Whole body and hindlimb cardiovascular responses of the anesthetized dog during CO hypoxia

1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
The Body ◽  
Whole Body ◽  
Total Resistance ◽  
Intact Group ◽  
Anesthetized Dogs

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.

The role of aortic chemoreceptors during severe CO hypoxia

1985 ◽  
Vol 63 (5) ◽  
pp. 509-514 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Whole Body ◽  
Limb Blood Flow ◽  
Intact Group ◽  
Anesthetized Dogs ◽  
Dialysis Method

The importance of aortic chemoreceptors in the circulatory responses to severe carbon monoxide (CO) hypoxia was studied in anesthetized dogs. The aortic chemoreceptors were surgically denervated in eight dogs prior to the induction of CO hypoxia, with nine other dogs serving as intact controls. Values for both whole body and hindlimb blood flow, vascular resistance, and O2 uptake were determined prior to and at 30 min of CO hypoxia in the two groups. Arterial O2 content was reduced 65% using an in situ dialysis method to produce CO hypoxia. At 30 min of hypoxia, cardiac output increased but limb blood flow remained at prehypoxic levels in both groups. This indicated that aortic chemoreceptor input was not necessary for the increase in cardiac output during severe CO hypoxia, nor for the diversion of this increased flow to nonmuscle tissues. Limb O2 uptake decreased during CO hypoxia in the aortic-denervated group but remained at prehypoxic levels in the intact group. The lower resting values for limb blood flow in the aortic-denervated animals required a greater level of O2 extraction to maintain resting O2 uptake. When CO hypoxia was superimposed upon this compensation, an O2 supply limitation occurred because the limb failed to vasodilate even as maximal levels for O2 extraction were approached.

The physiologic reserve in oxygen carrying capacity: studies in experimental hemodilution

1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Supply ◽  
The Body ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Oxygen Extraction Ratio ◽  
Acute Anemia ◽  
Total Body Oxygen

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.

Whole body and splanchnic oxygen consumption and blood flow after oral ingestion of fructose or glucose

1993 ◽  
Vol 264 (4) ◽  
pp. E504-E513 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
The Body ◽  
Splanchnic Blood Flow ◽  
Whole Body ◽  
Co2 Production ◽  
Arterial Blood ◽  
Splanchnic Oxygen

The contribution of the splanchnic tissues to the initial 2-h rise in whole body energy expenditure after ingestion of glucose or fructose was examined in healthy subjects. Indirect calorimetry and catheter techniques were employed to determine pulmonary gas exchange, cardiac output, splanchnic blood flow, splanchnic oxygen uptake, and blood temperatures before and for 2 h after ingestion of 75 g of either fructose or glucose in water solution or of water only. Fructose ingestion was found to increase total oxygen uptake by an average of 9.5% above basal levels; the corresponding increase for glucose was 8.8% and for water only 2.5%. The respiratory exchange ratio increased from 0.84 in the basal state to 0.97 at 45 min after fructose ingestion and rose gradually after glucose to 0.86 after 120 min. The average 2-h thermic effect, expressed as percent of ingested energy, was 5.0% for fructose and 3.7% for glucose (not significant). Splanchnic oxygen consumption did not increase measurably after ingestion of either fructose or glucose. The arterial concentration of lactate rose, arterial pH fell, and PCO2 remained essentially unchanged after fructose ingestion. Glucose, but not fructose, elicited increases in cardiac output (28%) and splanchnic blood flow (56%). Fructose, but not glucose, increased arterial blood temperature significantly. It is concluded that both fructose and glucose-induced thermogenesis occurs exclusively in extrasplanchnic tissues. Compared with glucose, fructose ingestion is accompanied by a more marked rise in CO2 production, possibly reflecting an increased extrasplanchnic oxidation of lactate and an accumulation of heat in the body.

Effects of i.v. amino acids on human splanchnic and whole body oxygen consumption, blood flow, and blood temperatures

1994 ◽  
Vol 266 (3) ◽  
pp. E396-E402 ◽  
Author(s):  
T. Brundin ◽  
J. Wahren
Keyword(s):  
Amino Acids ◽  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Amino Acid ◽  
The Body ◽  
Whole Body ◽  
Acid Infusion ◽  
Amino Acid Infusion ◽  
Splanchnic Oxygen

The thermic effect of amino acid administration was examined in healthy subjects. Pulmonary and splanchnic oxygen uptake, cardiac output, splanchnic blood flow, and blood temperatures were measured in eight healthy men before and during 2.5 h of intravenous infusion of 600 kJ of a mixture of 19 amino acids. Indirect calorimetry and catheter techniques were used, including thermometry in arterial and a hepatic venous blood. During the infusion, pulmonary oxygen uptake rose progressively from a basal value of 269 +/- 6 to 321 +/- 8 ml/min after 2.5 h. The splanchnic oxygen consumption increased from a basal level of 64 +/- 4 to a peak value of 91 +/- 7 ml/min after 2 h of infusion. The 2.5 h average splanchnic proportion of the amino acid-induced whole body thermogenesis was 51 +/- 11%. Cardiac output increased from 6.2 +/- 0.3 in the basal state to 7.3 +/- 0.4 l/min, whereas the splanchnic blood flow remained unchanged during the infusion period. The arteriohepatic venous oxygen difference increased from 51 +/- 4 in the basal state to 65 +/- 5 ml/l after 2 h of amino acid infusion. The blood temperature rose by approximately 0.25 degrees C during the amino acid infusion, reflecting an increased heat accumulation in the body. It is concluded that the splanchnic tissues account for approximately one-half of the amino acid-induced whole body thermogenesis, that amino acid infusion augments blood flow in the extrasplanchnic but not in the splanchnic tissues, and stimulates the accumulation of heat in the body most likely via a resetting of the central thermosensors.

Regional hemodynamic responses to hypoxia and hypermetabolism in polycythemic dogs

1989 ◽  
Vol 67 (1) ◽  
pp. 96-102 ◽  
Author(s):  
R. L. Stork ◽  
S. L. Dodd ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adverse Effects ◽  
Whole Body ◽  
Metabolic Demand ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Anesthetized Dogs ◽  
Resting Muscle ◽  
Increased Blood Flow

Normovolemic polycythemia did not improve the ability of either resting muscle or gut to maintain O2 uptake (VO2) during severe hypoxia because of the adverse effects of increased viscosity on blood flow to those regions. The present study tested whether increased metabolic demand would promote vasodilation sufficiently to overcome those effects. We measured whole body, muscle, and gut blood flow, O2 extraction, and VO2 in anesthetized dogs after increasing hematocrit to 65% and raising O2 demand with 2,4-dinitrophenol (n = 8). We also tested whether regional denervation (n = 8) and hypervolemia (n = 6) affected these responses. After raising hematocrit and metabolism, the dogs were ventilated with air, with 9% O2–91% N2, and again with air for 30-min periods. Reduced blood flow and increased O2 demand, caused by increased blood viscosity and 2,4-dinitrophenol, respectively, increased O2 extraction so that muscle VO2 was nearly supply limited in normoxia. Denervation showed that vasoconstriction had increased in gut and muscle with hypoxia onset but this was overcome after 15 min. By then, muscle was receiving a major portion of cardiac output, whereas gut showed little change. With hypervolemia cardiac output increased in hypoxia but neither gut nor muscle increased blood flow in those experiments. Because regional and whole body VO2 fell in all groups during hypoxia to the same extent found earlier in normocythemic dogs, any real benefit of polycythemia under the conditions of these experiments was dubious at best.

The effects of hyperoxia on oxygen uptake during acute anemia

1984 ◽  
Vol 62 (7) ◽  
pp. 809-814 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Cardiovascular Responses ◽  
Capillary Blood ◽  
Whole Body ◽  
Normobaric Hyperoxia ◽  
Blood Exchange ◽  
Variable Section ◽  
Bilateral Vagotomy

The effects of normobaric hyperoxia on the oxygen uptake [Formula: see text] and cardiovascular responses of the whole body and hindlimb during anemia were investigated. Anesthetized, paralyzed dogs were ventilated for 20-min periods with room air (normoxia), 100% O2 (hyperoxia), and returned to room air. Anemia (hematocrit = 15%) was then induced by isovolemic dextran-for-blood exchange and the normoxia, hyperoxia, normoxia sequence was repeated. Whole body [Formula: see text] and cardiac output rose following anemia, and then fell (p < 0.05) with hyperoxia during anemia. These responses were not abolished by β-blockade with propranolol (1 mg/kg, iv) or bilateral vagotomy. The hindlimb data for blood flow and [Formula: see text] were similar in direction to those of the whole body but were more variable. Section of the sciatic and femoral nerves did not appear to have significant effect on the limb responses to hyperoxia. The decrease in whole body and hindlimb [Formula: see text] with hyperoxia during anemia may have resulted from a redistribution of capillary blood flow away from exchange vessels in response to the elevated [Formula: see text].

Canine hindlimb blood flow and O2 uptake after inhibition of EDRF/NO synthesis

1994 ◽  
Vol 76 (3) ◽  
pp. 1166-1171 ◽  
Author(s):  
C. E. King ◽  
M. J. Melinyshyn ◽  
J. D. Mewburn ◽  
S. E. Curtis ◽  
M. J. Winn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Methyl Ester ◽  
Whole Body ◽  
O2 Uptake ◽  
Arterial Inflow ◽  
Anesthetized Dogs ◽  
Nos Inhibitor ◽  
The Right ◽  
Oxide Synthase

The nitric oxide synthase (NOS) inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) was used to determine whether the decrease in canine hindlimb blood flow (QL) with NOS inhibition would limit skeletal muscle O2 uptake (VO2). Arterial inflow and venous outflow from the hindlimb were isolated, and the paw was excluded from the circulation. Pump perfusion from the right femoral artery kept the hindlimb perfusion pressure near the auto-perfused level. Six anesthetized dogs received L-NAME (20 mg/kg i.v.), whereas another group of five dogs received the stereospecific enantiomer N omega-nitro-D-arginine methyl ester (D-NAME 20 mg/kg i.v.). Efficacy of NOS inhibition was tested with intra-arterial boluses of acetylcholine. QL was measured continuously, and whole body and hindlimb VO2 were measured 60 and 120 min after L-NAME or D-NAME. Whole body VO2 remained at control levels, but cardiac output decreased from 117 +/- 17 to 57 +/- 7 ml.kg-1.min-1 60 min after L-NAME (P < 0.05) and remained at that level for the duration of the experiment. Cardiac output was significantly higher in the D-NAME group than in the L-NAME group at 60 min. After L-NAME, QL fell 24% but VO2 increased from 5.2 +/- 0.4 to 7.4 +/- 0.6 ml.kg-1.min-1 (P < 0.05). No change in QL or VO2 occurred after D-NAME. NOS inhibition did not limit hindlimb VO2, despite decreases in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of alpha -adrenergic blockade during acute anemia

1982 ◽  
Vol 52 (1) ◽  
pp. 16-20 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Volume Expansion ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Peripheral Blood Flow ◽  
Adrenergic Blockade ◽  
Acute Anemia ◽  
Alpha Blockade ◽  
Total Body Oxygen

Studies were carried out in seven anesthetized paralyzed dogs to examine the importance of alpha -adrenergic tone in the cardiovascular responses during acute anemia. Data were obtained 1) at normal hematocrit (Hct), 2) during anemia produced by isovolemic hemodilution with dextran (Hct, 13–15%), 3) during anemia after alpha -blockade (alpha -bl) with phenoxybenzamine (3 mg/kg), and 4) following volume expansion during anemia with a red blood cell dextran solution. Cardiac output (QT), limb and total body oxygen uptake (VO2), and limb blood flow (QL) were determined. Both QT and QL increased during anemia (P less than 0.01), whereas limb resistance (RL) and total peripheral resistance (TPR) were decreased (P less than 0.01). No further change in either RL or TPR occurred with alpha -blockade anemia, but both QT and QL decreased (P less than 0.01). Whole-body VO2 increased during anemia and then declined with alpha -bl and anemia. Following volume expansion during anemia with alpha -bl, QT, QL, and whole-body VO2 increased. We conclude that alpha -adrenergic sympathetic tone to capacitance vessels is essential for the cardiac output increased during anemia, but has little or no effect on resistance vessels and hence distribution of peripheral blood flow.

Regional Blood Flow by Fractional Distribution of Indicators

1958 ◽  
Vol 193 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Leo A. Sapirstein
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
The Body ◽  
Arterial System ◽  
Whole Body ◽  
Blood Concentrations ◽  
Arterial Blood ◽  
The Brain ◽  
Fractional Uptake

K42 Cl, Rb86Cl and iodoantipyrine (I131) were given in single intravenous injections to rats. The isotope content of the organs and the arterial blood concentrations were studied as a function of time. K42Cl and Rb86Cl reached a stable level in all organs other than the brain in 6–9 seconds and maintained this level until 64 seconds. The arterial concentration curves for the isotopes showed that the injected dose was almost completely transferred into the arterial system at about 6–8 seconds. The isotopes showed subsequent recirculation amounting to about 40% of the original dose between the first recirculation and 64 seconds. The organs which displayed stability during the period of recirculation must have had extraction ratios from zero time less than 1.00 but equal to that of the whole body. The fractional uptake of indicator by such organs must therefore have been equal to their blood flow fraction of the cardiac output. The brain reached its maximum content of Rb86 and K42 in 5–6 seconds; both isotopes then disappeared rapidly. The brain was thus shown to have a lower extraction ratio toward these isotopes than the body as a whole; its flow fraction could not therefore be measured by their use. Most organs failed to show stability of their iodoantipyrine content between 9 and 64 seconds; this indicator is not suitable for the measurement of the flow fraction of such organs. By combining values for the cardiac output and the fractional uptake of K42 in dog organs, regional blood flow values were obtained. For those other organs where flow values by other methods are available, the agreement was good. The following blood flow values were obtained in the major organs of the dog: Heart (coronary flow), 1.0 ml/gm/min.; kidney, 3.0 ml/gm/min.; liver, 1.2 ml/gm/min. (0.4 ml/gm/min. hepatic artery, 0.8 ml/gm/min. portal vein); skin, 0.07 ml/gm/min.

Glucose and fatty acid metabolism in cows producing milk of low fat content

1974 ◽  
Vol 82 (1) ◽  
pp. 87-95 ◽  
Author(s):  
E. F. Annison ◽  
R. Bickerstaffe ◽  
J. L. Linzell
Keyword(s):  
Blood Flow ◽  
Milk Fat ◽  
The Body ◽  
Whole Body ◽  
Acetate Production ◽  
Entry Rate ◽  
Blood Concentrations ◽  
Body Tissues ◽  
High Starch ◽  
Starch Diet

SUMMARYThe effects of changing to a high starch: low roughage diet have been studied in two Friesian and two Jersey cows, surgically prepared for the simultaneous study of udder metabolism (arteriovenous difference x udder blood flow) and whole body turnover of milk precursors (isotope dilution).In the Friesian cows milk fat concentration was lower on the high starch diet but in the Jerseys fell only slightly in one animal. In both Friesians and in the one Jersey these changes were accompanied by an increase in total rumen VFA concentration. Rumen acetate concentration did not change but propionate doubled. Thus this confirms that the usually reported fall in ‘acetate:propionate ratio’ is due to a rise in propionate production rather than due to a fall in acetate production.There were significant falls in the blood concentrations of acetate and β-hydroxy-butyrate. The rate of extraction by the udder of acetate and β-hydroxybutyrate did not change but triglyceride extraction fell. Therefore since udder blood flow did not alter the uptake of all three fat precursors fell.The entry rate of glucose into the circulation and its contribution to total body CO2 increased. The entry rate and contribution to CO2 of acetate decreased but this was probably mainly due to a fall in endogenous acetate production by the body tissues. Plasma FFA concentration showed little change but the entry rate of palmitate fell on the high starch diet. There was also an increased proportion of unsaturated and trans fatty acids in the plasma and milk triglycerides.

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