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Biomedical subjects

S M Cain

Publications and source records attributed to S M Cain.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1982

A critical value for O2 transport in the rat.

Rat skeletal muscle O2 uptake (VO2) has been reported to be supply dependent even at normal blood flow rates. To find the point at which whole-animal VO2 became dependent on total O2 transport (TOT), intact anesthetized rats were ventilated under hypoxic, normoxic, and hyperoxic conditions while either normovolemic or hypovolemic. In this manner, TOT (cardiac output X arterial O2 content) was varied over a range of 5-80 ml . kg-1 . min-1 . VO2 was measured in a closed-circuit, double servospirometer system. O2 contents were measured in carotid artery and right heart blood. Arterial PCO2, pH, and rectal temperature were kept within normal limits. Above a TOT of 23 ml . kg-1 . min-1, reciprocal changes in O2 extraction and cardiac output maintained VO2 independently of TOT (VO2 = 17.9 +/- 1.3 ml . kg-1 . min-1). Below a TOT of 23 ml . kg-1 . min-1, Vo2 became linearly dependent upon TOT. For TOT between 5 and 16 ml . kg-1 . min-1, VO2 = 0.89 + 0.78 TOT (r = 0.98). These data indicate that above a critical TOT of approximately 23 ml . kg-1 . min-1, VO2 in anesthetized rats does not depend on TOT.

Animals↗
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

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

Effects of time and vasoconstrictor tone on O2 extraction during hypoxic hypoxia.

To test the role of peripheral vasoconstrictor tone in the efficient use of a limited O2 supply, three groups of anesthetized dogs were ventilated with 9.1% O2 until circulation failed. Two groups were alpha-blocked with phenoxybenzamine and one of those was volume expanded with dextran to restore blood pressure. After O2 utake was lowered in hypoxia, O2 uptake was linearly related to O2 delivery (cardiac output X arterial O2 content) with r = 0.94. The slope of that line was mathematically identical to the extraction ratio and it increased from 0.54 at 10 min to 0.87 at the end of hypoxia (r = 0.99). In both alpha-block groups O2 extraction remained constant with time, and O2 extraction in each alpha-block group was significantly less (P less than 0.01) than in the unblocked group. As further evidence of better O2 extraction, mixed venous partial O2 pressure was significantly less in the unblocked group, 6.2 +/- 3.4 Torr vs. 10.6 +/- 3.2 and 9.9 +/- 2.4 Torr with alpha block (P less than 0.01). Results after alpha-block indicated that a vigorous vasoconstrictor tone during hypoxia conserved O2 by promoting greater extraction by the tissues.

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↗
PubMed1977

Arterial lactate responses in dogs made apneic or breathing nitrogen.

O2 stores are kept more intact in apnea than in N2 breathing which removes O2stores from the body. If lactate moves readily into the circulation, arterial lactate should rise sooner with N2 breathing than with apnea because tissue O2 is lowered faster. This was tested in 10 anesthetized, paralyzed dogs made hypoxic both ways. Arterial and mixed venous blood were sampled every minute until circulation began to fail. Calculated changes in O2 stores would have supported control V O2 for 1.3 min with N2 and 2.7 min with apnea. The PVO2 at those times were 23.1 and 20.1 Torr. Although arterial lactate rose sooner with N2 than with apnea, the mean values for lactate increase for both N2 and apnea were fitted by a single curvilinear relation with PVO2. The PVO2 at which lactate first rosores were depleted. Latent period for lactate rise, therefore, was nearly the same as that for development of tissue hypoxia.

Animals↗
PubMed1977

pH effects on lactate and excess lactate in relation to O2 deficit in hypoxic dogs.

Both hypoxemia and alkalemia increase arterial lactate levels, but excess lactate (XL) may be better related to the true O2 deficit and less subject to the pH effect upon glycolysis. To test this idea, 50 anesthetized (30 ml/kg pentobarbital sodium) and paralyzed dogs in five groups were ventilated with low O2 mixtures. Arterial pH was altered by CO2, hyperventilation, and HCO3- so that the average pH of the five groups were 6.99, 7.21, 7.34, 7.53, and 7.54 (+ propranolol). Pyruvate and lactate levels rose at rates roughly corresponding to pH. In all animals, rise of lactate (deltaL), XL and net O2 deficit were linear with time and the slope accurately described the rate of rise. When the ratio of XL rate deltaL rate was plotted against pH, it increased toward unity as pH decreased to 6.9. The ratio of deltaL rate to true O2 deficit rate also showed a significant pH effect by increasing with pH. Ratio of XL rate to true O2 deficit rate, on the other hand, was independent of pH. XL may correct for red cell lactate production which is not affected by O2 supply but is influenced by pH.

Animals↗
PubMed1977

Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia.

Three groups of dogs were anesthetized, paralyzed, and ventilated at constant rates with the spleen clamped. Two groups were isovolemically hemodiluted with warm dextran and plasma to hematocrits just above and below that at which O2 uptake (VO2) could not be maintained at preanemic levels. One of these groups was given propranolol to reduce the cardiac output response to anemia. The third group was ventilated on a low O2 gas mixture to decrease oxygen uptake. VO2 was thus limited at a high-delivery O2 pressure (PO2) in anemia and a low-delivery PO2 in hypoxic hypoxia. VO2 was reduced at a mixed venous PO2 of 45 Torr in anemia and at 17 Torr in hypoxic hypoxia. VO2, mixed venous PO2, and O2 delivery decreased precipitously at hematocrits below 10%. Once VO2 was limited by O2 availability, a single linear relationship (r = 0.91) was found for percent VO2 as a function of total O2 delivery (cardiac output X arterial O2 content) during both anemic and hypoxic hypoxia. The critical value for O2 delivery was 9.8 ml/kg-min. When O2 supply became limiting, VO2 apparently was not diffusion limited because it was more dependent on volume delivery rates than on delivery PO2.

Anemia↗
PubMed1977

An analog approach to measuring O2 uptake on-line.

An analog circuit has been designed to provide a solution to the Haldane transformation that yields true O2 fraction. Incoming signals proportional to fractional concentration of CO2 and O2 in mixed expired gas are utilized in the circuit and the results are multiplied by a value proportional to ventilation. The final products are analog signals proportional to O2 uptake and CO2 output. The system is applicable to the anesthetized and paralyzed animal kept at a known constant ventilation. The final products are analog signals proportional to O2 uptake and CO2 output. The system is applicable to the anesthetized and paralyzed animal kept at a known constant ventilation. Diagrams of the circuit and expired gas collection and analysis arrangements are provided.

Animals↗
PubMed1975

Oxygen delivery and utilization in dogs with a sublethal dose of cobalt chloride.

Four groups of eight dogs each were anesthetized with pentobarbital, paralyzed with succinylcholine, and ventilated at constant rate. Control measurements were made for 30 min, then 15 mg/kg of cobaltous chloride was given slowly intravenously to one group. A second group was also given 1 mg/kg per h propranolol (beta-block); a third group was given NaHCO3 to correct pH changes after CoCl2; and a fourth group had both beta-block and NaHCO3. Vo2 was measured every 10 min for 4 h and blood was taken frequently for lactate, pyruvate, and blood gas measurements. Cobalt transiently decreased Vo2 in all groups but significantly more in those with beta-block (groups 2 and 4). Cardiac output and mean arterial pressure were also decreased in all groups but to similar extent. Recovery of Vo2 was complete, usually within 60 min with little evidence of deficit repayment. Total O2 transport (Q X Cao2) appeared to limit Vo2 below 12 ml/kg times min. Above that value, histotoxic effects of CoCl2 reduced Vo2 approximately 20%. Excess lactate (XL) in arterial blood was linearly correlated with measured O2 deficit during the acute reaction of CoCl2, in all but group 3, similar to results previously obtained in hypoxic hypoxia.

Animals↗
PubMed1975

Tissue oxygenation and splenic erythropoiesis during chronic hypoxia and hypercapnia.

Tissue (gas pocket) oxygen levels and erythropoietic activity were monitored in groups of rats chronically exposed to hypoxia (70 Torr PIO2), hypercapnia (60 Torr PICO2), or a combination of the two conditions. Arterial gas tensions and pH were also measured. Overall condition of the animals was assessed by comparison of growth rates with pair-fed controls. Hypoxic-hypercapnic pocket PO2 values (24-40 Torr) were similar to normoxic-normocapnic values (28-37 Torr), but greater than in hypoxia-normocapnia, and less than in normoxia-hypercapnia. Erythropoietic activity during hypoxia-hypercapnia ceased and the rats had a growth rate significantly below that of other groups. While chronic CO2 does increase tissue (pocket) oxygenation to near normal levels, probably due to increased ventilation and subsequently PaO2, the hypoxic-hypercapnic rats evidenced greater detrimental effects than did rats in hypoxic or hypercapnic environments.

Animals↗