Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study evaluated the regional release of cyclooxygenase products 4 h following 20 Gy gamma irradiation. Thoracic shielding reduced the radiation-induced increase in immunoreactive thromboxane B2 (iTxB2) excretion to control levels while abdominal shielding partially attenuated the altered excretion of this cyclooxygenase product. To assess the role the kidneys play in the radiation-induced increase in iTxB2 excretion, an in situ isolated perfused rat kidney model was developed. The excretion rate of iTxB2 from irradiated isolated perfused kidneys was not significantly different from sham-irradiated perfused kidneys. Radiation exposure did alter renal cyclooxygenase product release in that the excretion of immunoreactive prostaglandin E2 (iPG2) and immunoreactive 6-keto-PGF1 alpha was significantly increased (P less than 0.05) in irradiated isolated perfused kidneys. These data show that radiation-induced increases in iTxB2 excretion are primarily due to altered extrarenal synthesis and/or metabolism of this arachidonate metabolite.
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PMID:Regional release of cyclooxygenase products after radiation exposure of the rat. 309 35

We have tested the hypothesis that growth factor signaling pathways are augmented in hypertension, a disease associated with vascular smooth muscle cell growth. Thoracic aorta was dissected from deoxycorticosterone acetate-salt (DOCA-salt) and one kidney, one clip (1K, 1C) hypertensive rats and from sham normotensive rats for use in isolated tissue bath experiments. Systolic blood pressure was significantly higher in DOCA-salt and 1K, 1C than in normotensive sham rats: 192 +/- 7, 185 +/- 10, and 117 +/- 4 mmHg, respectively. Although virtually no contraction to epidermal growth factor (EGF) was observed in endothelium-denuded sham rat aorta [1 +/- 1% phenylephrine (PE) (10 micromol/l)-induced contraction], the maximal EGF-induced contraction was 45 +/- 7% in endothelium-denuded aorta from DOCA-salt hypertensive rats and 39 +/- 7% in aorta from 1K, 1C rats. Although slightly attenuated, a contraction to EGF was still observed in endothelium-intact aortic strips from 28-day DOCA-salt hypertensive rats. We also conducted concentration-response curves to EGF on days 1, 3, 5, 7, 14, and 21 of DOCA-salt therapy. A significant contraction to EGF in aorta from DOCA-salt rats was observed on day 14, when DOCA-salt rats had significantly higher blood pressure than sham rats: 188 +/- 6 and 122 +/- 3 mmHg, respectively. Transforming growth factor-alpha, an agonist of the EGF receptor, contracted DOCA-salt rat aorta (30 +/- 7% PE-induced contraction) but not sham aorta (3 +/- 3%). The EGF receptor tyrosine kinase inhibitor 4,5-dianilinophthalimide (10 micromol/l), the mitogen-activated protein kinase kinase inhibitor PD-098059 (10 micromol/l), and the L-type voltage-gated calcium channel inhibitor diltiazem (1 mol/l), but not the cyclooxygenase inhibitor indomethacin (10 micromol/l), virtually abolished EGF-induced contraction (85, 98, and 99% reduction, respectively). These data support a striking difference in EGF signaling between normotensive and hypertensive animals. Furthermore, they provide evidence that growth factors should be considered vasoconstrictors as well as growth modulators in hypertension.
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PMID:Epidermal growth factor: a potent vasoconstrictor in experimental hypertension. 1007 82

Analgesic management of postoperative pain associated with thoracic surgery remains a difficult clinical challenge. In the present study we used a thoracic muscle incision model to characterize pain-related behavior and changes in prostaglandin E2 (PGE2) in both thoracic cerebrospinal fluid (CSF) and incision site tissues. A deep muscle incision was made in the left thoracic region of rats anesthetized with isoflurane, propofol, or spinal bupivacaine. Thoracic CSF and incision site tissue concentrations of PGE2 were monitored for 6 h using microdialysis loop catheters. Postoperative pain-related behavior was assessed by recording exploratory locomotive activity. Thoracic muscle surgery decreased rearing and ambulation. Oral ketorolac or rofecoxib 3 mg/kg restored normal rearing and ambulation. Postoperative CSF PGE2 concentration increased most (threefold) with spinal anesthesia, and not at all with propofol. With surgery under isoflurane or spinal bupivacaine, presurgical oral administration of ketorolac or rofecoxib 3 mg/kg reduced postsurgical CSF PGE2 levels and tissue PGE2 levels. Intrathecal ketorolac (4 microg) reduced CSF PGE2 after surgery without affecting tissue PGE2 levels, whereas intrathecal L-745,337 (80 microg) did not reduce CSF PGE2. Thoracic surgical wounds increase pain-related behavior and CSF and tissue PGE2 levels, all of which can be attenuated by oral cyclooxygenase inhibitors.
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PMID:Upregulation of cerebrospinal fluid and peripheral prostaglandin E2 in a rat postoperative pain model. 1686 14