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Biomedical subjects

M J Joyner

Publications and source records attributed to M J Joyner.

At least 55 records · Page 3Linked to original sources
PubMed1998

Reduced leg blood flow during dynamic exercise in older endurance-trained men.

It is currently unclear whether aging alters the perfusion of active muscles during large-muscle dynamic exercise in humans. To study this issue, direct measurements of leg blood flow (femoral vein thermodilution) and systemic arterial pressure during submaximal cycle ergometry (70, 140, and 210 W) were compared between six younger (Y; 22-30 yr) and six older (O; 55-68 yr) chronically endurance-trained men. Whole body O2 uptake, ventilation, and arterial and femoral venous samples for blood-gas, catecholamine, and lactate determinations were also obtained. Training duration (min/day), estimated leg muscle mass (dual-energy X-ray absorptiometry; Y, 21.5 +/- 1.2 vs. O, 19.9 +/- 0.9 kg), and blood hemoglobin concentration (Y, 14.9 +/- 0.4 vs. O, 14.7 +/- 0.2 g/dl) did not significantly differ (P > 0.05) between groups. Leg blood flow, leg vascular conductance, and femoral venous O2 saturation were approximately 20-30% lower in the older men at each work rate (all P < 0.05), despite similar levels of whole body O2 uptake. At 210 W, leg norepinephrine spillover rates and femoral venous lactate concentrations were more than twofold higher in the older men. Pulmonary ventilation was also higher in the older men at 140 (+24%) and 210 (+39%) W. These results indicate that leg blood flow and vascular conductance during cycle ergometer exercise are significantly lower in older endurance-trained men in comparison to their younger counterparts. The mechanisms responsible for this phenomenon and the extent to which they operate in other groups of older subjects deserve further attention.

Adult↗
PubMed1998

Effects of nitric oxide synthase inhibition on cutaneous vasodilation during body heating in humans.

We sought to examine further the potential role of nitric oxide (NO) in the neurally mediated cutaneous vasodilation in nonacral skin during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured by using laser-Doppler flowmeters placed on both forearms. The NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) was given selectively to one forearm via a brachial artery catheter after marked cutaneous vasodilation had been established. During body heating, oral temperature increased by 1.1 +/- 0.1 degreesC while heart rate increased by 30 +/- 6 beats/min. Mean arterial pressure stayed constant at 84 +/- 2 mmHg. In the experimental forearm, cutaneous vascular conductance (CVC; laser-Doppler) decreased to 86 +/- 5% of the peak response to heating (P < 0.05 vs. pre-L-NMMA values) after L-NMMA infusion. In some subjects, L-NMMA caused CVC to fall by approximately 30%; in others, it had little impact on the cutaneous circulation. CVC in the control arm showed a similar increase with heating, then stayed constant while L-NMMA was given to the contralateral side. These results demonstrate that NO contributes modestly, but not consistently, to cutaneous vasodilation during body heating in humans. They also indicate that NO is not the only factor responsible for the dilation.

Adult↗
PubMed1998

Leg mass and lower body negative pressure tolerance in men and women.

To explore the hypothesis that lower body muscle mass correlates with orthostatic tolerance, 18 healthy volunteers (age 18-48 yr; 10 men, 8 women) underwent a graded lower body negative pressure (LBNP) protocol consisting of six, 5-min stages of suction up to 60 mmHg in 10-mmHg increments. Forearm blood flow, heart rate, and blood pressure were measured, and forearm vascular resistance was calculated. Leg muscle mass was assessed by dual-energy X-ray absorptiometry. All subjects received standard intravenous hydration for at least 8 h before the study. Six men and four women completed all stages of LBNP. Four men and four women developed presyncopal symptoms, including marked bradycardia and/or hypotension, at LBNP levels of 30 mmHg (n = 2;1 man, 1 woman), 40 mmHg (n = 2;1 man, 1 woman), and 50 mmHg (n = 4;2 men, 2 women). The presyncopal subjects had leg muscle masses ranging from 19.5 to 25.2 kg in men and from 11.7 to 16.6 kg in women. In subjects who completed all stages of LBNP, leg muscle mass ranged from 17.5 to 24.1 kg in men and from 10.4 to 18.0 kg in women. Leg muscle mass did not differ between presyncopal subjects and those who completed the protocol. Furthermore, there were no differences in the hemodynamic responses to LBNP between subjects with low vs. high leg mass. These data suggest that leg muscle mass is not a critical determinant of LBNP tolerance in otherwise healthy men and women.

Absorptiometry, Photon↗
PubMed1998

Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction.

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eight adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to approximately 20% maximal voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 120 mmHg for a 1-s period, then released as a simulation of the mechanical effect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscarinic blockade with atropine; and 3) after NO synthase inhibition with NG-monomethyl-L-arginine (L-NMMA) plus atropine. Forearm blood flow (FBF), measured by combined pulsed and echo Doppler ultrasound, was reduced at rest with L-NMMA-atropine compared with the other two conditions. After the single contraction, there were no effects of atropine, but L-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereas L-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation that L-NMMA reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of the hyperemia with exercise. It is unlikely that ACh and NO from the endothelium are involved in the dilator response to a single muscle contraction.

Acetylcholine↗
PubMed1997

Forearm sympathetic withdrawal and vasodilatation during mental stress in humans.

1. In humans, mental stress elicits vasodilatation in the muscle vascular beds of the forearm that may be neurally mediated. We sought to determine the extent to which this vasodilatation is due to sympathetic withdrawal, active neurogenic vasodilatation, or beta-adrenergically mediated vasodilatation. 2. We simultaneously measured forearm blood flow and muscle sympathetic nerve traffic to the forearm during mental stress in humans. In a second study, we measured forearm blood flow responses to mental stress after selective blockade of alpha-adrenergic neurotransmission in one forearm. In a final study, we measured forearm blood flow responses to mental stress after unilateral anaesthetic blockade of the stellate ganglion, alone or in combination with selective beta-adrenergic receptor blockade of the forearm. 3. During mental stress, muscle sympathetic nerve activity decreased from 5113 +/- 788 to 1509 +/- 494 total integrated activity min-1 (P < 0.05) and forearm vascular resistance decreased from 96 +/- 29 to 33 +/- 7 mmHg (dl of tissue) min ml-1 (P < 0.05). Considerable vasodilation was still elicited by mental stress after selective blockade of alpha-adrenergic neurotransmission. Vasodilatation also occurred during mental stress after stellate ganglion blockade. This dilatation was reduced by selective blockade of beta-adrenergic receptors in the forearm. 4. Our results support a role for both sympathetic withdrawal and beta-adrenergic vasodilatation as the major causes of the forearm vasodilatation during mental stress in humans.

Adolescent↗
PubMed1997

Evidence for nitric oxide-mediated sympathetic forearm vasodiolatation in humans.

1. Our aim was to determine if sympathetic vasodilatation occurs in the human forearm, and if the vasodilating substance nitric oxide contributes to this dilatation. We also sought to determine if the nitric oxide might be released as a result of cholinergic stimulation of the vascular endothelium. 2. Blood flow was measured in the resting non-dominant forearm with venous occlusion plethysmography. To increase sympathetic traffic to the resting forearm, rhythmic handgrip exercise to fatigue followed by post-exercise ischaemia was performed by the dominant forearm. A brachial artery catheter in the non-dominant arm was used to selectively infuse drugs. 3. During control conditions, there was mild vasodilatation in the resting forearm during exercise followed by constriction during post-exercise ischaemia. When exercise was performed after brachial artery administration of bretylium (to block noradrenaline release) and phentolamine (an alpha-adrenergic antagonist), profound vasodilatation was seen in the resting forearm during both exercise and post-exercise ischaemia. 4. When the nitric oxide synthase blocker NG-monomethyl-L-arginine (L-NMMA) was administered in the presence of bretylium and phentolamine prior to another bout of handgripping, little or no vasodilatation was seen either during exercise or post-exercise ischaemia. Atropine also blunted the vasodilator responses to exercise and post-exercise ischaemia after bretylium and phentolamine. 5. These results support the existence of active sympathetic vasodilatation in the human forearm and the involvement of nitric oxide in this phenomenon. They also suggest nitric oxide might be released as a result of cholinergic stimulation of the vascular endothelium.

Adrenergic Agents↗
PubMed1997

Does sympathetic activation blunt nitric oxide-mediated hyperemia in the human forearm?

To determine if the vasodilating substance nitric oxide (NO) interferes with the ability of sympathetic nerves to regulate blood flow in humans, forearm blood flow (FBF) was measured during brachial artery infusions of acetylcholine (ACh) to evoke endothelial NO release, and during infusions of the NO donor nitroprusside (NTP) in five healthy volunteers. Sympathetic activity was increased by application of lower body suction and antagonized by brachial artery infusions of phentolamine. In the control condition, FBF was 2.4 +/- 0.4 ml/100 ml per min and rose by 16.9 +/- 3.6 ml/100 ml per min during ACh at 16 micrograms/min and by 17.0 +/- 4.3 ml/100 ml per min at 64 micrograms/min. With suction, FBF was 1.7 +/- 0.6 ml/100 ml per min (p < 0.05 versus control) and rose by 11.4 +/- 3.2 ml/100 ml per min during ACh at 16 micrograms/min (p < 0.05 versus control). After phentolamine, FBF was 3.8 +/- 0.5 ml/100 ml per min at baseline (p < 0.05 versus control) and the increases in flow with ACh at either 16 or 64 micrograms/min were identical to control. During the control NTP trial, FBF rose by 6.3 +/- 1.1 ml/100 ml per min with NTP at 2.5 micrograms/min and by 12.1 +/- 1.4 ml/100 ml per min at 10 micrograms/min. Suction blunted and phentolamine augmented the increases in flow with NTP by approximately 50% (p < 0.05). Due to the unexpected results with ACh, the effects of suction and pharmacological sympathectomy with both phentolamine and bretylium on ACh-mediated dilation were evaluated with lower doses of ACh (8 and 32 micrograms/min) in six additional studies. Again, altered sympathetic activity had inconsistent effects on the rise in FBF with ACh administration. The effects of altered sympathetic activity on the blood flow responses to NTP indicate that sympathetic activity can modulate NO-mediated vasodilation, suggesting that NO does not have a major sympatholytic effect in the human forearm. That sympathetic activity did not consistently alter ACh-mediated vasodilation suggests that vasodilating mechanisms, in addition to NO release, can be activated by arterial administration of ACh in the human forearm.

Acetylcholine↗
PubMed1997

The effects of cross-linked hemoglobin on regional vascular conductance in dogs.

Hemoglobin (Hgb) solutions cause systemic vasoconstriction, which might limit their use as intraoperative blood substitutes. This constriction is thought to be caused by interaction between Hgb and nitric oxide (NO). To determine whether alpha-alpha cross-linked hemoglobin (XL-Hgb) interferes with NO-mediated vasodilation caused by acetylcholine (ACh) and sodium nitroprusside (NTP), we infused these compounds into the femoral, superior mesenteric, and circumflex coronary arteries of anesthetized dogs (n = 6) before and after partial exchange transfusion with XL-Hgb. Additional animals (n = 6) were studied after treatment with 5% albumin. XL-Hgb administration increased mean arterial pressure (MAP) from 81 +/- 5 to 112 +/- 8 (P < 0.05). Albumin reduced MAP from 84 +/- 4 mm Hg to 76 +/- 4 mm Hg (P < 0.05). Vascular conductance after XL-Hgb decreased in the femoral artery, was not changed in the mesenteric bed, and increased modestly in the coronary artery (from 0.19 +/- 0.03 to 0.26 +/- 0.02 mL x mm Hg(-1) x min(-1), P < 0.05). After albumin, conductance was unchanged in the femoral artery and increased in the mesenteric artery. Conductance also increased in the coronary bed (from 0.25 +/- 0.02 to 0.49 +/- 0.03 mL x mm Hg(-1) x min(-1), P < 0.05). The vasodilator response to ACh in the femoral or mesenteric beds was either unaffected or augmented by either XL-Hgb or albumin. In the coronary bed, XL-Hgb blunted the dilator responses to ACh and NTP, while albumin augmented the coronary dilator responses to ACh. In five additional dogs, the NO synthase inhibitor N(G)-monomethyl L-arginine caused MAP to increase from 85 +/- 4 to 90 +/- 8 mm Hg and blunted the coronary dilator responses to ACh by approximately 25%. Subsequent XL-Hgb administration caused a further increase in MAP to 112 +/- 19 mm Hg (P < 0.05) and also further blunted ACh-mediated vasodilator responses in the coronary circulation. XL-Hgb has complex effects on the circulatory system, including a reduction in the vasodilator responses to ACh and NTP in canine coronary arteries in vivo. The potential impact of these events on patients with significant coexisting disease is unclear.

Acetylcholine↗
PubMed1997

Vasovagal syncope and skeletal muscle vasodilatation: the continuing conundrum.

During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypotension, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed since vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In both cases, there is no bradycardia but hypotension during the syncopal attacks. The major site of the vasodilation is in skeletal muscle and muscle sympathetic nerve activity is suppressed just prior to and during vasovagal attacks, indicating that sympathetic withdrawal contributes to the dilation. However, the skeletal muscle vasodilation seen during syncope is greater than that caused by sympathetic withdrawal alone, and it is absent in limbs that have undergone surgical sympathectomy, or local anesthetic nerve block. These observations suggest a role for neurally mediated "active" vasodilation during syncope. The afferent neural pathways that evoke the profound vasodilation during vasovagal attacks remain the subject of debate. The neural pathways responsible for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, beta-adrenergic, and nitroxidergic (nitric oxide) vasodilator mechanisms are not essential to observe the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.

Adrenergic Fibers↗
PubMed1997

Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery.

The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + NG-monomethyl-L-arginine (L-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by approximately 71% (P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine + L-NMMA. Both drug conditions reduced FBF during exercise by approximately 10% compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + L-NMMA. Total FBF during 5 min of recovery was reduced with atropine + L-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise.

Acetylcholine↗
PubMed1997

Skeletal muscle mass and the reduction of VO2max in trained older subjects.

The role of skeletal muscle mass in the age-associated decline in maximal O2 uptake (VO2max) is poorly defined because of confounding changes in muscle oxidative capacity and in body fat and the difficulty of quantifying active muscle mass during exercise. We attempted to clarify these issues by examining the relationship between several indexes of muscle mass, as estimated by using dual-energy X-ray absorptiometry and treadmill VO2max in 32 chronically endurance-trained subjects from four groups (n = 8/group): young men (20-30 yr), older men (56-72 yr), young women (19-31 yr), and older women (51-72 yr). VO2max per kilogram body mass was 26 and 22% lower in the older men (45.9 vs. 62.0 ml.kg-1.min-1) and older women (40.0 vs. 51.5 ml.kg-1.min-1). These age differences were reduced to 14 and 13%, respectively, when VO2max was expressed per kilogram of appendicular muscle. When appropriately adjusted for age and gender differences in appendicular muscle mass by analysis of covariance, whole body VO2max was 0.50 +/- 0.09 l/min less (P < 0.001) in the older subjects. This effect was similar in both genders. These findings suggest that the reduced VO2max seen in highly trained older men and women relative to their younger counterparts is due, in part, to a reduced aerobic capacity per kilogram of active muscle independent of age-associated changes in body composition, i.e., replacement of muscle tissue by fat. Because skeletal muscle adaptations to endurance training can be well maintained in older subjects, the reduced aerobic capacity per kilogram of muscle likely results from age-associated reductions in maximal O2 delivery (cardiac output and/or muscle blood flow).

Absorptiometry, Photon↗
PubMed1997

Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans.

Our aim was to determine whether sympathetic withdrawal alone can account for the profound forearm vasodilation that occurs during syncope in humans. We also determined whether either vasodilating beta 2-adrenergic receptor or nitric oxide (NO) contributes to this dilation. Forearm blood flow was measured bilaterally in healthy volunteers (n = 10) by using plethysmography during two bouts of graded lower body negative pressure (LBNP) to syncope. In one forearm, drugs were infused via a brachial artery catheter while the other forearm served as a control. In the control arm, forearm vascular resistance (FVR) increased from 77 +/- 7 units at baseline to 191 +/- 36 units with -40 mmHg of LBNP (P < 0.05). Mean arterial pressure fell from 94 +/- 2 to 47 +/- 4 mmHg just before syncope, and all subjects demonstrated sudden bradycardia at the time of syncope. At the onset of syncope, there was sudden vasodilation and FVR fell to 26 +/- 6 units (P < 0.05 vs. baseline). When the experimental forearm was treated with bretylium, phentolamine, and propranolol, baseline FVR fell to 26 +/- 2 units, the vasoconstriction during LBNP was absent, and FVR fell further to 16 +/- 1 units at syncope (P < 0.05 vs. baseline). During the second trial of LBNP, mean arterial pressure again fell to 47 +/- 4 mmHg and bradycardia was again observed. Treatment of the experimental forearm with the NO synthase inhibitor NG-monomethyl-L-arginine in addition to bretylium, phentolamine, and propranolol significantly increased baseline FVR to 65 +/- 5 units but did not prevent the marked forearm vasodilation during syncope (FVR = 24 +/- 4 vs. 29 +/- 8 units in the control forearm). These data suggest that the profound vasodilation observed in the human forearm during syncope is not mediated solely by sympathetic withdrawal and also suggest that neither beta 2-adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.

Acetylcholine↗
PubMed1997

Nitric oxide and vasodilation in human limbs.

Both the skeletal muscle and skin of humans possess remarkable abilities to vasodilate. Marked vasodilation can be seen in these vascular beds in response to a variety of common physiological stimuli. These stimuli include reactive hyperemia (skin and muscle), exercise hyperemia (muscle), mental stress (muscle), and whole body heating (skin). The physiological mechanisms that cause vasodilation in response to these stimuli are poorly understood, and the substance(s) responsible for it remain unclear. In this context, recent attention has been focused on the possible contribution of nitric oxide (NO) to the regulation of hyperemic responses in human skin and skeletal muscle. The emerging picture is that NO is not an essential component of the dilator response seen during reactive hyperemia. However, it does appear that NO may play a modest role in exercise hyperemia. NO appears to play a major role in the skeletal muscle vasodilation seen in response to mental stress in humans. Preliminary evidence also indicates that NO is not essential for the normal dilator responses observed in the cutaneous circulation during body heating in humans, but this issue needs further study. There are a number of possible mechanisms that might mediate NO release in humans, and the role of these mechanisms in the various hyperemic responses is also poorly understood. The role of altered NO-mediated vasodilation in some disease states is also discussed. Whereas NO is a potent vasodilating substance, the actions of NO alone do not explain a variety of poorly understood vasodilator mechanisms in conscious humans. Much work remains for those interested in the role of NO in the regulation of blood flow to the skin and skeletal muscle of humans.

Animals↗
PubMed1996

Active vasodilation during fainting: a hypothesis revisited.

The current concept is that the vasodilation which contributes to fainting (vasovagal syncope) is caused entirely by withdrawal of sympathetic vasoconstrictor tone (i.e. passive vasodilation). This concept has supplanted the idea that an active, sympathetically mediated component to the vasodilation exists in humans. We have several lines of evidence suggesting that there can be sympathetically mediated active vasodilation in humans. We speculate that this active vasodilation may be linked to the release of the recently identified vasodilator nitric oxide. Along these lines, we have experimental evidence consistent with neurally mediated nitric oxide release during several types of sympathoexcitatory maneuvers in humans. We have also observed forearm vasodilation during a vasovagal response after alpha-adrenergic blockade of the forearm under study. These observations indicate that the potential role of active vasodilation during fainting in humans should be revisited.

History, 20th Century↗
PubMed1996

Propranolol blocks the hypophosphaturia of acute respiratory alkalosis in human subjects.

Respiratory alkalosis (RA) is seen in diverse clinical conditions including tissue hypoxia, malignancy, neurologic disorders, febrile states, pregnancy, and hepatic failure. Acute RA causes hypophosphaturia in rats, and this effect on renal phosphate handling is reversed by beta-adrenoreceptor antagonism. The objective of the present study was to determine the effect of acute RA on phosphate excretion in human patients in the absence and presence of beta-adrenoreceptor antagonism with propranolol. Twelve normal volunteers, 6 women and 6 men, were studied in two phases, once with placebo and once with intravenous infusion of propranolol. In both groups, 30-minute renal clearances were taken during normoventilation (NV) and during acute RA induced by voluntary hyperventilation. Acute RA produced a significant decrease in plasma phosphate (PPi) in the absence (deltaPPi = -0.16 +/- 0.03 mmol/L) and the presence (deltaPPi = -0.16 +/- 0.05 mmol/L) of propranolol. In the placebo group, fractional excretion of phosphate (FEPi) decreased from 24.1% +/- 3.4% in NV to 19.2% +/- 2.6% in RA. This was associated with a significant decrease in parathyroid hormone (PPTH), from 3.38 +/- 0.28 pmol/L in NV to 2.54 +/- 0.30 pmol/L in RA. In the propranolol group, FEPi did not change significantly, from 19.1% +/- 2.7% in NV to 18.7% +/- 3.0% in RA. This also occurred in the face of a decrease in PPTH, from 4.39 +/- 0.53 pmol/L in NV to 2.78 +/- 0.33 pmol/L in RA. Thus propranolol selectively changes the response of FEPi to acute RA while leaving the PPi and PPTH responses unaltered. This suggests that beta-adrenoreceptors play a role in the regulation of the response of renal phosphate handling during acute RA and that this role involves a direct tubular effect on phosphate reabsorption, independent of filtered load and hormonal status. We conclude that beta-adrenoreceptor antagonism blunts the hypophosphaturic effect of acute respiratory alkalosis in human subjects.

Adolescent↗
PubMed1996

Blood substitutes: fluids, drugs, or miracle solutions?

Oxygen-carrying volume-expanding solutions that can sustain life in the absence of red blood cells have been developed. Concerns about side effects, sources of hemoglobin, and the ultimate demonstration of efficacy will have to be satisfactorily addressed before anesthesiologists routinely administer such solutions in place of red cells during surgery.

Animals↗