PubMed Health⌕ Search

Biomedical subjects

C K Chapler

Publications and source records attributed to C K Chapler.

At least 55 records · Page 3Linked to original sources
PubMed1984

The effects of hyperoxia on oxygen uptake during acute anemia.

The effects of normobaric hyperoxia on the oxygen uptake (VO2) 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 VO2 and cardiac output rose following anemia, and then fell (p less than 0.05) with hyperoxia during anemia. These responses were not abolished by beta-blockade with propranolol (1 mg/kg, iv) or bilateral vagotomy. The hindlimb data for blood flow and VO2 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 VO2 with hyperoxia during anemia may have resulted from a redistribution of capillary blood flow away from exchange vessels in response to the elevated PO2.

Acute Disease↗
PubMed1983

Oxygen uptake and blood flow in canine skeletal muscle during moderate and severe anemia.

The metabolic and cardiovascular adjustments of the whole body and skeletal muscle were studied during moderate and severe acute anemia. In 15 anesthetized dogs, venous outflow from the gastrocnemius-plantaris muscle group was isolated. Cardiac output (QT) muscle blood flow (QM), total body and muscle oxygen uptake (VO2) were determined during a control period, and at 30 and 60 min of either (i) moderate anemia (n = 8) in which the mean hematocrit (Hct) was 25% or (ii) progressive anemia (n = 7) in which the mean Hct values were 25% at 30 min and 16% at 60 min of anemia. Muscle VO2, QT, and QM were increased in both groups at 30 min of anemia. By 60 min, QT and QM declined to preanemic control values in the moderate anemia group; whole body VO2 was maintained at the control level. Arterial oxygen transport was the same in the two groups at both 30 and 60 min of anemia despite the difference in Hct at 60 min. Muscle VO2 showed a further and similar rise in both groups between 30 and 60 min of anemia. These data show that the rise in muscle VO2 during acute anemia was not directly proportional to the degree of the hematocrit reduction. Further, the findings suggest that the muscle VO2 response was related to the decrease in arterial oxygen transport.

Anemia↗
PubMed1982

Hindlimb resistance in hypoxic dogs after adrenergic blockade or denervation.

Blood flow (Q) and O2 uptake (Vo2) were measured in the intact autoperfused left hindlimb (less paw) of anesthetized paralyzed dogs ventilated at constant rate with either room air (normoxia) or 9.1% O2 in N2 (hypoxia) for 20-min periods. One group of 10 dogs was given 3.0 mg/kg phenoxybenzamine (alpha-block) and was subjected to the sequence of normoxia, hypoxia, normoxia. The sequence was repeated after 1.0 mg/kg propranolol (beta-block). A second group of 10 was treated the same but was not given adrenergic blockers (no block). A third group of 10 was made hypoxic only once after the sciatic and femoral nerves to the prepared limb were severed (denervated). Decreased O2 availability during hypoxia limited both total and limb V02 in all cases. Limb Q did not change, but vascular resistance increased in the no-block group with onset of hypoxia and a brisk transient hyperemia occurred with reoxygenation. After both alpha- and beta-block no change occurred in limb resistance with reoxygenation. A similar result was obtained in the denervated limb. These results indicated that the transient hyperemia following hypoxia was the result of altered states of neurally mediated vascular tone, mostly sympathetic, and was not due to local metabolic vasodilation or altered blood levels of catecholamines during a 20-min period of hypoxia.

Animals↗
PubMed1982

Effects of alpha -adrenergic blockade during acute anemia.

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.

Acute Disease↗
PubMed1981

Peripheral vascular responses during acute anemia.

Peripheral vascular responses during acute anemia were studied in 19 anesthetized dogs. In one study (n = 9) hindlimb weight and venous pressures were measured prior to and during acute anemia produced by isovolemic dextran-for-blood exchange. In another series of five control and five anemic dogs (hematocrit = 14 +/- 1% (mean +/- SE)), flow to the limb was occluded and arterial and venous pressure changes in the occluded limb were measured as an index of neurally mediated alterations in limb vasomotor tone. Following reduction of the hematocrit to 14 +/- 0.3%, hindlimb weight decreased by an average of 10.0 g (P less than 0.01) at 15 min and 12.8 g (P less than 0.01) at 30 min of anemia. The decrease in limb weight was associated with a rise (P less than 0.01) in limb venous pressure. There was also a relatively greater degree of vasomotor tone in the occluded hindlimb of anemic dogs as compared with control animals. Although both arterial and venous pressure decreased in an occluded hindlimb following the production of anemia, the decreases in vascular pressures were significantly less than those observed in control experiments. It was not possible to distinguish between tone changes in arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone. arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone.

Acute Disease↗
PubMed1981

Blood flow and O2 uptake in dog hindlimb with anemia, norepinephrine, and propranolol.

To examine the relative importance of 1) reduced blood viscosity, 2) vasodilation mediated through beta-adrenergic receptors, and 3) sympathetic nerve activity on the regulation of limb blood flow during anemia, norepinephrine (NE) was infused in 10 anesthetized-paralyzed dogs at normal and reduced hematocrit (Hct). Cardiac output (QT), limb and total oxygen uptake (VO2)n and limb venous flow (QL) were determined. After a control period, NE (2 micrograms . kg-1 . min-1) was infused followed by another control period. The Hct was then reduced to 9% by isovolemic hemodilution with dextran, and data were obtained during anemia, anemia plus NE, and after isovolemic reinfusion of red blood cells (Hct 25%) during NE. Another 10 dogs were treated identically after propranolol (1.0 mg/kg) administration. At normal Hct, NE increased limb resistance (RL) (P less than 0.01) in the beta-block group; a decrease in RL (P less than 0.05) and a rise in QL (P less than 0.01) occurred in the no block group. QL and VO2 (limb and total) were not changed by NE. During anemia, RL was not altered in either group by NE; QT fell (P less than 0.05) in both, and QL decreased in the no block group. After reinfusion of cells, NE produced an increase in RL and total peripheral resistance (P less than 0.01) and a fall in QL (P less than 0.01) and QT (P less than 0.01) in both groups; limb and total VO2 rose in the no block group. We conclude that the reduction in viscosity prevented an increase in both RL and redistribution of QL during severe anemia (Hct 9%).

Anemia↗
PubMed1981

Effects of norepinephrine and alpha-block on O2 uptake and blood flow in dog hindlimb.

Norepinephrine (NE) may increase skeletal muscle O2 demand at the same time that it restricts O2 transport by vasoconstriction. We prevented vasoconstriction with 3.0 mg/kg phenoxybenzamine (alpha-Bl) in 10 anesthetized, paralyzed dogs ventilated at constant rate. Hindlimb and whole-body O2 uptake (VO2) and blood flow were measured for a 20-min control period, 20 min of NE infusion at 1 micrograms . kg-1 . min-1 either intravenously (iv) or intra-arterially (ia), and 20 min of recovery. The sequence was repeated for the other route of infusion. A second group of 10 without alpha-Bl was treated the same. Cardiac output increased with both ia and iv infusions in the no-block group and was unchanged in the alpha-Bl group. Limb blood flow increased 25% during the first 5 min of iv but decreased 40% with ia infusion in the no-block group. Whole-body VO2 was significantly increased 9% in both groups by both routes of NE. Limb VO2 was significantly decreased in the no-block group at 5 min of NE infusion iv when limb blood flow was increased. Limb VO2 did not change significantly in the alpha-Bl group with NE by either route. Hindlimb skeletal muscle did not participate in or contribute to the calorigenic effect of NE on the whole body, and that lack of effect was not due to any effect of NE on rate or distribution of blood flow in the limb.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of changes in blood flow, norepinephrine, and pH on oxygen uptake by resting skeletal muscle.

The purpose of this study was to examine the effects of norepinephrine infusion alone and during alkalosis on oxygen uptake in the dog gastrocnemius-plantaris muscle group under conditions of constant muscle blood flow. The animals were not cold acclimatized. Blood flow was pump controlled, alkalosis was produced by hyperventilation, and norepinephrine was infused intravenously at a rate of 1--1.5 micrograms/kg per minute. Alkalosis had no effect either alone or in combination with changes in blood flow. Similarly, changing blood flow from a low (0.10 +/- 0.02 mL/g muscle per minute (mean +/- SE)) to a high (0.34 +/- 0.04 mL/g muscle per minute) rate did not alter resting oxygen uptake. Norepinphrine caused an average increase of about 30% in resting muscle oxygen uptake which was sustained for the 15-min sampling period during a low flow-norepinephrine infusion and during the low and high blood flow-norepinephrine-alkalosis sampling periods. Norepinephrine infusion during the period of high muscle blood flow without alkalosis resulted in a transient increase followed by a decrease in muscle oxygen uptake. The data demonstrated that infusion of norepinephrine increased skeletal muscle oxygen uptake in "non-cold-acclimatized" dogs at low constant muscle blood flow. Further, without alkalosis, the norepinephrine effect at high flow was transient.

Alkalosis↗
PubMed1980

O2 extraction by canine hindlimb during alpha-adrenergic blockade and hypoxic hypoxia.

Hindlimb and total blood flow and O2 uptake were measured in anesthetized paralyzed dogs in which venous outflow from the left hindlimb (less paw) was directed through the femoral vein. After ventilation on room air, 10 dogs were given 3 mg/kg phenoxybenzamine + 10 ml/kg dextran and 10 other dogs were isovolemically exchanged with 10 ml/kg dextran without alpha-block while continuing to be ventilated on room air. All animals were then ventilated with 9.1% O2 in N2, followed by a recovery period on room air. Total and limb peripheral resistances were lowered by alpha-block, but total and limb blood flow changed little from control levels. Both total and limb O2 uptake were decreased below control values during hypoxia. Cardiac output and limb blood flow increased during hypoxia in both groups. Although alpha-block caused O2 extraction by the whole body to be less during hypoxia than in unblocked dogs, the hindlimb in both groups extracted O2 equally well. We concluded that skeletal muscle was not overperfused relative to O2 demand when alpha-blocked during hypoxia.

Animals↗
PubMed1979

Oxygen extraction by canine hindlimb during hypoxic hypoxia.

Regional and total blood flow and O2 uptake (VO2) were measured in 10 anesthetized paralyzed dogs in which venous outflow from the left hindlimb (less paw) was directed through the femoral vein. After being ventilated on room air during a 40-min control period, they were ventilated on 12.0% O2 for 40 min, 9.2% O2 for 40 min, and again on room air for 40 min. A second group of 10 was treated the same after they were given 1.0 mg/kg propranolol to block beta-adrenergic receptors. Neither limb blood flow nor cardiac output changed significantly during moderate hypoxia in either group; both increased in severe hypoxia but only in the no-beta-block group. Limb VO2 was not decreased significantly in either group during moderate hypoxia but total VO2 was decreased in the beta-block group. Total VO2 was decreased in both groups during severe hypoxia but limb VO2 was maintained in the beta-block group. beta-Block prevented the fall in total and limb peripheral resistance seen in severe hypoxia but did not alter the consistently more efficient utilization of total O2 delivery shown by the limb in comparison to the whole body by higher O2 extraction ratios and lower venous O2 pressure. beta-Vasodilator receptors evidently played an active part in the vasodilatation seen during severe hypoxia.

Animals↗
PubMed1978

O2 extraction by hind limb versus whole dog during anemic hypoxia.

The ability of the hind limb to obtain oxygen and maintain its O2 uptake in relation to the whole body during isovolemic hemodilution with dextran was measured in eight anesthetized, paralyzed dogs kept at constant ventilation. Hind limb venous outflow (ankle to upper thigh) was restricted by tourniquets to femoral vein. Hind limb blood flow, O2 uptake (VO2), cardiac output, and total VO2 were measured at normal hematocrit, at hematocrits just above (16%, stage 2) and just below (10%, stage II) that at which total VO2 could be maintained at the control level, and following isovolemic reinfusion of recovered red blood cells (Hct = 23%). VO2 was maintained at the control level in whole body and hind limb during stage I. Total VO2 decreased significantly in stage II (P less than 0.05), whereas limb VO2 did not. Hind limb had a consistently greater extraction ratio for O2 (P less than 0.01) and lower venous oxygen partial pressure than the body as a whole (P less than 0.01). In spite of limitations of O2 delivery by anemia to the point that total O2 demand was not met, there was no redistribution of blood flow away from or decreased demand for O2 by the hind limb, which was mostly skeletal muscle.

Anemia↗
PubMed1976

Metabolic intermediates and lactate diffusion in active dog skeletal muscle.

The concentration of several metabolic intermediates, blood flow (Q), oxygen uptake (VO2), and lactate release (La) were measured in the gastrocnemius muscle of anesthetized dogs. Muscle lactate concentration increased from 1.6 to 2.7 mumol/g wet wt (P less than 0.05) during 0.5-5 min of contractions at 5 twitches/s but was not different from the contralateral resting muscle at 15, 30, or 60 min. Glycerophosphate increased from 0.35 to 0.70 mumol/g wet wt (P less than 0.05) during 0.5-5 min of activity, whereas muscle pyruvate decreased from 0.09 to 0.07 mumol/g wet wt (P less than 0.05). The concentration of NAD did not change in 9 of 11 experiments during contractions, despite a 12- to 15-fold increase in La. Significant decreases in NAD were observed when Q was compromised by arterial occlusion during contractions. No demonstrable relationship existed between La and either the muscle lactate concentration or muscle-venous lactate concentration gradient. Q was positively correlated with both La and muscle lactate during the first 5-15 min of activity. We conclude that increased La or increased lactate concentration in muscle need not be associated with hypoxia and that Q has a major influence on La.

Animals↗