Effects of changes of pH and of carbon dioxide tension on left ventricular performance

Ng, M. L.; Levy, M; Zieske, HA

doi:10.1152/ajplegacy.1967.213.1.115

Cited by 114 publications

(30 citation statements)

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“…The results in the present experiments are in agreement with the common notion that CO 2 exerts a deleterious effect upon the isolated heart (15,(17)(18)(19)(20)(21)(22).…”

Section: Discussionsupporting

confidence: 92%

Mechanism of Action of Tris (Hydroxymethyl) Aminomethane on the Negative Inotropic Effect of Carbon Dioxide

González¹,

Cingolani²,

Mattiazzi³

et al. 1971

Circulation Research

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Administration of isotonic THAM to the blood of the heart-lung preparation induced a decrease in the negative inotropic effect of CO 2 , suggested by the fact that, at constant stroke work, an increase in Pco 2 of 26 ± 1.9 mm Hg was followed by an increase in left ventricular end-diastolic pressure (LVEDP) of 3.8 ± 0.2 mm Hg before the infusion of THAM; after THAM was given, a similar increase in Pco 2 induced an increase in LVEDP of 1.8 ± 0.2 mm Hg (P<0.01). When pH was increased by 0.15M NaHCO 3 , no changes in myocardial contractility or in the tolerance of the heart to CO 2 were found. On the other hand, hemodilution with isotonic sucrose reproduced the effect of THAM. Either sucrose or THAM produced a decrease in plasma Na. Myocardial contractility, previously increased by THAM or sucrose, returned to control after plasma Na was restored. When cat papillary muscles were immersed in Ringer's solution with normal (142 mn) and low (112 msi) Na concentration, it was observed that a similar increase in Pco 2 originated a smaller decrease in contractility when the muscles were in the low Na solution. It is concluded that the effect of THAM in the present experiments is due, at least to an important extent, to changes in extracellular Na.KEY WORDS myocardial contractility cat papillary muscle dog heart-lung preparation low extracellular [Na] extracellular pH hemodilution osmolarity• Tris (hydroxymethyl) aminomethane (THAM) is an amine buffer that was introduced in 1960 (1) in the clinical treatment of acid base disorders. Its use has been stimulated by the observation that it apparently buffers the intracellular as well as the extracellular space (2, 3).The cardiovascular actions of THAM have been extensively studied (4-12). It has been shown that the infusion of THAM in acidotic dogs increases myocardial contractile force (4-9) and that the replacement of NaHCO 3 by This study was supported in part by a grant from the Comision de Investigacion Cientifica, Universidad National de La Plata, Argentina.From the Institute de Fisiologia, Facultad de Ciencias Medicas, La Plata, Argentina.Dr. Gonzalez' present address is Department of Physiology, University of Kansas Medical Center, Kansas City, Kansas 66103.Received July 8, 1970. Accepted for publication November 5, 1970. THAM is associated with an increase in the developed tension of the isolated atrium (11). However, when THAM titrated to pH 7.4 is injected into the coronary circulation, no changes in myocardial contractile force are produced (9). In preliminary experiments from this laboratory (13) we observed that the administration of 0.3M THAM solution increased myocardial contractility in the isolated heart-lung preparation. On the other hand, the in vitro replacement of NaHCO.s by THAM was followed by an increase in contractility of cat papillary muscles only when a significant decrease in Na concentration of the medium was achieved (12).To supply further information about the effect of THAM upon myocardial contractility and the mechanism of its actio...

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“…The results in the present experiments are in agreement with the common notion that CO 2 exerts a deleterious effect upon the isolated heart (15,(17)(18)(19)(20)(21)(22).…”

Section: Discussionsupporting

confidence: 92%

Mechanism of Action of Tris (Hydroxymethyl) Aminomethane on the Negative Inotropic Effect of Carbon Dioxide

González¹,

Cingolani²,

Mattiazzi³

et al. 1971

Circulation Research

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“…In agreement with our findings, systemic pulmonary resistance. In contrast, hypocapnia-low pressure has been previously reported to decrease during alkalosis Pacoz, with a n~r m a l arterial pH-increased pulmonary in both humans (18) and animals (17,19). However, Rudolph pressure and pulmonary vascular resistance.…”

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confidence: 90%

Increased Arterial pH, Not Decreased PaCO2, Attenuates Hypoxia-Induced Pulmonary Vasoconstriction in Newborn Lambs

1986

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ABSTRACT. Mechanically induced hyperventilation is not the increase in pH, that improves these patients during used in the treatment of newborn infants with persistent respiratory alkalosis produced by mechanically induced hyperpulmonary hypertension syndrome to induce respiratory ventilation. alkalosis, which may attenuate their pulmonary vasocon-The purpose of the present study was to determine hovi striction. Whether this treatment is effective because of mechanically induced hyperventilation reverses hypoxia-induced the increase in arterial pH or the decrease in Pacoz was pulmonary vasoconstriction. For this purpose we compared the investigated in nine sedated, mechanically ventilated new-effects of three treatments-respiratory alkalosis, metabolic alborn lambs with hypoxia-induced pulmonary vasoconstric-kalosis, and hypocapnia-on hypoxia-induced pulmonary vasotion. We found that respiratory alkalosis and metabolic constriction in newborn lambs with mechanical lung factors held alkalosis were equally effective in attenuating hypoxia-constant. The strategy behind this approach was that if respirainduced pulmonary vasoconstriction, but that hypocapnia tory alkalosis reverses pulmonary vasoconstriction because of (low Pacoz with a normal arterial pH) was ineffective. the increase in pH, then metabolic alkalosis (increased pH antl These results indicate that increased arterial pH, not de-a normal Paco,) should have a similar effect. Conversely, if creased Paco2, attenuates hypoxia-induced pulmonary respiratory alkalosis reverses pulmonary vasoconstriction bevasoconstriction in newborn lambs and possibly the pul-cause of the decrease in Pace*, then hypocapnia (normal pH antl monary vasoconstriction in newborn infants with persistent a decreased Paco2) should have a similar effect. METHODSNine mixed breed newborn lambs (5.5 f 2.3 days; 4.4 k 1.0 kg) (mean f SD) were operated on under local anesthesia with Respiratory alkalosis, produced by mechanically induced hy-1 % lidocaine hydrochloride. Polyvinyl catheters were placed in perventilation, is the mainstay of treatment for newborn infants both hind 1% arteries and veins and advanced to the descending with persistent pulmonary hypertension syndrome. Respiratory aorta and inferior vena cava, respectively. A catheter alkalosis improves oxygenation and reverses pulmonary vasocon-Was also placed in a fore leg artery and passed retrograde to the striction by decreasing the mean pulmonary arterial pressure ascending aorta and positioned above the aortic valve to obtaiin when the arterial p~ is greater 7.55 and the paco2 is less arterial blood samples and measure systemic arterial pressure. A than 22 mm H~ ( 1 ,~) .whether these beneficial effects are caused no. 5 French end-hole, balloon-tip, flow-directed thermodi1utio:n by the increase in arterial pH or the decrease in Pace,, or by the catheter, with the proximal injection port 15 cm from the tip, alteration in mechanical lung factors necessary to produce res-was introduced into the internal jugular vein and advanced...

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“…[20][21][22][23][24] Walley et al reported that hypercapnic acidosis (PaCO 2 92 mmHg) decreases Ees by 19% in dogs anesthetized with fentanyl. 2 5 In contrast to previous studies in humans or dogs, hypercapnic acidosis caused bradycardia and reduced CO in our study of rabbits.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits

Mizukoshi

Sato

Yoshida

2001

Can J Anesth/J Can Anesth

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Purpose: We have previously observed that sympathetic blockade by epidural anesthesia (EA) modifies the cardiovascular response to marked hypercapnic acidosis in dogs. Our objective was to determine whether the combination of marked hypercapnic acidosis and EA reduce left ventricular contractility.Methods: We randomly assigned 22 Japanese white rabbits anesthetized with isoflurane (1.0%) to two groups according to the absence (control group, n=11) or presence (EA group, n=11) of thoracolumbar EA. After epidural injection (0.5 mL·kg -1 of 0.9% saline in the control group or 1% mepivacaine in the EA group) and during subsequent hypercapnia (mean arterial CO 2 tension 85 mmHg), we measured left ventricular pressure, left ventricular volume by using conductance catheter and plasma catecholamine concentrations. Left ventricular contractility was assessed by the slope of the linear approximation of the left ventricular end-systolic pressure-volume relationship, [i.e., end-systolic elastance (Ees)].Results: The combination of hypercapnic acidosis and thoracolumbar EA caused a 65% decrease in Ees (P <0.05). Hypercapnic acidosis alone caused a 16% decrease (P <0.05) and thoracolumbar EA alone caused a 49% decrease in Ees (P <0.05). In the EA group, epidural injection caused an 85% decrease in the epinephrine concentration (P <0.05) and a 39% decrease in the norepinephrine concentration (P <0.05), even during hypercapnic acidosis. However, in the control group, hypercapnic acidosis caused no change in the circulating epinephrine concentration but a 74% increase in the circulating norepinephrine concentration (P <0.05).

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Effects of changes of pH and of carbon dioxide tension on left ventricular performance

Cited by 114 publications

References 0 publications

Mechanism of Action of Tris (Hydroxymethyl) Aminomethane on the Negative Inotropic Effect of Carbon Dioxide

Mechanism of Action of Tris (Hydroxymethyl) Aminomethane on the Negative Inotropic Effect of Carbon Dioxide

Increased Arterial pH, Not Decreased PaCO2, Attenuates Hypoxia-Induced Pulmonary Vasoconstriction in Newborn Lambs

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits

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