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.

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 α-adrenergic receptors in carbon monoxide hypoxia

1986 ◽  
Vol 64 (11) ◽  
pp. 1442-1446 ◽  
Author(s):  
S. M. Villeneuve ◽  
C. K. Chapler ◽  
C. E. King ◽  
S. M. Cain
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Adrenergic Receptors ◽  
Muscle Blood Flow ◽  
Control Period ◽  
Arterial Oxygen ◽  
Adrenergic Blockade ◽  
Limb Blood Flow ◽  
Arterial Oxygen Content

The importance of α-adrenergic receptors in the cardiac output and peripheral circulatory responses to carbon monoxide (CO) hypoxia was studied in anesthetized dogs. Phenoxybenzamine (3 mg/kg i.v.) was injected to block α-receptor activity and the data obtained were then compared with those from a previous study of CO hypoxia in unblocked animals. Values for cardiac output, hindlimb blood flow, vascular resistance, and oxygen uptake were obtained prior to and at 30 and 60 min of CO hypoxia which reduced arterial oxygen content by approximately 50%. α-Adrenergic blockade resulted in a lower (p < 0.05) control value for cardiac output than observed in unblocked animals, but no differences were present between the two groups at 30 or 60 min of CO hypoxia. Similarly, limb blood flow was lower (p < 0.05) during the control period in the α-blocked group but rose to the same level as that in the unblocked animals at 60 min of COH. No change in limb blood flow occurred during CO hypoxia in the unblocked group. These findings demonstrated that during CO hypoxia (i) α-receptor mediated venoconstriction does not contribute to the cardiac output response and (ii) α-receptor mediated vasoconstriction probably does prevent a rise in hindlimb skeletal muscle blood flow.

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.

scholarly journals Resistance training increases basal limb blood flow and vascular conductance in aging humans

2006 ◽  
Vol 101 (5) ◽  
pp. 1351-1355 ◽  
Author(s):  
Maria M. Anton ◽  
Miriam Y. Cortez-Cooper ◽  
Allison E. DeVan ◽  
Daria B. Neidre ◽  
Jill N. Cook ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Strength Training ◽  
Whole Body ◽  
Control Group ◽  
Limb Blood Flow ◽  
Vascular Conductance ◽  
Femoral Blood Flow ◽  
Femoral Blood

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 ± 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 ± 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested ( P < 0.05). Whole body lean body mass increased ( P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55–60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.

The role of aortic chemoreceptors during acute anemia

1984 ◽  
Vol 62 (5) ◽  
pp. 519-523 ◽  
Author(s):  
P. C. Szlyk ◽  
C. King ◽  
D. B. Jennings ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Mean Value ◽  
Whole Body ◽  
Metabolic Responses ◽  
Limb Blood Flow ◽  
Acute Anemia ◽  
Control Value ◽  
Blood Exchange ◽  
Anesthetized Dogs ◽  
The Mean

The importance of aortic chemoreceptors in the circulatory and metabolic responses during acute anemia was studied in anesthetized dogs. Data were obtained from nine dogs in which the aortic chemoreceptors were surgically denervated prior to induction of anemia, and from seven sham-operated dogs. Cardiac output [Formula: see text], limb blood flow [Formula: see text], limb and whole body oxygen uptake [Formula: see text] were determined at normal hematocrit (Hct) and at 30 min of anemia (Hct = 13%) produced by isovolemic dextran-for-blood exchange. At 30 min of anemia, [Formula: see text] was increased from 91 to 186 mL∙kg−1∙min−1 (p < 0.01) and from 99 to 153 mL∙kg−1∙min−1 (p < 0.01) in the sham and denervated groups, respectively. The increase in [Formula: see text] during anemia was less (p < 0.05) in the aortic-denervated series. Limb flow was also increased during anemia in both groups (p < 0.01); the mean value of 89 mL∙kg−1∙min−1 in the denervated group was less than that of 130 mL∙kg−1∙min−1 observed in the sham animals (p < 0.05). Whole body [Formula: see text] decreased (p < 0.05) in the denervated group at 30 min of anemia; limb [Formula: see text] was maintained at the preanemic control value in both groups. The data indicate that during acute anemia the aortic chemoreceptors contribute to the increase in [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)

Cardiac Output Changes in Newborns With Hyperbilirubinemia Treated With Phototherapy

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Skin Blood Flow ◽  
Peripheral Blood ◽  
Cardiovascular Effects ◽  
Tissue Perfusion ◽  
Peripheral Blood Flow ◽  
Limb Blood Flow ◽  
Term Infants

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.

Role of adenosine in postprandial and reactive hyperemia in canine jejunum

1992 ◽  
Vol 263 (4) ◽  
pp. G487-G493 ◽  
Author(s):  
D. R. Sawmiller ◽  
C. C. Chou
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Concentration Difference ◽  
Adenosine Concentration ◽  
Anesthetized Dogs ◽  
Series Of Experiments ◽  
Increased Blood Flow

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.

Contribution of bile to postprandial intestinal hyperemia

1980 ◽  
Vol 238 (4) ◽  
pp. G284-G288 ◽  
Author(s):  
P. R. Kvietys ◽  
R. H. Gallavan ◽  
C. C. Chou
Keyword(s):  
Amino Acids ◽  
Blood Flow ◽  
Oleic Acid ◽  
Caproic Acid ◽  
Local Blood Flow ◽  
Vascular Effects ◽  
Bile Concentration ◽  
Anesthetized Dogs ◽  
Per Se

The role played by bile in postprandial intestinal hyperemia was examined by comparing the vascular effects of luminal placement of various nutrients with and without bile in situ jejunal segments of anesthetized dogs. The bile concentration was either 10 or 33% of that in the gallbladder. At these concentrations, bile per se in the jejunal lumen does not alter local blood flow. In the absence of bile, only glucose increased flow (+5% above control). With 10% bile, glucose and oleic acid increased flow by 10 and 24%, whereas with 33% bile, glucose, oleic acid, caproic acid, and amino acids increased flow by 22, 21, 12, and 12% above control, respectively. Triolein increased flow only after digestion by pancreatic enzymes and mixing with bile. Dipeptides did not alter flow with or without bile. Thus, bile plays an important role in postprandial intestinal hyperemia because it potentiates the glucose-induced hyperemia and because only in its presence can oleic acid, amino acids, caproic acid, and digested triolein increase intestinal blood flow.

In-situ generation of graphene network in silicon carbide fibers: Role of iodine and carbon monoxide

Carbon ◽  
2020 ◽  
Vol 158 ◽  
pp. 110-120
Author(s):  
Junsung Hong ◽  
Youngjin Ko ◽  
Kwang-Yeon Cho ◽  
Dong-Geun Shin ◽  
Prabhakar Singh ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Silicon Carbide ◽  
Silicon Carbide Fibers ◽  
In Situ Generation
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