scholarly journals Differential microcirculation dynamics during deliberate hypotension induced by nicardipine, PGE1 and trimethaphan in rat mesentery

1995 ◽  
Vol 42 (11) ◽  
pp. 1035-1039 ◽  
Author(s):  
Ko Takakura ◽  
Yoshihiro Sugiura ◽  
Yukio Goto
Keyword(s):  
Deliberate Hypotension ◽  
Rat Mesentery

Changes in rat mesentery interstitial matrix due to superfusate

1993 ◽  
Vol 265 (3) ◽  
pp. H852-H856 ◽  
Author(s):  
B. J. Barber ◽  
R. A. Babbitt ◽  
S. Dutta ◽  
S. Parameswaran
Keyword(s):  
Protein Content ◽  
Normal Saline ◽  
Protein Concentration ◽  
Matrix Protein ◽  
Protein Transport ◽  
Albumin Concentration ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Rat Mesentery ◽  
Sprague Dawley Rats

Animal preparations for microscopy often require a superfusate solution to cover surgically exposed tissue. There are few, if any, data concerning the effects of this solution on extravascular protein concentration and hydration. The effect of superfusion on mesenteric tissue in anesthetized male Sprague-Dawley rats was studied. Tissue samples were taken from nonsuperfused and superfused tissue and analyzed for hydration, albumin, and transferrin content. The mesenteric tissue interstitial matrix was rapidly altered by normal saline superfusate. After superfusion, there was a decrease (P < 0.01) in tissue albumin concentration from 1.17 +/- 0.27 to 0.10 +/- 0.08 g/dl (n = 9). Tissue hydration increased from 4.98 +/- 0.8 micrograms water/microgram dry wt in controls to 7.38 +/- 1.2 micrograms water/micrograms dry wt after superfusion. When a range of superfusate albumin concentrations was used (0, 1, 2, and 3 g/dl), tissue albumin concentration changed 0.59 +/- 0.09 g/dl for each gram per deciliter change in superfusate concentration (P < 0.0001). The large changes in interstitial matrix protein content and hydration suggest that superfusate solution effects need to be considered in microvascular protein transport experiments.

DELIBERATE HYPOTENSION IN THE CONTROL OF OPERATIVE BLEEDING*

2006 ◽  
Vol 115 (1) ◽  
pp. 341-347 ◽  
Author(s):  
James E. Eckenhoff ◽  
Estela Melman
Keyword(s):  
Deliberate Hypotension

Generalization of the Fahraeus principle for microvessel networks

1986 ◽  
Vol 251 (6) ◽  
pp. H1324-H1332 ◽  
Author(s):  
A. R. Pries ◽  
K. Ley ◽  
P. Gaehtgens
Keyword(s):  
Cross Sections ◽  
Flow Direction ◽  
Quantitative Information ◽  
Red Cells ◽  
Branch Points ◽  
Velocity Difference ◽  
Rat Mesentery ◽  
The Individual ◽  
Fahraeus Effect ◽  
Flow Cross

Microvessel hematocrits and diameters were determined in each vessel segment between bifurcations of three complete microvascular networks in rat mesentery. Classification of the segments as arteriolar, venular, or arteriovenular (av) was based on flow direction at branch points. Photographic and videomicroscopic mapping was used to obtain quantitative information on the architecture and topology of the networks. This topological information allowed the analysis of hematocrit distribution within a series of consecutive-flow cross sections, each of which carried the total flow through the network. The observed reduction of mean hematocrit in the more peripheral cross sections is explained by the presence of a “vessel” and a “network” Fahraeus effect. The vessel Fahraeus effect results from velocity difference between red cells and blood within the individual vessel segments due to the existing velocity and cell concentration profiles. The network Fahraeus effect is based on the velocity difference of red cells and blood caused by velocity and hematocrit heterogeneity between the vessels constituting any of the complete-flow cross sections. The network Fahraeus effect is found to account for approximately 20% of the total hematocrit reduction and increases toward the most distal cross sections.

LABETALOL VS. NITROPRUSSIDE FOR DELIBERATE HYPOTENSION

1988 ◽  
Vol 67 (Supplement) ◽  
pp. 58
Author(s):  
N. R. Fahmy ◽  
M. R. Bottros ◽  
J. Charchaflieh ◽  
N. Sunder
Keyword(s):  
Deliberate Hypotension

scholarly journals Determinants of valve gating in collecting lymphatic vessels from rat mesentery

2011 ◽  
Vol 301 (1) ◽  
pp. H48-H60 ◽  
Author(s):  
Michael J. Davis ◽  
Elaheh Rahbar ◽  
Anatoliy A. Gashev ◽  
David C. Zawieja ◽  
James E. Moore
Keyword(s):  
Pressure Gradient ◽  
Muscle Tone ◽  
Lymphatic Vessels ◽  
Vessel Diameter ◽  
Intraluminal Pressure ◽  
Pressure Gradients ◽  
Rat Mesentery ◽  
Temporal Relationships ◽  
Wide Range ◽  
Valve Opening

Secondary lymphatic valves are essential for minimizing backflow of lymph and are presumed to gate passively according to the instantaneous trans-valve pressure gradient. We hypothesized that valve gating is also modulated by vessel distention, which could alter leaflet stiffness and coaptation. To test this hypothesis, we devised protocols to measure the small pressure gradients required to open or close lymphatic valves and determine if the gradients varied as a function of vessel diameter. Lymphatic vessels were isolated from rat mesentery, cannulated, and pressurized using a servo-control system. Detection of valve leaflet position simultaneously with diameter and intraluminal pressure changes in two-valve segments revealed the detailed temporal relationships between these parameters during the lymphatic contraction cycle. The timing of valve movements was similar to that of cardiac valves, but only when lymphatic vessel afterload was elevated. The pressure gradients required to open or close a valve were determined in one-valve segments during slow, ramp-wise pressure elevation, either from the input or output side of the valve. Tests were conducted over a wide range of baseline pressures (and thus diameters) in passive vessels as well as in vessels with two levels of imposed tone. Surprisingly, the pressure gradient required for valve closure varied >20-fold (0.1–2.2 cmH2O) as a passive vessel progressively distended. Similarly, the pressure gradient required for valve opening varied sixfold with vessel distention. Finally, our functional evidence supports the concept that lymphatic muscle tone exerts an indirect effect on valve gating.

Role of adenosine in noradrenergic neurotransmission in spontaneously hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson
Keyword(s):  
Plasma Levels ◽  
Spontaneously Hypertensive Rat ◽  
Base Line ◽  
Inhibitory Effects ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Rat Mesentery ◽  
Wistar Kyoto

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.

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