Oxygen requirements of the dyskinetic myocardial segment

1989 ◽  
Vol 257 (4) ◽  
pp. H1184-H1191 ◽  
Author(s):  
P. A. Gayheart ◽  
J. Vinten-Johansen ◽  
W. E. Johnston ◽  
T. O. Hester ◽  
A. R. Cordell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Arteries ◽  
Dose Response ◽  
Contractile Function ◽  
Myocardial Segment ◽  
Response Curves ◽  
Intracoronary Infusion ◽  
Oxygen Requirements ◽  
Measure Oxygen Consumption

Oxygen requirements of a noncontracting myocardial segment subjected to passive systolic stretch (dyskinesis) have not been well described. The purpose of this study was to measure oxygen consumption (MVO2) of a myocardial segment made dyskinetic by intracoronary infusion of lidocaine. In 12 anesthetized open-chest dogs, segmental shortening was measured sonomicrometrically in regions perfused by the left anterior descending (LAD) and circumflex (Cfx) coronary arteries. MVO2 was measured by arterial-venous oxygen content differences and transmural blood flow. Dose-response curves to intracoronary lidocaine showed that complete dyskinesis was achieved by a 0.25-mg/ml dose of lidocaine, whereas the Cfx region maintained a constant level of segmental shortening. MVO2 of the LAD segment was similar to that of the Cfx segment under control conditions. With lidocaine-induced dyskinesis, MVO2 in the arrested segment was reduced by 33% (P less than 0.05), despite the loss of contractile function. When bulging was prevented by ventricular unloading, MVO2 in the arrested segment decreased to 2.65 ml O2.min-1.100 g-1 (i.e., basal oxygen requirements). In conclusion, MVO2 in a pharmacologically arrested myocardial segment undergoing systolic bulging is paradoxically high relative to both basal requirements and MVO2 in the normally contracting segment.

Effect of solute-coupled volume absorption on oxygen consumption in cat ileum.

1979 ◽  
Vol 236 (2) ◽  
pp. E198
Author(s):  
J D Valleau ◽  
D N Granger ◽  
A E Taylor
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Absorption ◽  
Tyrode Solution ◽  
Recovery Method ◽  
Volume Absorption ◽  
All Solutions ◽  
Volume Recovery ◽  
Oxygen Requirements ◽  
Increased Blood Flow

The effects of solute-coupled volume absorption on blood flow, oxygen consumption, and vascular resistance were analyzed in autoperfused segments of cat ileum. Intestinal absorption was stimulated by placing either Tyrode solution, Tyrode + glucose, or Tyrode + taurocholate into the ileal lumen. Net volume absorption rates (Jv,m) were determined using a volume recovery method. Oxygen consumption (VO2) increased during the absorption of all solutions. The absorption of Tyrode solution plus glucose caused the greatest increase in VO2, whereas Tyrode plus taurocholate resulted in the smallest increase. For Tyrode solution and Tyrode plus glucose absorption, the increased VO2 was due predominantly to an increased blood flow, whereas the increased VO2 with taurocholate resulted from an increased oxygen extraction. A linear relationship between the change in VO2 during transport and Jv,m was aquired for Tyrode solution, and Tyrode + glucose. The results indicate that the oxygen requirements of the absorbing intestine are dependent on both the rate of transport and the solutes being transported.

Coronary hyperperfusion augments myocardial oxygen consumption

1996 ◽  
Vol 271 (4) ◽  
pp. H1384-H1393 ◽  
Author(s):  
Y. Ishibashi ◽  
J. Zhang ◽  
D. J. Duncker ◽  
C. Klassen ◽  
T. Pavek ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Systolic Thickening ◽  
Subepicardial Layer ◽  
Systolic Wall Thickening

This study was performed to test the hypothesis that increases in myocardial oxygen consumption (MVo2) and myocardial contractile function during exercise are flow limited. Studies were performed in 15 chronically instrumented normal dogs. MVo2 and regional percent systolic wall thickening were measured during control conditions and during maximal vasodilation produced by infusion of adenosine (20-75 micrograms.kg-1.min-1) or adenosine combined with nitroglycerin (0.4 micrograms.kg-1.min-1; TNG) into the left anterior descending coronary artery during a three-stage graded treadmill exercise protocol. Adenosine and adenosine plus TNG significantly increased coronary blood flow by 298 +/- 26 and 306 +/- 24%, respectively, at rest and by 134 +/- 7 and 145 +/- 9%, respectively, during the heaviest level of exercise (each P < 0.01). Adenosine and adenosine plus TNG increased MVo2 at rest, but this was associated with a parallel increase in heart rate, so that MVo2 per beat was not significantly changed. Systolic wall thickening was also not changed by hyperperfusion during resting conditions. However, MVo2 per beat was increased by 12 +/- 4% with adenosine and by 13 +/- 5% with adenosine plus TNG during moderate exercise and by 23 +/- 5% with adenosine and by 27 +/- 4% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). Systolic thickening of the full left ventricular wall did not change during hyperperfusion, but thickening in the subepicardial layer was increased by 14 +/- 3% with adenosine and 18 +/- 3% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). There was no difference in wall thickening between adenosine and adenosine plus TNG. These findings imply that the increases in MVo2 which occur during exercise are limited by coronary blood flow.

Responses of blood flow, oxygen consumption, and contractile function to inotropic stimulation in stunned canine myocardium

1994 ◽  
Vol 127 (5) ◽  
pp. 1251-1262 ◽  
Author(s):  
Tetsuo Hashimoto ◽  
Denis B. Buxton ◽  
Janine Krivokapich ◽  
Herbert W. Hansen ◽  
Michael E. Phelps ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Contractile Function ◽  
Inotropic Stimulation ◽  
Canine Myocardium

The relationship between the thermogenic response of brown adipose tissue and age during noradrenaline infusion in the young rabbit

1985 ◽  
Vol 63 (10) ◽  
pp. 1215-1220
Author(s):  
W. H. Harris ◽  
D. O. Foster ◽  
B. E. Nadeau
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Age Groups ◽  
Brown Fat ◽  
Young Rabbit ◽  
Morphological Evidence ◽  
Response Curves ◽  
Total Blood ◽  
Noradrenaline Infusion ◽  
Brown Adipose

This work was undertaken to determine if the thermogenic activity of brown fat decreased with age in young rabbits despite the morphological evidence indicating persistence of the brown adipocytes at 4 weeks of age. Data obtained by infusing five doses of noradrenaline and measuring oxygen consumption were used to construct cumulative dose–response curves for five age groups between 3 and 32 days of age. Blood flow to brown fat and other tissues was measured by the microsphere method at 1 and 3 weeks of age. The noradrenaline-induced increase in oxygen consumption when expressed as a percentage of resting oxygen consumption in millilitres per 100 g of body weight decreased (p < 0.05) with age. However, the absolute noradrenaline-induced increase in metabolic rate (millilitres per minute) increased with age. Total blood flow to brown fat (millilitres per minute) during noradrenaline infusion was unchanged between 1 and 3 weeks of age, but when the blood flow was expressed in millilitres per minute per gram of tissue flow decreased significantly (p < 0.05) probably because of infiltration of brown fat with white fat. These data suggest that the amount of brown fat and its thermogenic capacity remain relatively constant between 1 and 3 weeks of age, but as a thermogenic organ, brown fat becomes proportionally less effective with age because of the large increase in body mass.

Cardamist - a glyceryl trinitrate aerosol

1967 ◽  
Vol 5 (2) ◽  
pp. 8-8
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Heart Disease ◽  
Glyceryl Trinitrate ◽  
Coronary Arteries ◽  
Sublingual Administration ◽  
Vascular Bed ◽  
Anginal Pain ◽  
Coronary Vasodilatation ◽  
Local Accumulation

Glyceryl trinitrate is the best drug for preventing anginal pain.1 It is often assumed to dilate coronary arteries, but measurements of myocardial blood flow in man have failed to show that sublingual administration of the drug increases flow in patients with diseased coronary arteries.2 Local accumulation of metabolites during angina is believed to cause coronary vasodilatation: whether any drug can cause further local vasodilatation is uncertain. However, dilatation of the vascular bed may occur when the drug is injected into the coronary arteries of patients with ischaemic heart disease.3 The drug lowers arterial pressure both at rest and during exercise and it diminishes cardiac oxygen consumption. Thus it may help by reducing the metabolic requirements of the heart.1

Comparison of the effects of several endotoxin preparations on body temperature and metabolic rate in the rat

1989 ◽  
Vol 67 (9) ◽  
pp. 1011-1014 ◽  
Author(s):  
M. A. Horan ◽  
R. A. Little ◽  
N. J. Rothwell ◽  
P. J. L. M. Strijbos
Keyword(s):  
Oxygen Consumption ◽  
Body Temperature ◽  
Dose Response ◽  
Similar Pattern ◽  
Low Doses ◽  
Response Curves ◽  
Maximal Increase ◽  
Bacterial Endotoxins ◽  
Higher Doses ◽  
Phenol Extract

The effects of several bacterial endotoxins on body temperature and resting oxygen consumption [Formula: see text] were compared in normal rats. Low doses (0.05 mg/kg, i.m.) of 0127:B8 phenol-extracted endotoxin caused significant increases in both parameters. Maximal febrile responses (+1.6 °C) occurred at a dose of 0.05 mg/kg, but higher doses produced smaller effects. The maximal increase in [Formula: see text] (17%) occurred at doses of 0.5–1.0 mg/kg. A TCA extract of the same strain of endotoxin elicited a similar pattern of responses but was less potent than the phenol extract, whereas another endotoxin 026:B6 (TCA extract) was much less potent. The data illustrate the importance of constructing dose–response curves when comparing different endotoxins and indicate that in the rat, oxygen consumption provides a useful index of the response to pyrogens.Key words: fever, endotoxin, temperature, oxygen consumption, rat.

Combined effects of autoregulation and vasoconstrictors on hindquarters vascular resistance

1990 ◽  
Vol 258 (4) ◽  
pp. H1032-H1041 ◽  
Author(s):  
G. A. Meininger ◽  
J. P. Trzeciakowski
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Dose Response ◽  
Perfusion Pressure ◽  
Combined Effects ◽  
Ang Ii ◽  
Response Curves ◽  
Local Pressure ◽  
Pressure Flow ◽  
Dose Dependent

Relative contributions of local autoregulatory tone and vasoconstrictor tone to skeletal muscle vascular resistance were studied in anesthetized rats during hypertension produced by vasoconstrictor infusion. Rats were instrumented with a Doppler flow probe on the sacral aorta (SA) to measure blood flow and to allow calculation of vascular resistance. An occluder was placed on the SA and used to produce stepwise reductions in local perfusion pressure. Pressure-flow curves for the hindquarters were obtained in the absence and presence of elevated mean arterial pressure (MAP) produced by infusion of angiotensin II (ANG II; 50-1,247 ng.kg-1.min-1) or phenylephrine (PE; 2.5-12.4 micrograms.kg-1.min-1). Both ANG II and PE infusion increased MAP. For example, MAP was increased by ANG II from 91 to 134 mmHg and by PE from 89 to 156 mmHg. In addition, infusions of ANG II and PE produced dose-dependent rightward shifts in the hindquarters pressure-flow relationship. To examine the effect of pressure on the dose-response relationships of ANG II or PE, local perfusion pressure was adjusted to remain constant at various pressure levels that were independent of MAP during drug infusions. This produced a series of distinct dose-response curves with each curve defined by a different pressure level and with each characterized by a different maximum change in vascular resistance. If local perfusion pressure was not held constant but was permitted to increase with MAP, a compound dose-response curve was obtained in which the combined effects of the change in local pressure (i.e., autoregulation) and vasoconstrictor dose on vascular resistance could be discerned. These data demonstrate that hindquarters blood flow autoregulation continues to occur in the presence of vasoconstrictors. Consequently, autoregulatory mechanisms may be stimulated by any increase in MAP whether associated with systemic vasoconstrictor infusion or activation of neurohumoral pressor systems. The result is an amplified rise in local vascular resistance.

Intestinal microvascular responsiveness to norepinephrine in chronic portal hypertension

1991 ◽  
Vol 260 (4) ◽  
pp. H1135-H1143 ◽  
Author(s):  
T. Joh ◽  
D. N. Granger ◽  
J. N. Benoit
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Dose Response ◽  
Vessel Diameter ◽  
Maximal Response ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Cross Sectional ◽  
On Line

Effects of chronic prehepatic portal hypertension on intestinal microvascular sensitivity to norepinephrine (NE) were studied. Normal and portal hypertensive rats were anesthetized, and the intestine was prepared for in vivo microscopic observation. The preparation was transferred to a video microscope and a first-, second-, or third-order submucosal arteriole (i.e., 1A, 2A, or 3A, respectively) selected for study. Microvascular diameter and arteriolar erythrocyte velocity were measured on-line, and arteriolar blood flow was subsequently calculated as the product of velocity and vessel cross-sectional area. Once steady-state conditions were reached, the preparation was exposed to incremental doses of NE and microvessel responses were recorded. Cumulative log dose-response curves relating the change in arteriolar blood flow and vessel diameter to NE concentration were constructed for each group of arterioles and the ED50 for maximal response obtained from each dose-response relationship. NE ED50 for 1A blood flow was significantly higher in portal hypertensive rats (2.57 +/- 0.25 microM) compared with control rats (1.48 +/- 0.19 microM). Analysis of the diameter responses of 1A, 2A, and 3A indicated that the loss of vascular NE sensitivity in chronic portal hypertension was localized to the terminal submucosal arterioles (2A and 3A). No differences in the diameter response of 1A were observed between normal and portal hypertensive rats. Separate experiments were conducted to test if glucagon, a known mediator of the hyperdynamic intestinal circulation in portal hypertension, could acutely alter NE responsiveness in normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Contractile actions of C5a on isolated porcine coronary resistance and conductance arteries

1997 ◽  
Vol 272 (1) ◽  
pp. H12-H16 ◽  
Author(s):  
S. V. Rendig ◽  
S. Gray ◽  
E. A. Amsterdam
Keyword(s):  
Coronary Arteries ◽  
Dose Response ◽  
Thromboxane A2 ◽  
Physiological Salt Solution ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Response Curves ◽  
Resistance Vessels ◽  
Dose Response Curves ◽  
Endothelium Dependent Relaxation

The comparative effects of the complement component C5a on coronary resistance and conductance arteries have not been evaluated. To clarify the coronary contractile actions of this anaphylatoxin, we studied the effects of C5a on development of isometric tension in isolated porcine coronary conductance and resistance arteries. Internal diameters of conductance and resistance vessels were 367 +/- 21 and 88 +/- 4 microns, respectively. Vessel ring segments were suspended in a microvessel myograph, stretched to the peaks of their length-tension curves, and precontracted with 30 mM K+ physiological salt solution. Dose-response curves to C5a (2, 10, and 50 nM) were obtained. At 50 nM, the C5a-induced increase in tension in resistance arteries (4.1 +/- 0.9 to 5.7 +/- 1.4 mN, 35.8 +/- 3.4%) was significantly greater (P < 0.05) than in conductance arteries (10.7 +/- 2.2 to 12.4 +/- 2.6 mN, 15.6 +/- 3.0%). A specific thromboxane A2 receptor antagonist, SQ-29548, virtually eliminated C5a-induced increases in tension. C5a did not impair endothelium-dependent relaxation in either conductance or resistance vessels, as indicated by the half-maximal effective dose (ED50) calculated from bradykinin dose-response curves before and after exposure of the vessels to 50 nM C5a (resistance: pre-C5a ED50 = 2 nM, post-C5a ED50 +/- 3 nM; conductance: pre-C5a ED50 +/- 13 nM, post-C5a ED50 +/- 14 nM). These results indicate that 1) C5a has a greater vasoconstrictive effect on isolated porcine resistance than conductance coronary arteries; 2) C5a-induced coronary constriction is mediated by thromboxane A2; and 3) C5a does not impair endothelium-dependent relaxation of isolated porcine coronary arteries.

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