Regional blood flow and O2 transport during hypoxic and CO hypoxia in neonatal and adult sheep

1985 ◽  
Vol 248 (1) ◽  
pp. H118-H124 ◽  
Author(s):  
R. C. Koehler ◽  
R. J. Traystman ◽  
M. D. Jones
Keyword(s):  
Skeletal Muscle ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Small Intestine ◽  
Regional Blood Flow ◽  
Hypoxic Hypoxia ◽  
Age Group ◽  
Lung Inflation ◽  
Adult Sheep ◽  
O2 Transport

We compared regional blood flow in unanesthetized newborn lambs with that in adult sheep during acute, isocapnic hypoxic hypoxia [HH, 40-50% reduction of arterial O2 content (CaO2)]. The HH response in lambs and adults was qualitatively similar in heart, brain, and skeletal muscle, where flow increased; and in spleen, where it decreased. The response differed in skin and kidney, where flow decreased in lambs and was unchanged in adults, and in small intestine, where it was unchanged in lambs and increased in adults. Thus vasoconstriction during HH was less prominent in skin, kidney, and small intestine in adults. However, the trend toward lesser vasoconstriction in the adult cannot be attributed to a diminishing carotid chemoreflex and/or a more prominent vasodilatory lung inflation reflex because the same trend occurred during carbon monoxide hypoxia (COH). COH reduces CaO2 but stimulates neither the carotid chemoreflex nor, since hyperpnea is absent, the lung inflation reflex. Within each age group the responses to COH and HH were qualitatively the same. These data therefore provide no evidence for an active carotid chemoreflex in unanesthetized postnatal sheep. This is either because the peripheral circulatory effect of the chemoreflex is suppressed by the lung inflation reflex or, less likely, because the chemoreflex does not operate in the sheep at this level of HH.

scholarly journals Comparison of Cerebrovascular Response to Hypoxic and Carbon Monoxide Hypoxia in Newborn and Adult Sheep

1984 ◽  
Vol 4 (1) ◽  
pp. 115-122 ◽  
Author(s):  
Raymond C. Koehler ◽  
Richard J. Traystman ◽  
Scott Zeger ◽  
Mark C. Rogers ◽  
M. Douglas Jones
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Age Groups ◽  
Hypoxic Hypoxia ◽  
Dissociation Curve ◽  
Oxyhemoglobin Dissociation Curve ◽  
Adult Sheep ◽  
Control Value ◽  
Oxyhemoglobin Dissociation

Cerebral blood flow (CBF) responses to two types of isocapnic hypoxia, hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH), were examined in seven unanesthetized adult sheep by the radiolabeled microsphere technique. Comparisons were made with newborn lambs (5–12 days old) previously studied under similar conditions. The arterial O2 content (Cao2) was reduced in a graded manner to 50–60% of the control value. During HH, CBF increased to maintain cerebral O2 delivery (Cao2 x CBF) in both adults and newborns; however, cerebral O2 uptake (CMRO2) did not change. Although CMRO2 was higher in newborns, the responses of CBF/CMRO2 to HH did not differ significantly in newborns and adults. In newborns, regional CBF showed that brainstem areas were particularly responsive to HH. In both age groups, CBF increased to a greater extent with COH than with HH for similar reductions in Cao2. This resulted in an increase in cerebral O2 delivery with COH. The degree to which COH differed from HH correlated with the magnitude of the leftward shift of the oxyhemoglobin dissociation curve that accompanies COH. In adults, CMRO2 fell by 16% with COH but was maintained in newborns. We conclude that maintenance of cerebral O2 delivery during acute, isocapnic HH is a property of CBF regulation common to both newborn and adult sheep. During COH, the position of the oxyhemoglobin dissociation curve is an additional factor that sets the level of O2 delivery. The fetal conditions of low Cao2 and a left-shifted oxyhemoglobin dissociation curve may have provided the newborn with a microcirculation better suited for maintaining CMRO2 during COH.

Regional blood flow in newborn piglets during environmental cold stress

1986 ◽  
Vol 251 (3) ◽  
pp. G308-G313 ◽  
Author(s):  
S. R. Mayfield ◽  
B. S. Stonestreet ◽  
A. M. Brubakk ◽  
P. W. Shaul ◽  
W. Oh
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Small Intestine ◽  
Cold Stress ◽  
Vascular Resistance ◽  
Oxygen Delivery ◽  
Regional Blood Flow ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Newborn Piglets

Regional blood flow, oxygen delivery, and vascular resistance were determined in newborn piglets during a successful homeothermic response to environmental cold stress. Eight 3- to 4-day-old awake piglets were studied in a thermoneutral environment and 30, 45, and 60 min after onset of environmental cold stress. During cold stress, blood flow was significantly increased to skeletal muscle, the thermogenic organ, and decreased to the small intestine (P less than 0.05). Because arterial oxygen content (CaO2) was stable during the study, changes in oxygen delivery (CaO2 X blood flow) paralleled blood flow. Vascular resistance during cold stress was significantly decreased in skeletal muscle and increased in both the adrenals and the small intestine (P less than 0.05). We conclude that, during successful thermogenesis, the redistribution of cardiac output toward the thermogenic organ (skeletal muscle) is associated with a significant decrease in intestinal blood flow and oxygen delivery. This is not a passive process as evidenced by the coincident observation of increased intestinal vascular resistance.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

scholarly journals Coronary and cerebral metabolism-blood flow coupling and pulmonary alveolar ventilation-blood flow coupling may be disabled during acute carbon monoxide poisoning

2020 ◽  
Vol 129 (5) ◽  
pp. 1039-1050
Author(s):  
Ronald F. Coburn
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Cerebral Metabolism ◽  
Carbon Monoxide Poisoning ◽  
Alveolar Ventilation ◽  
Physiological Adaptation ◽  
Acute Carbon Monoxide Poisoning ◽  
Flow Coupling ◽  
Adaptation Mechanisms

This article introduces and supports a postulate that the tissue hypoxia component of carbon monoxide poisoning results in part from impairment of physiological adaptation mechanisms whereby tissues can match regional blood flow to O2 uptake, and the lung can match regional blood flow to alveolar ventilation.

scholarly journals Hmox1 (Heme Oxygenase-1) Protects Against Ischemia-Mediated Injury via Stabilization of HIF-1α (Hypoxia-Inducible Factor-1α)

2020 ◽  
Author(s):  
Louise L. Dunn ◽  
Stephanie M.Y. Kong ◽  
Sergey Tumanov ◽  
Weiyu Chen ◽  
James Cantley ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Heme Oxygenase ◽  
Hypoxia Inducible Factor ◽  
Ischemic Injury ◽  
Heme Oxygenase 1 ◽  
Wild Type ◽  
Tissue Necrosis ◽  
Hypoxia Inducible Factor 1Α

Objective: Hmox1 (heme oxygenase-1) is a stress-induced enzyme that catalyzes the degradation of heme to carbon monoxide, iron, and biliverdin. Induction of Hmox1 and its products protect against cardiovascular disease, including ischemic injury. Hmox1 is also a downstream target of the transcription factor HIF-1α (hypoxia-inducible factor-1α), a key regulator of the body’s response to hypoxia. However, the mechanisms by which Hmox1 confers protection against ischemia-mediated injury remain to be fully understood. Approach and Results: Hmox1 deficient ( Hmox1 –/– ) mice had impaired blood flow recovery with severe tissue necrosis and autoamputation following unilateral hindlimb ischemia. Autoamputation preceded the return of blood flow, and bone marrow transfer from littermate wild-type mice failed to prevent tissue injury and autoamputation. In wild-type mice, ischemia-induced expression of Hmox1 in skeletal muscle occurred before stabilization of HIF-1α. Moreover, HIF-1α stabilization and glucose utilization were impaired in Hmox1 –/– mice compared with wild-type mice. Experiments exposing dermal fibroblasts to hypoxia (1% O 2 ) recapitulated these key findings. Metabolomics analyses indicated a failure of Hmox1 –/– mice to adapt cellular energy reprogramming in response to ischemia. Prolyl-4-hydroxylase inhibition stabilized HIF-1α in Hmox1 –/– fibroblasts and ischemic skeletal muscle, decreased tissue necrosis and autoamputation, and restored cellular metabolism to that of wild-type mice. Mechanistic studies showed that carbon monoxide stabilized HIF-1α in Hmox1 –/– fibroblasts in response to hypoxia. Conclusions: Our findings suggest that Hmox1 acts both downstream and upstream of HIF-1α, and that stabilization of HIF-1α contributes to Hmox1’s protection against ischemic injury independent of neovascularization.

Age-related changes in regional blood flow in the rat

1985 ◽  
Vol 249 (3) ◽  
pp. H485-H491 ◽  
Author(s):  
R. F. Tuma ◽  
G. L. Irion ◽  
U. S. Vasthare ◽  
L. A. Heinel
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Index ◽  
Regional Blood Flow ◽  
Adult Rats ◽  
Blood Flows ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Regional Blood Flows ◽  
Central Hemodynamic

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.

Effects of insulin-like growth factor-I and LR3IGF-I on regional blood flow in normal rats

1997 ◽  
Vol 155 (2) ◽  
pp. 351-358 ◽  
Author(s):  
CM Gillespie ◽  
AL Merkel ◽  
AA Martin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Arterial Blood ◽  
Cardiovascular Side Effects ◽  
Igf I ◽  
The Central Nervous System ◽  
The Brain ◽  
Infusion Period

Two studies were conducted to investigate the haemodynamic effects of IGF-I and its analogue LR3IGF-I in normal anaesthetised rats. Infusion of IGF-I intravenously, at a dose of 125 micrograms/kg/h, for 20 min in the first study resulted in renal blood flow being significantly elevated by 35% above baseline. Mean arterial blood pressure (MABP) at this IGF-I dose fell by 18% of baseline, with LR3IGF-I also causing a significant decline in MABP (by 15%) at the dose of 125 micrograms/kg/h. In the second study the intravenous administration of IGF-I or LR3IGF-I, at a dose of 125 micrograms/kg/h, over a period of 60 min, resulted in MABP being significantly lowered by 25% of baseline values. Regional blood flow rates were determined using radioactive microspheres, 15 microns in diameter, injected systemically at the end of the peptide infusion period. The gastrocnemius, a representative skeletal muscle, was the only vascular region to show a significant increase in blood flow after IGF-I (by 58%) or LR3IGF-1 (by 308%) infusion. Vascular resistance in the brain was significantly reduced after infusion of IGF-I (by 60%) or LR3IGF-I (by 48%) as compared with vehicle. Skeletal muscle vascular resistance was also reduced by IGF-I (by 41%) and more particularly by LR3IGF-I (by 77%) in comparison to vehicle. These alterations to vascular tone produced by IGF infusion may be related to the central nervous system and systemic cardiovascular side-effects that have been reported during IGF-I administration in humans.

Effects of intra-arterial arginine-vasopressin infusions on peripheral blood flows in conscious dogs

1986 ◽  
Vol 71 (6) ◽  
pp. 713-721 ◽  
Author(s):  
Jean-Francois Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Small Intestine ◽  
Arginine Vasopressin ◽  
Muscle Blood Flow ◽  
Plasma Concentrations ◽  
Abdominal Fat ◽  
Conscious Dogs ◽  
Bone Blood Flow ◽  
Blood Flows

1. We reported in an earlier study that intravenous infusions of arginine-vasopressin (AVP), 220 pg min−1 kg−1 for 1 h, substantially reduced blood flow to the skin, skeletal muscle, pancreas, colon, small intestine, abdominal fat and myocardium [1] in conscious dogs. In the present study, we infused AVP directly into the artery supplying these organs and tissues in order to determine the relative contribution of local versus systemic mechanisms in the vascular resistance changes previously observed. 2. Regional blood flows were measured with radioactive microspheres in conscious, chronically instrumented dogs before and during intra-arterial infusions of AVP administered into the left axillary artery (n = 6), the left coronary artery (n = 6), and the cranial mesenteric artery (n = 6). The infusion rates were calculated to increase local, target organ plasma concentrations of AVP to the levels reached in our previous study while minimizing systemic changes. 3. Left axillary AVP artery infusion significantly reduced skin and compact bone blood flow, but had no effect on skeletal muscle blood flow. Intra-coronary AVP infusion had no effect on myocardial blood flow nor on cardiac output. Intramesenteric AVP infusion had no effect on blood flow to the colon, small intestine and abdominal fat, but significantly reduced blood flow to those areas of the pancreas which received blood from the cannulated artery. 4. Measurements in a limited number of dogs indicated that the local axillary and mesenteric venous levels of AVP were similar when the hormone was infused systemically at a rate of 220 pg min−1 kg−1 or intra-arterially at a lower rate. 5. These findings suggest that the increase in resistance measured in the skeletal muscle, small intestine, colon and abdominal fat after systemic administration of small amounts of AVP results in large part from indirect mechanisms. Direct vasoconstrictor effects of AVP at these plasma concentrations appear limited to the skin, the pancreas and the compact bones.

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