scholarly journals In vivo imaging with a water immersion objective affects brain temperature, blood flow and oxygenation

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Morgane Roche ◽  
Emmanuelle Chaigneau ◽  
Ravi L Rungta ◽  
Davide Boido ◽  
Bruno Weber ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Temperature ◽  
Water Immersion ◽  
Phosphorescence Lifetime ◽  
Cranial Window ◽  
Hemoglobin Saturation ◽  
Tissue Po2 ◽  
Physiological Values ◽  
Water Immersion Objective

Previously, we reported the first oxygen partial pressure (Po2) measurements in the brain of awake mice, by performing two-photon phosphorescence lifetime microscopy at micrometer resolution (Lyons et al., 2016). However, this study disregarded that imaging through a cranial window lowers brain temperature, an effect capable of affecting cerebral blood flow, the properties of the oxygen sensors and thus Po2 measurements. Here, we show that in awake mice chronically implanted with a glass window over a craniotomy or a thinned-skull surface, the postsurgical decrease of brain temperature recovers within a few days. However, upon imaging with a water immersion objective at room temperature, brain temperature decreases by ~2–3°C, causing drops in resting capillary blood flow, capillary Po2, hemoglobin saturation, and tissue Po2. These adverse effects are corrected by heating the immersion objective or avoided by imaging through a dry air objective, thereby revealing the physiological values of brain oxygenation.

scholarly journals Author response: In vivo imaging with a water immersion objective affects brain temperature, blood flow and oxygenation

2019 ◽  
Author(s):  
Morgane Roche ◽  
Emmanuelle Chaigneau ◽  
Ravi L Rungta ◽  
Davide Boido ◽  
Bruno Weber ◽  
...  
Keyword(s):  
Blood Flow ◽  
In Vivo Imaging ◽  
Brain Temperature ◽  
Water Immersion ◽  
Author Response ◽  
Water Immersion Objective

Critical P O 2 of skeletal muscle in vivo

1999 ◽  
Vol 277 (5) ◽  
pp. H1831-H1840 ◽  
Author(s):  
Keith N. Richmond ◽  
Ross D. Shonat ◽  
Ronald M. Lynch ◽  
Paul C. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Tension ◽  
Muscle Blood Flow ◽  
Interstitial Oxygen ◽  
Local Conditions ◽  
Phosphorescence Lifetime ◽  
Nadh Fluorescence

The main purpose of this study was to determine the interstitial oxygen tension at which aerobic metabolism becomes limited (critical [Formula: see text]) in vivo in resting skeletal muscle. Using an intravital microscope system, we determined the interstitial oxygen tension at 20-μm-diameter tissue sites in rat spinotrapezius muscle from the phosphorescence lifetime decay of a metalloporphyrin probe during a 1-min stoppage of muscle blood flow. In paired experiments NADH fluorescence was measured at the same sites during flow stoppage. NADH fluorescence rose significantly above control when interstitial[Formula: see text] fell to 2.9 ± 0.5 mmHg ( n = 13) and was not significantly different (2.4 ± 0.5 mmHg) when the two variables were first averaged for all sites and then compared. Similar values were obtained using the abrupt change in rate of[Formula: see text] decline as the criterion for critical [Formula: see text]. With a similar protocol, we determined that NADH rose significantly at a tissue site centered 30 μm from a collecting venule when intravascular[Formula: see text] fell to 7.2 ± 1.5 mmHg. The values for critical interstitial and critical intravascular[Formula: see text] are well below those reported during free blood flow in this and in other muscle preparations, suggesting that oxygen delivery is regulated at levels well above the minimum required for oxidative metabolism. The extracellular critical[Formula: see text] found in this study is slightly greater than previously found in vitro, possibly due to differing local conditions rather than a difference in metabolic set point for the mitochondria.

Branchial and systemic roles of adenosine receptors in rainbow trout: an in vivo microscopy study

1996 ◽  
Vol 271 (3) ◽  
pp. R661-R669 ◽  
Author(s):  
L. Sundin ◽  
G. E. Nilsson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Rainbow Trout ◽  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Water Immersion ◽  
Cardiovascular Effects ◽  
Secondary System ◽  
A1 Receptor

The purinergic branchial vasomotor control in rainbow trout (Oncorhynchus mykiss) was studied using an epi-illumination microscope equipped with a water-immersion objective. Cardiac output (Q), heart rate, and dorsal (PDA) and ventral (PVA) aortic pressures were recorded simultaneously. Prebranchial injection of adenosine or the A1-receptor agonist N6-cyclopentyl-adenosine (CPA) constricted the distal portion of the filament vasculature, which coincided with an increase of PVA. The A2-receptor agonist PD-125944 was without effect. After adenosine and CPA injection, an overflow of blood to the secondary system was repeatedly observed unless blood flow came to a complete stop. The lack of a concomitant reduction of Q suggested a redistribution of blood to the secondary system and to more proximal parts of the filament. The branchial effects of adenosine and CPA were completely blocked by the unspecific adenosine receptor antagonist amino-phylline and the specific A1-receptor antagonist N6-cyclopen-tyltheophylline. The results suggest that A1-receptors alone mediate the branchial vasoconstriction observed. Thus the responses of the branchial vasculature to adenosine include a vasoconstriction of the filament vasculature mediated via specific A1 receptors and a redistribution of blood flow to the secondary system and to proximal parts of the filament. Additional cardiovascular effects of adenosine included decreased systemic vascular resistance and heart rate.

scholarly journals Rethinking the Conditions and Mechanism for Glymphatic Clearance

2021 ◽  
Vol 15 ◽  
Author(s):  
Craig F. Ferris
Keyword(s):  
Blood Flow ◽  
Cerebral Spinal Fluid ◽  
Brain Temperature ◽  
New Model ◽  
Glymphatic System ◽  
Critical Studies ◽  
Circadian Changes ◽  
Cranial Window ◽  
The Brain ◽  
By Products

Critical studies that form the foundation of the glymphatic system and the clearance of metabolic by-products of unwanted proteins from the brain are reviewed. Concerns are raised about studying glymphatic flow in anesthetized animals and making assumptions about the whole brain based upon data collected from a cranial window on the cortex. A new model is proposed arguing that the flow of cerebral spinal fluid and parenchymal clearance in the perivascular system of unwanted proteins is regulated by circadian changes in brain temperature and blood flow at the level of the microvasculature.

Tissue gas tensions in experimental anemia

1963 ◽  
Vol 18 (4) ◽  
pp. 734-738 ◽  
Author(s):  
D. Bartlett ◽  
S. M. Tenney
Keyword(s):  
Blood Flow ◽  
Hemoglobin Concentration ◽  
Threshold Concentration ◽  
Alveolar Ventilation ◽  
Rate Process ◽  
Dissociation Curve ◽  
Diffusion Factor ◽  
Flow Response ◽  
Physiological Values

“Tissue-venous” O2 and CO2 tensions were determined by the subcutaneous gas pocket technique in rats with induced anemia of varying severity. Correlative ventilatory and metabolic measurements were made under light anesthesia. Gas pocket CO2 tension remained unchanged in all animals, but O2 tension decreased in anemic animals. Making use of the gas pocket tensions, rat blood nomogram, and certain assumptions, largely supported by the other measurements, a number of physiological values were calculated. From these it was concluded that in the anemic animal alveolar ventilation remained unchanged but, in the region of the gas pocket, blood flow increased with every decrement of hemoglobin concentration below the normal value. There was no “threshold” concentration of hemoglobin below normal at which point the blood flow response was initiated—the response was a continuous one. An in vivo slope value of the CO2 blood dissociation curve was derived and this was shown to vary directly with the hemoglobin concentration. Finally, the rate of disappearance of gas from the subcutaneous pocket suggested that there was a diffusion factor, in addition to blood flow, which played a role in the rate process. Submitted on November 13, 1962

scholarly journals Geometric Features of the Pial Arteriolar Networks in Spontaneous Hypertensive Rats: A Crucial Aspect Underlying the Blood Flow Regulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Dominga Lapi ◽  
Martina Di Maro ◽  
Nicola Serao ◽  
Martina Chiurazzi ◽  
Maurizio Varanini ◽  
...  
Keyword(s):  
Blood Flow ◽  
Peripheral Resistance ◽  
Hypertensive Rats ◽  
Cross Sectional ◽  
Spontaneously Hypertensive ◽  
Adult Age ◽  
Cranial Window ◽  
Frequency Components ◽  
Geometric Arrangements

BackgroundSeveral studies indicate that hypertension causes major changes in the structure of the vessel wall by affecting the regulation of blood supply to the tissues. Recently, it has been observed that capillary blood flow is also considerably influenced by the structural arrangement of the microvascular networks that undergo rarefaction (reduction of the perfused vessel number). Therefore, this study aimed to assess the geometric arrangements of the pial arteriolar networks and the arteriolar rhythmic diameter changes in spontaneously hypertensive rats (SHRs).MethodsFluorescence microscopy was utilized to observe in vivo the pial microcirculation through a closed cranial window. Pial arterioles were classified according to Strahler’s method. The arteriolar rhythmic diameter changes were evaluated by a generalization short-time Fourier transform.ResultYoung SHRs showed four orders of vessels while the adult ones only three orders. The diameter, length, and branching number obeyed Horton’s law; therefore, the vessels were distributed in a fractal manner. Larger arterioles showed more asymmetrical branches than did the smaller ones in young SHRs, while in adult SHRs smaller vessels presented asymmetrical branchings. In adult SHRs, there was a significant reduction in the cross-sectional area compared with the young SHRs: this implies an increase in peripheral resistance. Young and adult age-matched normotensive rats did not show significant alterations in the geometric arteriolar arrangement with advancing age, both had four orders of arteriolar vessels, and the peripheral resistance did not change significantly. Conversely, the frequency components evaluated in arteriolar rhythmic diameter changes of young and adult SHRs showed significant differences because of a reduction in the frequency components related to endothelial activity detected in adult SHRs.ConclusionIn conclusion, hypertension progressively causes changes in the microarchitecture of the arteriolar networks with a smaller number of vessels and consequent reduced conductivity, characteristic of rarefaction. This was accompanied by a reduction in the formation and release of independent and dependent – endothelial nitric oxide components regulating arterial vasomotion.

Changes in arterioles, arteries, and local perfusion of the brain stem during hemorrhagic hypertension

1996 ◽  
Vol 270 (4) ◽  
pp. H1350-H1354 ◽  
Author(s):  
K. Toyoda ◽  
K. Fujii ◽  
S. Ibayashi ◽  
S. Sadoshima ◽  
M. Fujishima
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Basilar Artery ◽  
Doppler Flowmetry ◽  
Large Arteries ◽  
Cerebrovascular Resistance ◽  
Cranial Window ◽  
Arterial Blood ◽  
The Brain

Cerebral arterioles have been regarded as the primary sites of autoregulatory responses, whereas the role of large arteries in the cerebral autoregulation is poorly understood. The goal of this study was to determine in vivo whether the basilar artery and its primary branches act as resistance vessels under hypotensive conditions by simultaneously measuring their diameters and local brain stem blood flow with laser-Doppler flowmetry. In 10 anesthetized rats, blood flow to the brain stem was well maintained during stepwise hemorrhagic hypotension when mean arterial blood pressure fell from 116 +/- 3 to 50 mmHg and decreased gradually between 50 and 30 mmHg. Diameter of the basilar artery (n = 10) and its large branches (n = 22), measured through an open cranial window, increased by 10% from the baseline value at 50 mmHg and reached their maximum at 30 mmHg (314 +/- 9 from 244 +/- 6 mum, and 149 +/- 4 from 117 +/- 3 mum, respectively). Small branches (n = 15) dilated to a larger extent compared with the larger arteries throughout hypotension and reached the maximum at 30 mmHg (69 +/- 3 from 48 +/- 2 mum). Below 30 mmHg, there was a steep fall in blood flow and reduction in diameter of all-sized arteries. Thus small vessels contribute to reductions in cerebrovascular resistance throughout the entire autoregulatory-range in the brain stem circulation. Large arteries, such as the basilar artery and its branches, also contribute to reductions in cerebrovascular resistance around the lower limits of cerebral blood flow autoregulation and may thus play a significant role in maintaining blood flow to the brain stem during severe systemic hypotension.

Enhanced oxygenation in vivo by allosteric inhibitors of hemoglobin saturation

1993 ◽  
Vol 265 (4) ◽  
pp. H1450-H1453 ◽  
Author(s):  
S. R. Khandelwal ◽  
R. S. Randad ◽  
P. S. Lin ◽  
H. Meng ◽  
R. N. Pittman ◽  
...  
Keyword(s):  
Intraperitoneal Administration ◽  
Thigh Muscle ◽  
Dissociation Curve ◽  
Allosteric Inhibitors ◽  
Hemoglobin Saturation ◽  
Tissue Po2 ◽  
In Vivo Effects ◽  
O2 Dissociation Curve ◽  
O2 Dissociation

The in vivo effects on hemoglobin (Hb)-O2 affinity and tissue PO2 were investigated after intraperitoneal administration of 2-[4-(((dichloroanilino)-carbonyl)methyl)phenoxyl]-2-methyl propionic acid (RSR4; 150 mg/kg) or its 3,5-dimethyl derivative (RSR13; 300 mg/kg) in C3Hf/Sed mice. The Hb-O2 dissociation curve was plotted from tail vein blood samples using an O2 dissociation analyzer before and up to 160 min after compound administration. Twenty to 40 min after injection, the PO2 at 50% saturation of hemoglobin (Hb P50) increased by a mean of 25% (range 18-31%) after RSR4 and 53% (range 36-76%) after RSR13. Tissue PO2 was continuously measured using an O2 microelectrode in thigh muscle before and up to 40 min after RSR4 or RSR13 injection. Twenty to 40 min after administration, tissue PO2 increased by a mean of 78% (range 30-127%) after RSR4 and 66% (range 39-97%) after RSR13 administration in anesthetized mice. No change in tissue PO2 was seen in anesthetized controls.

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