Blood flow and tissue-pO2 in the trained and untrained gastrocnemius muscle of the anesthetized guinea pig

1975 ◽  
Vol 34 (1) ◽  
pp. 33-42 ◽  
Author(s):  
C. Doermer ◽  
W. Schroeder
Keyword(s):  
Blood Flow ◽  
Guinea Pig ◽  
Gastrocnemius Muscle ◽  
Tissue Po2

Catecholamine and serotonin concentrations in fetal guinea-pig brain: relation to regional cerebral blood flow and oxygen delivery in the growth-restricted fetus

1996 ◽  
Vol 8 (3) ◽  
pp. 355 ◽  
Author(s):  
A Jensen ◽  
HJ Klonne ◽  
A Detmer ◽  
AM Carter
Keyword(s):  
Blood Flow ◽  
Guinea Pig ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Tissue Concentrations ◽  
Blood Flows ◽  
Arterial Blood ◽  
Tissue Po2 ◽  
The Brain ◽  
Neurotransmitter Metabolism

To test the hypothesis that intrauterine growth restriction (IUGR) would lead to altered neurotransmitter metabolism in the brain because of poorer oxygenation, blood flows and tissue concentrations of noradrenaline, dopamine, serotonin and their metabolites were measured in 14 parts of the brain of guinea-pig fetuses at 61-64 days' gestation. Eight fetuses with IUGR induced by uterine artery ligation were compared with 8 controls. Regional brain blood flows were determined by the microsphere method and tissue concentrations of monoamines by HPLC with electrochemical detection. The oxygen content of preductal arterial blood was significantly lower in IUGR fetuses than in controls (2.3 +/- 0.6 v. 3.5 +/- 0.5 mM; P < 0.001). Although this was compensated by increases in blood flow to many areas of the brain, significant decreases occurred in oxygen delivery to the temporal and occipital cortex, hippocampus and cerebellum of IUGR fetuses. In contrast, oxygen delivery to brainstem areas was maintained. Noradrenaline concentrations were closely similar in brains from the two groups, except for an increase in the caudate nucleus of IUGR fetuses. Dopamine concentrations were significantly elevated in brainstem areas. Concentrations of 3,4-dihydroxyphenylglycol (DOPEG), a noradrenaline metabolite, and 3,4-dihydroxyphenylacetic acid (DOPAC), a dopamine metabolite, showed a similar pattern of increase in brains of IUGR fetuses, possibly resulting from increased synthesis of noradrenaline and dopamine rather than from decreased degradation. Concentrations of serotonin were significantly higher in frontal and temporal cortex of IUGR fetuses, and the serotonin metabolite 5-HIAA increased significantly in cortical areas. Changes in neurotransmitter metabolism could not be related to oxygen supply, since serotonin concentrations increased in the forebrain, despite reduced oxygen delivery and the known dependence of tryptophan-5-hydroxylase on tissue PO2, and dopamine levels were elevated in the brainstem, where the oxygen supply was maintained.

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

Brain adaptation to chronic hypobaric hypoxia in rats

1992 ◽  
Vol 72 (6) ◽  
pp. 2238-2243 ◽  
Author(s):  
J. C. LaManna ◽  
L. M. Vendel ◽  
R. M. Farrell
Keyword(s):  
Blood Flow ◽  
Motor Cortex ◽  
Microvessel Density ◽  
Hypobaric Hypoxia ◽  
Regional Blood Flow ◽  
Oxygen Availability ◽  
Sensory Cortex ◽  
Hypoxic Exposure ◽  
Normal Brain ◽  
Tissue Po2

Rats were exposed to hypobaric hypoxia (0.5 atm) for up to 3 wk. Hypoxic rats failed to gain weight but maintained normal brain water and ion content. Blood hematocrit was increased by 48% to a level of 71% after 3 wk of hypoxia compared with littermate controls. Brain blood flow was increased by an average of 38% in rats exposed to 15 min of 10% normobaric oxygen and by 23% after 3 h but was not different from normobaric normoxic rats after 3 wk of hypoxia. Sucrose space, as a measure of brain plasma volume, was not changed under any hypoxic conditions. The mean brain microvessel density was increased by 76% in the frontopolar cerebral cortex, 46% in the frontal motor cortex, 54% in the frontal sensory cortex, 65% in the parietal motor cortex, 68% in the parietal sensory cortex, 68% in the hippocampal CA1 region, 57% in the hippocampal CA3 region, 26% in the striatum, and 56% in the cerebellum. The results indicate that hypoxia elicits three main responses that affect brain oxygen availability. The acute effect of hypoxia is an increase in regional blood flow, which returns to control levels on continued hypoxic exposure. Longer-term effects of continued moderate hypoxic exposure are erythropoiesis and a decrease in intercapillary distance as a result of angiogenesis. The rise in hematocrit and the increase in microvessel density together increase oxygen availability to the brain to within normal limits, although this does not imply that tissue PO2 is restored to normal.

scholarly journals Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling

2021 ◽  
Author(s):  
Friedrich Ihler ◽  
Saskia Freytag ◽  
Benedikt Kloos ◽  
Jennifer Lee Spiegel ◽  
Frank Haubner ◽  
...  
Keyword(s):  
Animal Model ◽  
Blood Flow ◽  
Guinea Pig ◽  
Cochlear Blood Flow ◽  
Pig Animal Model

Effects of Electrical Stimulation of the Superior Cervical Ganglion on Cochlear Blood Flow in Guinea Pig

1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Cochlear Blood Flow ◽  
Cervical Ganglion ◽  
Stimulation Of

Effect of terbutaline sulphate on ovarian, uterine and maternal placental blood flow in the anaesthetized guinea pig

1978 ◽  
Vol 53 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Lena Mårtensson ◽  
Per-Ove B. Sjöquist ◽  
Leif Bjellin ◽  
Anthony M. Carter
Keyword(s):  
Blood Flow ◽  
Guinea Pig ◽  
Terbutaline Sulphate ◽  
Placental Blood ◽  
Placental Blood Flow

Chronic CO inhalation and carotid body catecholamines: testing of hypotheses

1989 ◽  
Vol 67 (1) ◽  
pp. 239-242 ◽  
Author(s):  
S. Lahiri ◽  
D. G. Penney ◽  
A. Mokashi ◽  
K. H. Albertine
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Direct Action ◽  
Systemic Effect ◽  
Hypoxic Hypoxia ◽  
Tissue Blood Flow ◽  
Catecholamine Content ◽  
Carotid Bodies ◽  
Significant Stimulation ◽  
Tissue Po2

The purpose of this study was twofold: one concerns carotid blood flow and tissue PO2 and the other the effect of chronic hypoxic hypoxia on enhanced catecholamine content. The rationale was that chronic CO inhalation would not mimic the effect of hypoxia on the carotid body if its tissue blood flow is sufficiently high to counteract the effect of CO on O2 delivery and, hence, on tissue PO2. The differential effects of CO on the carotid body and erythropoietin-producing tissue would also indicate that the effect of hypoxic hypoxia on the carotid body is the result of a direct action of a local low O2 stimulus rather than secondary to a systemic effect initiated by other O2-sensing tissues. To test these alternatives we studied the effects of chronic CO inhalation on carotid body catecholamine content and hematocrit in the rats, which were exposed to an inspired PCO of 0.4–0.5 Torr at an inspired PO2 of approximately 150 Torr for 22 days. The hematocrit of CO-exposed rats was 75 +/- 1.1% compared with 48 +/- 0.7% in controls. Dopamine and norepinephrine content of the carotid bodies (per pair) was 5.88 +/- 0.91 and 3.02 +/- 0.19 ng, respectively, in the CO-exposed rats compared with 6.20 +/- 1.0 and 3.29 +/- 0.6 ng, respectively, in the controls. Protein content of the carotid bodies (per pair) was 18.4 +/- 1.6 and 20.5 +/- 0.9 micrograms, respectively. Thus, despite a vigorous erythropoietic response, the CO-exposed rats failed to show any significant stimulation of carotid body in terms of the content of either catecholamine or protein. The results suggest that carotid body tissue PO2 is not compromised by moderate carboxyhemoglobinemia because of its high tissue blood flow and that the chronic effect of hypoxic hypoxia on carotid body is direct.

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