Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats

1996 ◽  
Vol 216 (3) ◽  
pp. 175-178
Author(s):  
W Min Li
Keyword(s):  
Anesthetized Rats ◽  
Systemic Hypoxia

Dissociation between skeletal muscle microvascular Po2and hypoxia-induced microvascular inflammation

2003 ◽  
Vol 94 (6) ◽  
pp. 2323-2329 ◽  
Author(s):  
Sidharth Shah ◽  
Julie Allen ◽  
John G. Wood ◽  
Norberto C. Gonzalez
Keyword(s):  
Blood Flow ◽  
Microvascular Blood Flow ◽  
Phosphorescence Quenching ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Systemic Hypoxia ◽  
Individual Contributions ◽  
Microvascular Inflammation ◽  
Quenching Method ◽  
The Individual

Systemic hypoxia (SHx) produces microvascular inflammation in mesenteric, cremasteric, and pial microcirculations. In anesthetized rats, SHx lowers arterial blood pressure (MABP), which may alter microvascular blood flow and microvascular Po2(PmO2) and influence SHx-induced leukocyte-endothelial adherence (LEA). These experiments attempted to determine the individual contributions of the decreases in PmO2, venular blood flow and shear rate, and MABP to the hypoxia-induced increase in LEA. Cremaster microcirculation of anesthetized rats was visualized by intravital microscopy. PmO2was measured by a phosphorescence-quenching method. SHx [inspired Po2of 70 Torr for 10 min, MABP of 65 ± 3 mmHg, arterial Po2(PaO2) of 33 ± 1 Torr] and cremaster ischemia (MABP of 111 ± 7 mmHg, PaO2of 86 ± 3 Torr) produced similar PmO2: 7 ± 2 and 6 ± 2 Torr, respectively. However, LEA increased only in SHx (1.9 ± 0.9 vs. 11.2 ± 1.1 leukocytes/100 μm, control vs. SHx, P < 0.05). Phentolamine-induced hypotension (MABP of 55 ± 4 mmHg) in normoxia lowered PmO2to 26 ± 6 Torr but did not increase LEA. Cremaster equilibration with 95% N2-5% CO2during air breathing (PaO2of 80 ± 1 Torr) lowered PmO2to 6 ± 1 Torr but did not increase LEA. On the other hand, when cremaster PmO2was maintained at 60–70 Torr during SHx (PaO2of 35 ± 1 Torr), LEA increased from 2.1 ± 1.1 to 11.1 ± 1.5 leukocytes/100 μm ( P < 0.05). The results show a dissociation between PmO2and LEA and support the idea that SHx results in the release of a mediator responsible for the inflammatory response.

Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats

1996 ◽  
Vol 216 (3) ◽  
pp. 175-178 ◽  
Author(s):  
Wei Min Li ◽  
Akio Sato ◽  
Atsuko Suzuki ◽  
Andrzej Trzebski
Keyword(s):  
Anesthetized Rats ◽  
Systemic Hypoxia

scholarly journals Role of the Kölliker-Fuse nucleus in cardiovascular responses to hypoxia and baroreceptor activation in anesthetized rats

Bioimpacts ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 55-61
Author(s):  
Nafiseh Mirzaei-Damabi ◽  
Bahar Rostami ◽  
Masoumeh Hatam
Keyword(s):  
Intravenous Injection ◽  
Significant Role ◽  
Cardiovascular Effect ◽  
Respiratory Control ◽  
Cardiovascular Responses ◽  
Anesthetized Rats ◽  
Systemic Hypoxia ◽  
Induced Hypertension ◽  
Baroreceptor Activation

<span style="color: #1f497d;">Introduction: Parabrachial Kölliker-Fuse (KF) complex, located in dorsolateral part of the pons, is involved in the respiratory control, however, its role in the baroreflex and chemoreflex responses has not been established yet. This study was performed to test the contribution of the KF to chemoreflex and baroreflex and the effect of microinjection of a reversible synaptic blocker (Cocl2) into the KF in urethane anesthetized rats. <br /> <span style="color: #1f497d;">Methods: Activation of chemoreflex was induced by systemic hypoxia caused by N2 breathing for 30 seconds "hypoxic- hypoxia methods" and baroreflex was evoked by intravenous injection (i.v.) of phenylephrine (Phe, 20 µg /kg/0.05–0.1 mL). N2 induced generalized vasodilatation followed by tachycardia reflex and Phe evoked vasoconstriction followed by bradycardia.<br /> <span style="color: #1f497d;">Results: Microinjection of Cocl2 (5 mM/100 nL/side) produced no significant changes in the Phe-induced hypertension and bradycardia, whereas the cardiovascular effect of N2 was significantly attenuated by the injection of CoCl2 to the KF. <br /> <span style="color: #1f497d;">Conclusion: The KF played no significant role in the baroreflex, but could account for cardiovascular chemoreflex in urethane anesthetized rats.

Mesenteric microvascular inflammatory responses to systemic hypoxia are mediated by PAF and LTB4

2003 ◽  
Vol 94 (6) ◽  
pp. 2313-2322 ◽  
Author(s):  
Alfred J. Casillan ◽  
Norberto C. Gonzalez ◽  
Jennifer S. Johnson ◽  
Dawn R. S. Steiner ◽  
John G. Wood
Keyword(s):  
Inflammatory Response ◽  
Vascular Permeability ◽  
Inflammatory Responses ◽  
Platelet Activating Factor ◽  
Ros Generation ◽  
Leukocyte Adherence ◽  
Anesthetized Rats ◽  
Systemic Hypoxia ◽  
Paf Receptor ◽  
Web 2086

Systemic hypoxia produces a rapid microvascular inflammatory response characterized by increased reactive oxygen species (ROS) levels, leukocyte-endothelial adherence and emigration, and increased vascular permeability. The lipid inflammatory mediator leukotriene B4 (LTB4) is involved in the early hypoxia-induced responses (ROS generation and leukocyte adherence). Whether other lipid inflammatory mediators participate in this phenomenon is not known. The objective of these experiments was to study the role of platelet-activating factor (PAF) in the microvascular inflammatory response to hypoxia and its potential interactions with LTB4 in this response. Intravital microscopy was used to examine mesenteric venules of anesthetized rats. We found that WEB-2086, a PAF receptor antagonist, completely prevented the increase in ROS levels and leukocyte adherence during a brief reduction in inspired Po 2 to anesthetized rats; administration of either WEB-2086 or the LTB4 antagonist LTB4-DMA attenuated leukocyte emigration and the increase in vascular permeability to the same extent during prolonged systemic hypoxia in conscious rats. Furthermore, no additive effect was observed in either response when both antagonists were administered simultaneously. This study demonstrates a role for PAF in the rapid microvascular inflammatory response to hypoxia, as well as contributions of PAF and LTB4 to the slowly developing responses observed during sustained hypoxia. The incomplete blockade of the hypoxia-induced increases in vascular permeability and leukocyte emigration by combined administration of both antagonists indicates that factors in addition to LTB4 and PAF participate in these phenomena.

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