Effect of pacing on oxygen supply-to-consumption ratio in ischemic myocardium

1985 ◽  
Vol 249 (2) ◽  
pp. H249-H254
Author(s):  
G. J. Grover ◽  
H. R. Weiss

This study was performed to determine if the partially occluded myocardium could maintain its O2 supply-to-consumption ratio during atrial pacing. In 14 open-chest anesthetized dogs, the left anterior descending coronary artery was occluded to 50% of base-line flow, and in half of the dogs the hearts were paced to 50% above base-line heart rate. Blood flows were determined by use of microspheres before and after occlusion, and O2 supply-consumption variables were determined by use of microspectrophotometry. After occlusion in control and paced groups, blood flow was depressed in the ischemic region compared with the nonischemic region. In paced animals, blood flows in all regions were significantly higher compared with their respective values in nonpaced animals. After pacing, mean O2 consumption was 34% higher (53% in the occluded region) compared with control animals. The O2 supply-to-consumption ratio was similar in the occluded region of paced animals compared with the same region in controls. This ratio was lower in ischemic regions of both groups compared with their respective nonischemic regions. This indicates that, despite a reduced O2 supply-to-consumption ratio in the ischemic area, an unutilized reserve of flow exists.

1975 ◽  
Vol 39 (2) ◽  
pp. 235-241 ◽  
Author(s):  
R. Lemen ◽  
J. G. Jones ◽  
P. D. Graf ◽  
G. Cowan

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.


1977 ◽  
Vol 233 (2) ◽  
pp. H217-H221 ◽  
Author(s):  
T. B. Allison ◽  
J. W. Holsinger

The effects of atrial pacing on tissue metabolite levels known to be sensitive to ischemia were examined. Anesthetized dogs were thoracotomized and a pacing electrode was sutured to the right atrium. Pacing at rates of 200 or 250 beats/min (10 animals per group) was performed for 15 min after base-line hemodynamic data had been obtained. At the end of the pacing period, a transmural biopsy was taken, frozen in liquid nitrogen, and sectioned into subepicardial, midmyocardial, and subendocardial layers. ATP, phosphocreatine, lactate, and glycogen were extracted and analyzed. Significant (P less than 0.001) transmural gradients of each of these metabolites existed in the control group. Pacing had no significant (P greater than 0.2) effect on any metabolite from layer to layer at 200 or 250 beats/min. However, indices of heart work (i.e., contractility (dP/dt), stroke work, and stroke volume) demonstrated significant reductions (P less than 0.01) due to pacing, while circumflex artery blood flow increased more than twofold (P less than 0.001) at the highest rate. These data suggest that physiologic autoregulation occurred during pacing and protected the subendocardium from stress-induced ischemic insult.


1985 ◽  
Vol 59 (4) ◽  
pp. 1258-1265 ◽  
Author(s):  
E. L. Dove ◽  
P. G. Katona

To quantify the immediate isocapnic respiratory response to baroreceptor stimulation, pressure in the isolated externally perfused carotid sinuses (CS) of 24 vagotomized alpha-chloralose-anesthetized dogs was increased selectively during either inspiration or expiration as a step (from time of onset to end of respiratory phase) or a pulse (500 ms). The rise time (150 ms), base-line pressure (80 mmHg), and stimulus magnitude (40 mmHg) were similar for the two stimuli. The time of stimulus onset (delay), expressed as a percent of control time of inspiration (TI) or expiration (TE), was varied. TI, TE, and tidal volume (VT) were expressed as percent changes from control. Stimuli delivered early in inspiration lengthened TI [23.5 +/- 6.4% (SE) for step and 11.7 +/- 6.3% for pulse stimuli at 5% delay] more effectively than late stimuli. VT was essentially unaltered. In contrast, step stimuli delivered during expiration caused a lengthening of TE (32.7 +/- 6.3% at 5% delay) that did not depend on the delay (up to 75%). Very late (85%) pulse stimuli lengthened TE (15.2 +/- 5.7%) more effectively than early stimuli. For both stimuli, the expiratory VT was unaltered. When the responses are compared before and after separation of the blood supply of the carotid bodies from the CS region and when they are compared before and after inhibition of reflex systemic hypotension by ganglionic blockade, the observed responses were shown to be due solely to CS baroreceptor stimulation and not to alterations in carotid body blood flow or reflex changes in systemic cardiovascular variables.


1976 ◽  
Vol 54 (3) ◽  
pp. 347-356 ◽  
Author(s):  
Stephen D. Guthrie ◽  
Quillian R. Murphy

The epinephrine-induced loss and subsequent uptake of K+ by the liver was studied by measuring hepatic arterio–venous K+ differences and splanchnic blood flows in anesthetized dogs with chronically implanted portal vein catheters and celiac and superior mesenteric artery flow probes. When epinephrine was administered intraportally, neither α- nor β-adrenergic blockade, singly or in combination, had significant effects upon the hyper-kalemic or the hypokalemic phases in either hepatic venous or systemic arterial blood. It was concluded that the movements of K+ into and out of the liver caused by epinephrine are not mediated by the classical adrenergic receptors as defined by inhibition by specific blocking agents.


1988 ◽  
Vol 255 (6) ◽  
pp. E812-E823
Author(s):  
H. J. Adrogue ◽  
Z. Chap ◽  
Y. Okuda ◽  
L. Michael ◽  
C. Hartley ◽  
...  

The determinants of the altered glucoregulation in acidosis were investigated in anesthetized dogs. Because CO2 rapidly equilibrates and its effects are mediated by pH changes, CO2 inhalation was examined. Plasma acid-base composition, glucose, insulin, glucagon, and blood flows were evaluated before and after an intravenous glucose load (1.2 +/- 0.1 g/kg body wt) in normal and acidotic dogs with flow probes and catheters chronically implanted in the portal circulation. A simultaneous infusion of phentolamine (5 micrograms.kg-1.min-1), propranolol (3.5 micrograms.kg-1.min-1), both, or none was used. All acidemic dogs had lower hepatic extraction of insulin and greater hyperglycemia after the glucose challenge; thus the adrenergic system is not critical for these responses. Because arterial insulin levels were either normal (propranolol) or increased (all others) in acidosis, insulin resistance was likely. Insulin infusion (2 and 4 mU.kg-1.min-1) with euglycemic clamp and [3-3H]glucose documented that acidemia decreases peripheral glucose utilization and the insulin suppression of hepatic glucose production. Acidemia also enhances plasma glucagon levels, yet this effect plays a limited role in the observed hyperglycemia.


1988 ◽  
Vol 254 (3) ◽  
pp. H417-H424 ◽  
Author(s):  
H. F. Downey ◽  
G. F. Merrill ◽  
S. Yonekura ◽  
N. Watanabe ◽  
C. E. Jones

Responses to norepinephrine (NE) before and after treatment with adenosine deaminase (ADA) were examined in anesthetized dogs. In four dogs repeatable changes in coronary blood flow, myocardial oxygen extraction and consumption, left ventricular +dP/dtmax, and heart rate (HR) were demonstrated during two successive intracoronary infusions of 0.13 micrograms.kg-1.min-1 NE. In eight dogs, the NE-induced hyperemia was decreased from +150 to +67%, the change in myocardial oxygen consumption (MVo2) was attenuated from +177 to +101% by ADA, and the increase in HR was reduced from +28 to +16%. In six dogs, the increase in HR caused by NE before ADA was maintained after ADA by atrial pacing. The NE-induced hyperemia and the increase in MVo2 were again decreased by ADA. Similar results were observed in 12 other dogs with hearts paced at a constant, elevated rate during control as well as during both infusions of NE. In all groups, the O2 extraction response to increased MVo2 increased and the flow response decreased after ADA. In six dogs nitroprusside was infused during NE after ADA. When coronary flow was restored to the same level observed before deaminase, MVo2 was not diminished. These results support a role for adenosine in the coronary functional hyperemia accompanying NE activation of the canine myocardium.


1989 ◽  
Vol 256 (4) ◽  
pp. H1176-H1184 ◽  
Author(s):  
H. Murakami ◽  
S. J. Kim ◽  
H. F. Downey

To determine whether right coronary (RC) flow reserve persists at perfusion pressures below the apparent autoregulatory range, the RC artery of 18 anesthetized dogs was cannulated and perfused at controlled pressures. RC blood flow (RCBF) fell from 65.3 +/- 6.1 to 33.7 +/- 2.3 ml.min-1.100 g-1 as RC perfusion pressure (RCPP) was reduced from 80 to 40 mmHg. At 40 mmHg, intracoronary adenosine increased RCBF by 97.9 +/- 10.6 ml.min-1.100 g-1 (P less than 0.001). RCBF fell to 9.5 +/- 1.7 ml.min-1.100 g-1 at 20 mmHg, and RCBF did not significantly increase during adenosine, although RC vasodilation was observed in four dogs. Regional right ventricular (RV) blood flows at RCPP of 80 and 40 mmHg were measured by radioactive microsphere technique. Before adenosine infusion, RCBF was distributed uniformly across the RV free wall at normal and low perfusion pressures. During adenosine infusion, blood flow in both regions increased significantly, but the flow reserve was greater in the subendocardial region at both normal and reduced pressures. RV myocardial O2 consumption (MVo2) was decreased significantly at 40 mmHg, however, there was no evidence of ischemia at this pressure, since the RV lactate extraction ratio was normal (n = 8). Thus RV O2 demand fell when RC O2 supply was reduced, although a flow reserve was available. RV MVo2 was restored to normal when right coronary flow reserve was mobilized by adenosine infusion. For RCBF from 65 to 365 ml.min-1.100 g-1, RC venous O2 content rose and RV MVo2 was essentially constant.(ABSTRACT TRUNCATED AT 250 WORDS)


1981 ◽  
Vol 240 (2) ◽  
pp. H262-H273
Author(s):  
T. R. Harris ◽  
K. A. Overholser ◽  
R. G. Stiles

We have extended earlier studies on coronary vascular permeability-surface area (PS) for [14C]sucrose to include observations of the transcoronary flow resistance before and after partial occlusion of the left anterior descending coronary artery. Multiple-tracer (MT) studies were conducted on 13 anesthetized dogs by inserting an isotope mixture (125I-albumin, 51Cr-red blood cells, [14C]sucrose, 3HOH) into a cannula connecting the carotid and the left anterior descending coronary artery. Analysis of blood sampled from the coronary sinus allowed calculation of PS, extravascular 3HOH volume (VT), and extravascular [14C]sucrose volume (VS). Flow reduction significantly reduced VT and VS and increased PS/VT relative to base line. Coronary resistance distal to the obstruction (R) decreased significantly immediately after flow reduction but then, over the low-flow period, increased significantly above this initial low-flow value. The mean R during reduced flow normalized to R immediately after flow reduction (Ri) correlated significantly with PS/VT during ischemia. Because R/Ri is not correlated with VT alone, we speculate that capillary permeability alterations may play a role in the deterioration of myocardial perfusion during ischemia.


1985 ◽  
Vol 59 (6) ◽  
pp. 1986-1990 ◽  
Author(s):  
A. N. Freed ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes

We studied the effects of the flow of dry air on collateral tone in the lung periphery. A bronchoscope was wedged in sublobar segments of anesthetized dogs, and measurements of collateral resistance (Rcs) were recorded before and after flow was increased from 200 to 2,000 ml/min for a 5-min period. Five minutes after exposure was completed, Rcs increased by an average of 117 +/- 25.2% (SE) over control. Maximum Rcs occurred 5 min after the challenge was concluded and required 48 +/- 10.5 min to return to base line. When flow rate was held constant and exposure period varied, Rcs increased with increased stimulus duration. With exposure times held constant, the response of the collateral system was positively associated with changes in stimulus strength (flow rate). No refractory period was observed with repetitive challenges. Finally, when dry air (delivered at 22 degrees C) and conditioned air (i.e., delivered at 28 degrees C; relative humidity = 80%) challenges were alternated in the same wedged segment, dry air produced a mean increase in Rcs of 93.2%, whereas challenge with warm moist air increased Rcs only 33.5%. Regardless of which challenge was presented first, dry air consistently produced a greater constrictor response. This response is similar to that observed in cold air- and exercise-induced asthma and indicates that the lung periphery in dogs, like larger airways in asthmatic subjects, has the potential to increase tone when exposed to dry air. Peripheral airways in dogs thus constitute a model that can be used for the investigation of exercise-induced asthma.


1987 ◽  
Vol 63 (5) ◽  
pp. 1829-1836 ◽  
Author(s):  
P. Hanly ◽  
A. Sienko ◽  
R. B. Light

Acute bilateral Pseudomonas aeruginosa pneumonia was induced in 10 anesthetized dogs, after which five dogs received intravenous indomethacin (2 mg/kg) (indomethacin group), whereas five others were infused with saline (2 ml/kg) (control group). Plasma levels of 6-ketoprostaglandin F1 alpha(6-keto-PGF1 alpha) and thromboxane B2 (TxB2), stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), respectively, were measured by radioimmunoassay. Although TxB2 levels were not different before and after inoculation in either group, 6-keto-PGF1 alpha levels increased from their base-line value in each animal as pneumonia developed (indomethacin group: less than 100 to 330 +/- 90 pg/ml; control group: less than 100 to 630 +/- 300 pg/ml). Both prostaglandins fell to less than 100 pg/ml in each dog after indomethacin infusion, whereas they remained elevated in the control group after infusion of normal saline. Perfusion of consolidated lung regions (Qp/QT), measured with radioactive microspheres and expressed as a percent of total pulmonary blood flow, was dramatically reduced after indomethacin (35 +/- 3 to 16 +/- 1%) with consequent improvement in pulmonary shunt (Qs/QT: 30 +/- 8 to 18 +/- 6%) and arterial O2 tension (PaO2: 123 +/- 25 to 274 +/- 77 Torr). These parameters remained unchanged or deteriorated further in the control group after infusion of saline. Three additional dogs with Pseudomonas pneumonia were studied in which the indomethacin-induced reduction in Qp/QT was substantially but not completely reversed by intravenous infusion of PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)


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