INFLUENCE OF ACIDEMIA ON LEFT VENTRICULAR FUNCTION IN THE NEWBORN LAMB

PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.

2012 ◽  
Vol 303 (9) ◽  
pp. H1135-H1142 ◽  
Author(s):  
Sarah Mahne ◽  
Gin C. Chuang ◽  
Edward Pankey ◽  
Lucy Kiruri ◽  
Philip J. Kadowitz ◽  
...  

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.


1991 ◽  
Vol 260 (3) ◽  
pp. H702-H712 ◽  
Author(s):  
K. R. Walley ◽  
D. J. Cooper

To determine the causes of impaired left ventricular function during hypovolemic shock we measured diastolic and end-systolic pressure-volume relationships and hemodynamics. Left ventricular pressure (Millar catheter) and volume (3 ultrasonic crystal pairs) were measured in six open-chest, chloralose-morphine anesthetized, juvenile pigs. After baseline measurements, the pigs were bled and maintained at a mean aortic pressure of 50 cmH2O for 7 +/- 1 h. After resuscitation with all shed blood, left ventricular function was markedly impaired as indicated by increased end-diastolic pressure (20.3 vs. 8.7 cmH2O at baseline, P less than 0.05), decreased aortic pressure (36% of baseline, P less than 0.01), and decreased stroke volume (50% of baseline, P less than 0.01). Systolic contractility was increased (P less than 0.05), but diastolic compliance was greatly reduced due to decreased diastolic maximum (52% of baseline, P less than 0.01) and equilibrium volumes (57% of baseline, P less than 0.01). We conclude that impaired left ventricular function during hypovolemic shock is due entirely to increased diastolic stiffness. These results can theoretically be accounted for by a 20% reduction in myocardial muscle length with no change in muscle stress-strain characteristics. This may be the physiological expression of morphologically observed myocardial "zonal lesions" of hypovolemic shock.


1981 ◽  
Vol 4 (1) ◽  
pp. 28-33 ◽  
Author(s):  
A. S. Iskandrian ◽  
B. L. Segal ◽  
A. Hamid HAKKI

1980 ◽  
Vol 238 (2) ◽  
pp. H257-H262
Author(s):  
J. C. Werner ◽  
J. C. Lee ◽  
S. E. Downing

We have shown previously that insulin reduces myocardial injury associated with norepinephrine (NE) infusion in the rabbit (Am. J. Pathol. 93:399--353, 1978). In the present study, left ventricular function (LVF) was assessed from afterload curves obtained by progressive aortic constriction 2--4 days following NE infusion. The initial slope of the function curves (SFC), maximum dP/dt and left ventricular end-diastolic pressure at 120 mmHg ((LVEDP120) were used for comparison. In 4 controls, SFC averaged 23.8 mmHg/cmH2O. In 10 rabbits given NE, the mean slope was 8.4 (P less than 0.01). However, animals pretreated with insulin before being given NE did not differ from controls (SFC, 19.7 mmHg/cmH2O). These performance data were supported by measurements of LVEDP120, which were 2.8, 12.3 and 3.1 cmH2O, respectively (P less than 0.05 and less than 0.02). In spite of the higher LVEDP, max dP/dt120 was significantly lower in the NE group than in the group given insulin. Histological findings and postmortem measurements of LV volume and mass were consistent with the observed differences in LVF. It is concluded that NE damage reduces LVF and this is largely prevented by pretreatment with insulin.


2001 ◽  
Vol 101 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Yuji HARA ◽  
Mareomi HAMADA ◽  
Yuji SHIGEMATSU ◽  
Bonpei MURAKAMI ◽  
Kunio HIWADA

Congestive heart failure is a common and serious complication in patients undergoing chronic dialysis. However, there have been no studies on preferential medical therapies to improve left ventricular function in haemodialysis patients. β-Blocker treatment is known to improve left ventricular function in patients with dilated cardiomyopathy; moreover, plasma levels of noradrenaline and natriuretic peptides are sensitive markers of left ventricular dysfunction. The present study investigated whether β-blocker treatment could improve left ventricular function in haemodialysis patients with a dilated left ventricle. Our study group comprised 14 haemodialysis patients with a dilated left ventricle, who had undergone maintenance haemodialysis for a mean of 11 years. The following haemodynamic parameters were evaluated before and after 4 months of treatment with the β-blocker metoprolol: left ventricular dimension at end-systole and end-diastole, and fractional shortening. Plasma levels of noradrenaline, atrial natriuretic peptide and brain natriuretic peptide were also determined. Dry body weight and haemoglobin concentration showed no significant change after compared with before treatment with metoprolol. Heart rate decreased significantly, from 79±9 beats/min to 69±9 beats/min, but systolic blood pressure remained unchanged. The left ventricular dimension both at end-systole and at end-diastole was decreased, and fractional shortening increased significantly. Plasma levels of noradrenaline did not change significantly, but those of atrial natriuretic peptide and brain natriuretic peptide decreased markedly [from 100±89 pg/ml to 46±29 pg/ml (P = 0.0051) and from 549±516 pg/ml to 140±128 pg/ml (P = 0.0035) respectively]. In conclusion, β-blocker therapy with metoprolol can markedly attenuate left ventricular remodelling and decrease the plasma levels of natriuretic peptides in haemodialysis patients with a dilated left ventricle.


1994 ◽  
Vol 35 (2) ◽  
pp. 260-260
Author(s):  
Marcel Jij Albers ◽  
Frank Van Bel ◽  
Robert Jm Klautz ◽  
Paul Steendijk ◽  
Jaap Ottenkamp ◽  
...  

Author(s):  
Claire Colebourn ◽  
Jim Newton

This chapter reviews the structure and physiology of the left ventricle and details assessment methods and their safe usage. It looks in detail at the effects of critical illness on left ventricular function, specifically including the effect of sepsis, ischaemia, and drug toxicity.


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