Effect of hypoxemia and hypercapnia on regional distribution of myocardial blood flow

1965 ◽  
Vol 208 (6) ◽  
pp. 1211-1216 ◽  
Author(s):  
William D. Love ◽  
Myra D. Tyler
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Coronary Blood Flow ◽  
Regional Distribution ◽  
Fick Principle ◽  
The Right ◽  
Isotope Content ◽  
Coronary Sinus Blood ◽  
Normal Difference

The effect of hypoxia and hypercapnia on regional coronary blood flow and vascular resistance (CVR) was studied in dogs without thoracotomy. Gas tensions were varied by ventilation at controlled rates with gas mixtures containing 4–100% O2 and 0–24% CO2. After 10 min intravenous infusion of Rb86, the animals were killed and the heart isotope content determined. Blood flow to the left ventricle was calculated by the Fick principle from the isotope uptake and the mean difference in radioactivity of arterial and coronary sinus blood. Patterns of flow elsewhere were estimated from the rates of regional Rb86 clearance. Myocardial Rb86 clearance in the right and left ventricles has been previously shown to be closely related to the rate of coronary blood flow. Hypoxemia and severe hypercapnia (pCO2 above 100 mm Hg) both produced a profound fall in CVR. With hypoxemia this decrease was more marked in the right ventricle. Elevation of pCO2 exaggerated the normal difference in Rb86 uptake between inner and outer thirds of the wall of the left ventricle, while hypoxemia reversed the normal gradients. Hypercapnia did not affect these gradients in the right ventricle, but hypoxemia significantly reduced them.

Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle

2005 ◽  
Vol 230 (8) ◽  
pp. 507-519 ◽  
Author(s):  
Pu Zong ◽  
Johnathan D. Tune ◽  
H. Fred Downey
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Coronary Blood Flow ◽  
Oxygen Demand ◽  
Coronary Vasodilation ◽  
External Work ◽  
Coronary Conductance ◽  
The Right

Few studies have investigated factors responsible for the O2 demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which Is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are Identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O2 demand has not been defined. At rest, the left ventricle extracts ~75% of the O2 delivered by coronary blood flow, whereas right ventricular O2 extraction Is only ~50%. As a result, resting right coronary venous PO2 is ~30 mm Hg, whereas left coronary venous PO2 is ~20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O2 as the left ventricle. Endogenous nitric oxide impacts the right ventricular O2 demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O2 extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O2 consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O2 extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO2 decreases to ~20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO2 has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion.

Alterations of coronary blood flow and reserve with aging in Fischer 344 rats

1989 ◽  
Vol 256 (1) ◽  
pp. H66-H73 ◽  
Author(s):  
R. Hachamovitch ◽  
P. Wicker ◽  
J. M. Capasso ◽  
P. Anversa
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Pressure Overload ◽  
Fischer 344 Rats ◽  
Time Intervals ◽  
Vascular Reserve ◽  
Fischer 344 ◽  
The Right

To determine whether aging affects the coronary circulation, left and right ventricular coronary blood flow and vascular resistance at rest and after maximal vasodilation were measured by left atrial injection of radioactive microspheres in conscious, unrestrained male Fischer 344 rats at 4, 12, and 20 mo of age. As a function of age, maximal coronary blood flow per 100 g of tissue decreased by 43% in the left ventricle at both 12 and 20 mo, whereas a 44 and a 47% reduction was found in the right side of the heart at the same time intervals. Minimal coronary vascular resistance per 100 g of myocardium increased by 56 and 36% in the left ventricle and by 48 and 44% in the right at 12 and 20 mo, respectively. No change was found in total minimal coronary resistance for either ventricle despite an increase in myocardial mass. Maximal coronary blood flow per 100 g to the endocardium was depressed more than epicardial flow, leading to a 24% reduction in the endocardial-to-epicardial flow ratio at 20 mo. Coronary vascular reserve per 100 g, expressed as the increase in coronary blood flow during maximal coronary vasodilation, was greater in the right than in the left ventricle at all ages. It is concluded that the changes in coronary hemodynamics associated with maturation and aging are comparable with those seen in pressure overload hypertrophy with an increased vulnerability potential of the myocardium to ischemic episodes, particularly of the subendocardial region of the left ventricle.

Regional variation in pericardial contact pressure in the canine ventricle

1988 ◽  
Vol 255 (6) ◽  
pp. H1370-H1377 ◽  
Author(s):  
B. D. Hoit ◽  
W. Y. Lew ◽  
M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Contact Pressure ◽  
Regional Variation ◽  
Left Atrial ◽  
Regional Distribution ◽  
Lateral Wall ◽  
Cardiac Volume ◽  
Pericardial Pressure ◽  
The Right

We studied eight open-chest dogs to determine whether there is regional variation in pericardial contact pressure (PCP). Flat, air-filled balloons were used to measure PCP simultaneously over the lateral walls of the right and left ventricles while cardiac volume was varied by dextran infusion. End-diastolic and mean PCP were significantly higher over the left than right ventricle at high (20.3 +/- 1.0 mmHg) and middle levels (13.7 +/- 0.9 mmHg) of left atrial pressure. At high left atrial pressures, the end-diastolic PCP over the lateral left ventricle was 9.1 +/- 2.4 mmHg compared with 4.3 +/- 2.3 mmHg over the lateral right ventricle (P less than 0.05). At middle levels of left atrial pressures, end-diastolic PCP was 6.2 +/- 3.5 mmHg over the left ventricle and 1.5 +/- 2.4 mmHg over the right ventricle (P less than 0.05). These variations in PCP persisted after severing the pericardial diaphragmatic attachments and after turning the dogs such that one or the other balloon was dependent. Regional distribution of PCP was studied by positioning a single balloon sequentially at multiple ventricular sites. PCP was consistently higher over the lateral wall of the left ventricle than either the anterior or posterior walls of the right or left ventricle. After aortic occlusion, end-diastolic PCP increased more over the left than right ventricle. In contrast, with pulmonary artery occlusion, end-diastolic PCP increased more over the right than left ventricle. Pericardial pressure varies regionally, and a single pericardial pressure may be an oversimplification when used to describe pericardial restraint on the cardiac volume.

Relationship of blood flow and myocardial Rb86 clearance in right and left ventricles

1963 ◽  
Vol 205 (2) ◽  
pp. 382-384 ◽  
Author(s):  
William D. Love ◽  
Lawrence P. O'Meallie
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Venous Blood ◽  
Percentage Error ◽  
Fick Principle ◽  
Mean Error ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Relationship Of

The rate of myocardial clearance of Rb86 from arterial blood and the rate of coronary blood flow were studied simultaneously during a 10-min period of isotope infusion in dogs. In order to measure blood flow to the right and left ventricles separately using the Fick principle, venous blood was obtained from an anterior cardiac vein and from the coronary sinus. The relationship of myocardial blood flow and Rb86 clearance was not detectably different in the right and left ventricles. The percentage error in predicting flow from clearance rose as the values increased. At rates of flow below 6 ml/g 10 min the mean error was 4.7%. From 6 to 12 ml/g 10 min the mean error was 10.0% in controls and 14.4% in a group with pulmonary embolism or obstruction of the pulmonary artery. Since the clearance technique does not require catheterization of a cardiac vein, this method can be used to study coronary blood flow under conditions approximating the undisturbed state.

Effects of cardiac sympathetic nerve stimulation on regional coronary blood flow

1987 ◽  
Vol 252 (2) ◽  
pp. H269-H274
Author(s):  
C. W. Haws ◽  
L. S. Green ◽  
M. J. Burgess ◽  
J. A. Abildskov
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Coronary Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Beta Blockade ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Cardiac Nerve

The purpose of this study was to examine the effects of cardiac sympathetic nerve stimulation on regional coronary blood flow following beta-blockade. In 17 anesthetized dogs treated with propranolol (2 mg/kg iv) regional myocardial perfusion was measured (microspheres) during control and during stimulation of the ventrolateral, ventromedial, or recurrent cardiac nerve (8–10 V, 4-ms pulses at 10 Hz for 30 s). Ventrolateral nerve stimulation produced 25.5 +/- 3.4 and 23.5 +/- 3.1% (mean +/- SE) decreases in coronary blood flow in the posterior and lateral quadrants of the left ventricle. These changes were significantly greater than the 8.5 +/- 2.9, 11.5 +/- 3.0, and 3.7 +/- 2.8% decreases in the anterior and septal left ventricle and right ventricle, respectively (P less than 0.01). Ventromedial nerve stimulation produced 18.6 +/- 2.8, 15.4 +/- 2.8, and 10.1 +/- 3.2% decreases in flow in the anterior, septal, and lateral left ventricle, respectively. These changes were significantly greater than the 5.3 +/- 3.8 and 9.9 +/- 3.6% decrease in the posterior left ventricle and right ventricle (P less than 0.01). Recurrent cardiac nerve stimulation produced 16.4 +/- 2.1, 15.6 +/- 2.2, and 13.6 +/- 2.5% decreases in flow in the anterior and septal left ventricle and right ventricle, respectively. These changes were significantly greater than the 5.2 +/- 3.2 and 5.4 +/- 3.0% changes in the posterior and lateral quadrants (P less than 0.01). Ventrolateral nerve stimulation resulted in a small but significant increase in the endocardial-to-epicardial blood flow ratio in the posterolateral left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrastructural and functional features of the developing mammalian heart: a brief overview

1995 ◽  
Vol 7 (3) ◽  
pp. 451 ◽  
Author(s):  
JJ Smolich
Keyword(s):  
Blood Flow ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Postnatal Development ◽  
Vascular Resistance ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
The Right

The heart undergoes marked ultrastructural alterations during fetal and postnatal development. Early in fetal development, cardiac myocytes contain abundant pools of glycogen, scattered mitochondria and sparse, peripheral myofibrils. Transverse tubules are absent, and sarcoplasmic reticulum and intercalated discs are poorly developed. During late fetal and early postnatal development, myofibrils extend into the myocyte interior and attain a mature appearance, and the glycogen pools are reduced in size. In addition, transverse tubules develop and the morphological appearance of the sarcoplasmic reticulum and intercalated disc becomes increasingly complex. Experimental studies in sheep, corroborated by clinical studies in humans, also point to marked functional changes during development. In the fetus, the right ventricle is the dominant pumping chamber because right ventricular output exceeds left ventricular output, while pulmonary arterial and aortic pressures are similar. This functional difference is reflected in myocardial blood flow patterns, with blood flow to the right ventricle exceeding that to the left ventricle. The ventricular outputs equalize after birth, but a functional left ventricular dominance rapidly emerges following a postnatal increase in systemic vascular resistance and a decrease in pulmonary vascular resistance. This postnatal switchover in functional dominance is accompanied by a corresponding alteration in the relative level of ventricular myocardial blood flows. Consistent with right ventricular dominance in utero, myocytes in the right ventricle of the fetal sheep are larger and contain more myofibrillar material than those in the left ventricle. Left ventricular myocytes become larger than right ventricular myocytes after birth, but this adaptation to altered postnatal haemodynamics requires some weeks to become fully established.

Right Ventricular Perfusion

2018 ◽  
Vol 128 (1) ◽  
pp. 202-218 ◽  
Author(s):  
George J. Crystal ◽  
Paul S. Pagel
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Coronary Circulation ◽  
Contractile Function ◽  
Left Ventricular ◽  
Oxygen Extraction ◽  
Pulmonary Arterial ◽  
The Right

Abstract Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in reduced extravascular compressive forces and myocardial oxygen demand. Right ventricular perfusion has eight major characteristics that distinguish it from left ventricular perfusion: (1) appreciable perfusion throughout the entire cardiac cycle; (2) reduced myocardial oxygen uptake, blood flow, and oxygen extraction; (3) an oxygen extraction reserve that can be recruited to at least partially offset a reduction in coronary blood flow; (4) less effective pressure–flow autoregulation; (5) the ability to downregulate its metabolic demand during coronary hypoperfusion and thereby maintain contractile function and energy stores; (6) a transmurally uniform reduction in myocardial perfusion in the presence of a hemodynamically significant epicardial coronary stenosis; (7) extensive collateral connections from the left coronary circulation; and (8) possible retrograde perfusion from the right ventricular cavity through the Thebesian veins. These differences promote the maintenance of right ventricular oxygen supply–demand balance and provide relative resistance to ischemia-induced contractile dysfunction and infarction, but they may be compromised during acute or chronic increases in right ventricle afterload resulting from pulmonary arterial hypertension. Contractile function of the thin-walled right ventricle is exquisitely sensitive to afterload. Acute increases in pulmonary arterial pressure reduce right ventricular stroke volume and, if sufficiently large and prolonged, result in right ventricular failure. Right ventricular ischemia plays a prominent role in these effects. The risk of right ventricular ischemia is also heightened during chronic elevations in right ventricular afterload because microvascular growth fails to match myocyte hypertrophy and because microvascular dysfunction is present. The right coronary circulation is more sensitive than the left to α-adrenergic–mediated constriction, which may contribute to its greater propensity for coronary vasospasm. This characteristic of the right coronary circulation may increase its vulnerability to coronary vasoconstriction and impaired right ventricular perfusion during administration of α-adrenergic receptor agonists.

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