Ropivacaine attenuates pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung☆

2000 ◽  
Vol 25 (2) ◽  
pp. 187-194
Author(s):  
L FISCHER ◽  
C HONEMANN ◽  
J PATRIE ◽  
M DURIEUX ◽  
G RICH
Keyword(s):  
Thromboxane A2 ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Thromboxane A2 Analogue

Ropivacaine attenuates pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung

2000 ◽  
Vol 25 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Lars G. Fischer ◽  
Christian W. Hönemann ◽  
James T. Patrie ◽  
Marcel E. Durieux ◽  
George F. Rich
Keyword(s):  
Thromboxane A2 ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Thromboxane A2 Analogue

Thromboxane A2 analogue contracts predominantly the hepatic veins in isolated canine liver

1996 ◽  
Vol 52 (6) ◽  
pp. 483-495 ◽  
Author(s):  
H. Urayama ◽  
T. Shibamoto ◽  
H.-G. Wang ◽  
S. Koyama
Keyword(s):  
Thromboxane A2 ◽  
Hepatic Veins ◽  
Thromboxane A2 Analogue

Metabolic and respiratory hydrogen ion effects on hypoxic pulmonary vasoconstriction

1984 ◽  
Vol 57 (2) ◽  
pp. 545-550 ◽  
Author(s):  
C. Marshall ◽  
L. Lindgren ◽  
B. E. Marshall
Keyword(s):  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Regression Equations ◽  
Rat Lung ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Ion Effects

Hypoxic pulmonary vasoconstriction (HPV) was studied in the ventilated-perfused rat lung in vitro. Respiratory acidosis and alkalosis were obtained by ventilating with 2, 7, or 10% CO2 (21% O2-balance N2). Metabolic acidosis and alkalosis were produced by the addition of 0.9 N NaHCO3 or 1 N lactic acid to the perfusate at constant PCO2. At each pH the pressor responses to 2 and 4% O2 were compared with the maximum pressor response (R%max) obtained with zero O2 and 5% CO2 at a normal pH (approximately 7.35). HPV was maximal when the [H+] was between 38 and 50 nM and was attenuated by changes of pH in either direction. Both respiratory and metabolic pH changes had similar effects. The combined linear regression equations were as follows: with 2% O2 the response to acidosis was R%max = 101.37 – 0.52 [H+] and to alkalosis was R%max = 2.03 [H+] - 3.85; with 4% O2 the response to acidosis was R%max = 56.88 – 0.3 [H+] and to alkalosis was R%max = 1.16 [H+] - 4.95. These effects were not due to changes of ionized calcium.

Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion

1997 ◽  
Vol 82 (2) ◽  
pp. 592-598 ◽  
Author(s):  
Richard H. Turnage ◽  
John L. Lanoue ◽  
Kevin M. Kadesky ◽  
Yan Meng ◽  
Stuart I. Myers
Keyword(s):  
Intestinal Ischemia ◽  
Thromboxane A2 ◽  
Microvascular Permeability ◽  
Sprague Dawley ◽  
Pulmonary Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor ◽  
Krebs Buffer

Turnage, Richard H., John L. LaNoue, Kevin M. Kadesky, Yan Meng, and Stuart I. Myers. Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion. J. Appl. Physiol. 82(2): 592–598, 1997.—This study examines the hypothesis that intestinal reperfusion (IR)-induced pulmonary thromboxane A2(TxA2) release increases local microvascular permeability and induces pulmonary vasoconstriction. Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of IR. Sham-operated animals (Sham) served as controls. After IR or Sham, the pulmonary vessels were cannulated, and the lungs were perfused in vitro with Krebs buffer. Microvascular permeability was quantitated by determining the filtration coefficient ( K f), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, imidazole (TxA2 synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then K f, Ppa, Ppv, and Ppc were again measured. The K fof lungs from IR animals was four times greater than that of Sham ( P = 0.001), and Rt was 63% greater in the injured group ( P = 0.01). Pc of IR lungs was twice that of controls (5.4 ± 1.0 vs. 2.83 ± 0.3 mmHg, IR vs. Sham, respectively; P < 0.05). Imidazole or SQ-29,548 returned K fto baseline measurements ( P < 0.05) and reduced Rt by 23 and 17%, respectively ( P < 0.05). IR-induced increases in Pc were only slightly reduced by 500 μg/ml imidazole (14%; P = 0.05) but unaffected by lower doses of imidazole (5 or 50 μg/ml) or SQ-29,548. These data suggest that IR-induced pulmonary edema is caused by both increased microvascular permeability and increased hydrostatic pressure and that these changes are due, at least in part, to the ongoing release of TxA2.

Platelet-activating factor increases platelet-dependent glycoconjugate secretion from tracheal submucosal gland

1989 ◽  
Vol 257 (6) ◽  
pp. L373-L378 ◽  
Author(s):  
T. Sasaki ◽  
S. Shimura ◽  
K. Ikeda ◽  
H. Sasaki ◽  
T. Takishima
Keyword(s):  
Platelet Activating Factor ◽  
Thromboxane A2 ◽  
Submucosal Gland ◽  
Thromboxane Receptor ◽  
Significant Stimulation ◽  
Submucosal Glands ◽  
Dose Dependent Fashion ◽  
Thromboxane Receptor Antagonist ◽  
Dose Dependent ◽  
Thromboxane A2 Analogue

Using isolated glands from feline trachea, we examined the effect of platelet-activating factor (PAF) on radiolabeled glycoconjugate release and glandular contraction by measuring induced tension in the absence or presence of platelets. PAF alone did not produce any significant glandular contraction nor any significant change in glycoconjugate release from isolated glands. In the presence of purified platelets containing no plasma, PAF (10(-8) to 10(-5) M) produced significant glycoconjugate secretion in a dose-dependent fashion, but it produced no significant glandular contraction. PAF-evoked glycoconjugate secretion was time dependent, reaching a peak response of 277% of control 15-30 min after the exposure of isolated glands to 10(-5) M PAF in the presence of platelets and returning to 135% of controls at 2 h. Platelets alone did not produce any significant stimulation in glycoconjugate release. CV-3988, a known PAF antagonist, inhibited the secretory response to PAF. Methysergide, a known antagonist to receptors for 5-hydroxytryptamine, did not alter PAF-evoked glycoconjugate secretion. Both indomethacin and SQ 29,548, a thromboxane receptor antagonist, abolished the PAF-evoked glycoconjugate secretion from isolated submucosal glands. Epithiomethanothromboxane A2, a stable thromboxane A2 analogue, produced a significant increase in glycoconjugate secretion in a dose-dependent fashion. These findings indicate that PAF increases glycoconjugate release in the presence of platelets and that the increase is dependent on some aspect of platelet function, namely thromboxane generation.

scholarly journals Effects of Nitroglycerin on Stable Thromboxane A2 Analogue-Induced, Nifedipine-Resistant Contraction in Canine Basilar Artery

1990 ◽  
Vol 54 (2) ◽  
pp. 237-240 ◽  
Author(s):  
Hachiro USUI ◽  
Yoshinobu AKIMOTO ◽  
Kazuyoshi KURAHASHI ◽  
Hiroaki SHIRAHASE ◽  
Motohatsu FUJIWARA ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Thromboxane A2 ◽  
Canine Basilar Artery ◽  
Thromboxane A2 Analogue
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