i! -' :.;; -' u.. Q a: 32..: 27 t OFF C s TM (MNUT) Fig. 2. Artic fl during H-A () and ' H-N (A). ( = significantly different frm cntrl, P <.5) mixture cntaining 2-5% CO2 and 25% O2 in N2. The animal as then sitched t rm air and CV parameters recrded fr anther minutes and the results cnsidered as recvery (recv). An hur later the buffering capacity f the bld as increased by a sl intravenus infusin f a ne mlar slutin f TRAM in nrmal saline (.5 ml/kg/min), 2 The animal as then expsed t the same gas mixture and the same level f hypercapnia as induced. Here the reductin f bld ph as minimal, hence this cnditin is cnsidered as hypercapnia ith nrmal arterial ph (H-N; Table T). Respiratry rates, tidal vlume and ther ere kept cnstant in rder t ler the interactin lung stretch receptrs ith the direct and reflex f hypercapnia n the CVS as much as pssible.3 All recrdings ere made n an 8 channel 342

3 G.A. Dehghani, Ph.D., and A. Khshbaten, Ph.D. 6 Table. Arterial bld gases during hypercapnia ith nrmal ph.+. :x: 4 «a: 2 "- OFF CO2 Cntrl 7.42 ±.2 3.8±.3 2 ± 8 xpt min ± ±.6 2 ± 9 xpt min ±.9 6. ±.6 5 ±9 xpt min ± ± 3.6 6±6 Recv min ± m 48.±3. 4±9 Recv min ± ± 3. 5±9 Recv min ± m 38.3 ± ± 9 S Values are expressed as mean ± S. '" Values are significantly different frm cntrl at P::;.5. TM (MNUT Fig. 3. Right atrial pressure during H-A () and H-N (A). Z :: 36 -J 32 :: '" ::c.s 28 x : a.. f- 24 ON C2 OFF C , ,, TM (MNUTl Fig. 4. Ttal peripheral resistance during H-A () and H-N (A). plygraph. Mean arterial bld pressre (Pa) and mean right atrial pressure (PRA) ere recrded cntinuusly by damping pressre traces electrn;cally. Mean and pulsatile artic fl ere reccrded by cnnecting the fl prbe t a Carlina fl meter attached t the plygraph. n recrding the mean artic fl (Qa), zer fl as taken t the prtin f the recrd preceding the sharp systlic upstrke. Ttal peripheral resistance (TPR), excluding crnary resistance, as calculated by dividing Pa minus PRA in mmhg by artic fl in ml/ min. Statistical analysis All results ere expressed as means and standard errr f the mean. The data ere analyzed using analysis f variance. Duncan's ne multiple range test as used t find statistical differences beteen the means hen the prbability value as equal t r less than.5 (P,;.5). RSULTS Tables and sh bld ph and gas values during the experiment. n R-A the increased PaC2 as accmpanied by a cncmitant reductin in pra, but in R-N the changes in pha ere statistically insignificant. Cardiac perfrmance Fig. shs that heart rate (RR) decreased significantly dring R-N hereas this respnse as reversed t tachycardia during R-A. Fig. 2 represents that there ere significant and similar increments in Qa in bth cnditins. Full recvery ccrred minutes after cessatin f hypercapnia. Right atrial pressure (PRA) Fig. 3 shs that there as a significant increase in PRA nly dring the first minutes f R-A. Arterial vascular tne and bld pressure Fig. 4 shs that there is a 2% reductin in the values f TPR dring hypercapnia. As shn in Fig. 5, there as a slight decrease in the values f Pa dring the first t minutes f R-N hich later n reversed t a significant rise. Whereas during R-A, Pa increased right aay, after stabilizatin these increments ere % and 2%, respectively. These changes returned back t cntrl values after sitching the cat t rm air. DSCUSSON Many studies have evaluated the effects f hypercapnia n the CVS, but almst nne have differentiated the respnses f this system t hypercapnia ithut the influence f arterial acidsis. arlier reprts have shn that a cncmitant elevatin f PaC2 and acidsis uld affect CVS activity in the 343

4 Cardivascular Respnse t Hypercapnia and ph in Cat dg, but these reprts are debatable.!",6,2 n this study e frrst tried t see if there uld be any differences beteen the effects f hypercapnia n the CVS f the cat frm that f the dg. Then e tried t frnd ut hether cntrlling the ph f arterial bld uld alter these respnses t hypercapnia. Respiratry rate and tidal vlume ere kept cnstant during the experiment t diminish the interactin f lung stretch reflexes ith that f arterial chemreceptrs, as prved t be the case.9 Acute hypercapnia lers intercellular and cerebrspinal fluid ph independent f arterial bld ph,3 and activates sympathetic gastric nerves via central chemreceptrs independent f arterial chemreceptrs.4 Therefre, in this study the lcal effects f hypercapnia n pacemaker cells, mycardium, vascular beds and hpefully the central nervus system remained cnstant in bth cnditins t eliminate their interactins ith chemreceptr reflexes as much as pssible. The results f this study uld give us a ne insight cncerning the influences f hypercapnia alne and in cnjunctin ith acidsis n the CVS f the cat. The lcal influences f hypercapnia and acidsis are shn t be vasdilatin and cardiac depressin.',ll On the ther hand, arterial chemreceptrs (ab and cb) hich directly sense H in cncentratins and arterial bld gases are shn t have different sensitivities t PaC2 and pha, 2,5,9 and their separate r cmbined stimulatin have varius influences f the CVS,6,7,l,3 t is interesting t nte that the cardiac system shed a cmplicated respnse t bth types f hypercapnia. There as an increase in cardiac utput (Fig. 2), and althugh heart rate increased during H-A, this respnse as cmpletely ppsite during H-N (Fig. ). These results made us believe that nt nly are CVS respnses f the cat t hypercapnia different frm that f the dg but als that the presence r absence f acidsis makes the hle Stry different. The increased cardiac utput might be the utcme f augmented mycardial cntractility and venus return,5 because the negative chrntrpic effects f hypercapnia during H-N culd nt alter this elevatin. n islated preparatins, lactic acidsis has been shn t have negative intrpic and chrntrpic effects n the heart,l2 hereas stimulatin f arterial chemreceptrs have ppsite effects thrugh sympathetic stimulatin and increased adrenal secretin f epinephrine.6, Hypercapnia independent f arterial acidsis lers the intracellular ph f mycardial cells.!,4 Therefre, the level f intracellular ph as (hpefully) identical in bth cnditins. f this is the case the decreased heart rate bserved during H-N culd be attributed t intracellular acidsis as cncluded by Rthe et ai, and a eaker stimulatry respnse f arterial chemreceptrs Time (minutes) Fig. 5. Mean arterial pressure during H-A () and H-N (A) ( = significantly different frm each ther, P <.5). t hypercapnia in the absence f acidsis. Hence in the presence f acidsis, hypercapnia culd vercme the depressing effects f intracellular acidsis due t strnger stimulatin f cb chemreceptrs.6,9 Venus return is anther factr hich directly influences cardiac utput. PRA is a gd indicatr f the increment f venus return hen there is a cncmitant increment in cardiac utput in the nrmal functining heart. Althugh in this study e culd nt directly measure mycardial cntractility, frm the results f ther investigatrs e can say that there as an increase in cardiac perfrmance mainly in respnse t stimulatin f arterial chemreceptrs.6, 3 Furthermre, Rthe et a. shed that hypercapnia increased capacitance vessel tne thrugh arterial chemreceptr stimulatin. Therefre, the significant elevatin f PRA bserved during H-A accmpanying the increased cardiac utput is a gd sign f the increment f venus return (Fig. 3). TPR in cnjuctin ith the measurement f arterial bld pressure Clearly bviated the respnses f the arterial system t H-A and H-N. There as a significant reductin in TPR in bth cnditins (Fig. 4) hich is in agreement ith the results f Rthe et ai, t has been shn that H-A prduces mderate arterilar vasdilatin in the dg. Despite ur expectatin that TPR uld decrease much mre during hypercapnia the presence f arterial acidsis, e fund that ch,m:es',> ere similar in bth cnditins (Fig. 4). Pkrski et have shn that metablic acidsis mainly stilnula«, ab.9 Althugh stimulatin f ab by arterial might have increased sympath-adrenal activity mre during H-A, it seems that it as nt diminish the direct lcal vasdilatry effects f as reprted by thers.!o,,3 344

5 G.A. Dehghani, Ph.D., and A. Khshbaten, Ph.D. levatin f cardiac utput in the presence f arterial vasdilatin in this study is the main cause f increased Pa (Fig. 5). arlier reprts have reiterated that cmbined stimulatin f bth ab and cb uld vercme the direct vasdilatry influences f systemic hypxia in the cat.' Althugh arterial vessels had a vasdilatry respnse t hypercapnia (Fig. 4), e still think that cmbined stimulatins f ab and cb ere the main cause f a much greater increase in Pa during H A. The ler activity f ab during H-N made the elevatin f Pa less prnunced than hat as bserved during H-A (Fig. 5). n summary, the results f this study indicated that a cmbinatin f arterial acidsis and hypercapnia has a greater and mre frceful stimulatry influence n arterial chemreceptrs. This stimulatin eliminates the direct depressing effects f hypercapnia and acidsis n arterial bld pressure, cardiac perfrmance and heart rate. RFRNCS. Bang OH, Cafe F, Walk: M, Lipania JG: Cardivascular respnses t hypxia and varying pe2 in aake dg. J Appi Physi27(2): 24 28, Bisc T, Purves M, Sampsn SR: The frequency f nerve impulses in single cartid bdy chemreceptr afferent fibers recrded in viv ith intact circulatin. J Physil (Land) 28: 2-3, Dehghani GA, Msavi SM: nteractins f arterial chemreceptrs and pulmnary stretch reflexes in circulatry regulatins in the cat. JMS 8(3,4): 53-58, Dning S, Mitchell JR, Wallace GA: Cardivascular respnses t ischemia, hypxia, and hypercapnia f the central nervus system. Am J Physil 24(5): , Fitzgerald RS, Dehghani GA: Neural respnses f the cat cartid and artic bdies t hypercapnia and hypxia. J Appl Physil 52 (3): 569-6, Fitzgerald RS, Dehghani GA, Sham JSK, Shirahata M, Mitzner W: Peripheral chemreceptr mdulatin f pulmnary vasculature in the cat. J Appl Physil 73: 2-29, Kimura A, Sat A, Sat Y, Trzebski A: Rle f the central and arterial chemreceptrs in the respnse f gastric tne and mtility t hypxia, hypercapnia and hypcapnia in rats. J Autn Syst 45(): 77 85, Parker P, Dabney JM, Sctt JB, Haddy FJ: Reflex vascular respnses in kidney, ileum, and frelimb t cartid stimulatin. Am J Physi22 8(): 46-5, Pkrski M, Lahiri S: Artic and cartid chemreceptr respnses t metablic acidsis in the cat. Am J Physil 224: R , Raff H, Shinsak J, Dallman MF: Renin and ACTH respnses t hypercapnia and hypxia after chrnic cartid chemdenervatin. Am J Physil247: R42-47, Rthe CF, Maass M, Flanagan AD: ffects f hypercapnia and hypxia n the cardivascular system; vascular capacitance and artic chemreceptrs. Am J Physil 259: H932-9, Shapir J: Functinal and metablic respnses f islated hearts t acidsis: effects f sdium bicarbnate and carbicarb. Am J Physil258(6 pt. 2): H835-9, Stern S, Rappaprt : Cmparisn f the reflex elicited frm cmbined r separate stimulatin f artic and cartid chemreceptrs n mycardial cntractility, cardiac utput, and systemic resistance. Circ Res 2: , Wasser JS, nman KC, Arendt A, Laler RG, Jacksn DC: 3P-NMR measurements f phi and high-phsphates in islated turtle hearts during anxia and acidsis. Am J Physil259(3 pt 2): R52-3, «

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