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 excitatory innervation of isolated thoracic duct segments was studied using tissue bath techniques. No spontaneous activity was present in longitudinal or helical strips obtained from a portion of the thoracic duct cephalad to the hilum of the lung. Norepinephrine (10(-8) to 10(-5) M) and tyramine (3 x 10(-5) M) produced contractions that were antagonized by phentolamine (2 x 10(-5) M) and phenoxybenzamine (10(-7) M). Acetylcholine (10(-7) to 10(-4) M) produced contractions that were antagonized by atropine (5 x 10(-9) M). Thoracic duct strips also contracted in response to field electrical stimulation, and maximal responses were obtained with a stimulus of 15 V, 15 Hz, and 1-ms pulse duration. These electrically induced contractions were abolished by tetrodotoxin (5 x 10(-7) M), phentolamine (2 x 10(-5) M), phenoxybenzamine (10(-7) M), and guanethidine (3 x 10(-6) M), but not by atropine (10(-6) M). We conclude that smooth muscle of the canine thoracic duct contains alpha-adrenergic and acetylcholine receptors, both of which cause contraction when stimulated. However, only the alpha-receptors appear to be innervated.
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PMID:Evidence for alpha-adrenergic innervation of the isolated canine thoracic duct. 625 35

The alpha adrenoceptor properties of the rabbit ear artery and thoracic aorta were assessed using isolated blood vessel rings mounted in tissue baths. Labetalol, an alpha and beta receptor antagonist, caused dose-dependent contractions in control, reserpinized and surgically denervated ear arteries. This contraction was inhibited by phentolamine and abolished by the irreversible alpha receptor antagonist, N,N'-bis-(O-methoxy-benzylaminohexyl) cystamine tetrahydrochloride. Thoracic aorta failed to respond to labetalol. Using labetalol as an antagonist against methoxamine, labetalol pA2 values were 7.4 +/- 0.3 (95% confidence interval) and 7.13 +/- 0.25 in ear artery and aorta, respectively. Thus, labetalol had the same affinity for the alpha receptors of these two vessels but was an alpha agonist only in the ear artery. Norepinephrine ED50 values and dissociation constants (KA) were determined by analysis of dose-response data with and without partial inactivation of alpha receptors by phenoxybenzamine. Ear artery and aorta norepinephrine ED50 values, 4.24 (2.24-8.03) X 10(-8) M and 2.48(1.64-3.76) X 10(-8) M, respectively, were not significantly different. In contrast, norepinephrine KA values differed by a factor of 32, 4.11 (3.02-5.60) X 10(-6) M and 1.29 (0.85-1.94) X 10(-7) M, respectively. Receptor reserves were also markedly different in these vessels. Thus, ED50 was achieved with 1% receptor occupancy in ear artery as compared to 16% receptor occupancy in aorta. It is concluded that the alpha receptors of ear artery and aorta are both qualitatively and quantitatively different.
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PMID:Qualitative and quantitative differences between the postsynaptic alpha adrenoceptors of rabbit ear artery and thoracic aorta. 629 3

Noradrenaline (NA) release in the rat lumbar spinal cord (L3-4) in response to variable intensity, selective stimulation of large (A-beta), small myelinated (A-delta), and unmyelinated (C) afferent fibers was examined by in vivo microdialysis with high performance liquid chromatography and electrochemical detection. Application of 100 mM K+ solution via the dialysis probe increased NA in the dialysate. Thoracic segment transection rostral to the probe depressed the NA level. Transcutaneous stimulation of peripheral nerves had the following effects: 1) High intensity stimulation of afferent A-delta or C fibers increased spinal NA release, which was decreased by thoracic spinal cord transection. 2) Stimulation of afferent A-beta or A-delta fibers at low intensity did not affect the NA level. 3) High intensity stimulation of afferent A-beta fibers depressed NA release in half of the trials. Results indicate that many NA-containing nerve terminals that innervate the lumbar spinal cord originate from supraspinal structures. Somatic neural inputs from afferent C fibers and high-threshold A-delta, but not A-beta nor low-threshold A-delta fibers, activate the descending NA system and release the NA in the spinal cord. The descending NA system may participate in antinociception.
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PMID:Activation of descending noradrenergic system by peripheral nerve stimulation. 805 46

The purpose of this study was to assess the endocrine status, thoracic impedance, blood concentration, and hemodynamic dose-responses using different angles of passive head-up tilt (HUT) ranging from 12 degrees to 70 degrees in the same subjects. Measurements were performed during 20 min supine position (pre-HUT), 30 min upright (HUT12, HUT30, HUT53, or HUT70), and 20 min supine (post-HUT); subjects 70 min in the supine position only (HUT0) served as resting controls. Norepinephrine increased above resting control values by 19, 44, 80, and 102%; epinephrine by 30, 41, 64, and 68%; aldosterone by 29, 62, 139, and 165%; plasma renin activity n. s., 41, 91, and 89%; vasopressin n.s., 27, 47, and 59%; thoracic bioimpedance n. s., 8, 13, and 16%; heart rate n. s., 5, 26, and 45%, and mean arterial pressure n. s., 5, 7, and 10%; at min 27 of HUT12, HUT30, HUT53, and HUT70, respectively. Pulse pressure decreased with HUT53 and HUT70 by 4 and 10%. Hematocrit increased by 0.2, 1.7, 6.3, and 7.2%, respectively. Blood density increased by 2.3 and 3.0 g/l, plasma density by 1.7 and 1.8 g/l with HUT53 and HUT70. After finishing HUT, heart rate fell to values which stayed below pre-HUT, and also below resting control levels for > or = 5 min ("post-orthostatic bradycardia") even after the lowest orthostatic load (HUT12). Thoracic impedance and arterial pressure remained increased after terminating HUT30, HUT53, and HUT70. In conclusion, passive orthostatic loading of different extent produces specific dose-responses of different magnitude in the endocrine system, blood composition, thoracic impedance, and hemodynamic variables. The heart rate is depressed even after HUT12, while arterial blood pressure and thoracic impedance exceed pre-stimulus levels after greater head-up tilt, indicating altered cardiovascular response after passive orthostasis.
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PMID:Cardiovascular and hormonal changes with different angles of head-up tilt in men. 1130 Feb 29

The aim of our study was to quantitate, in the same test subjects, hormonal, thoracic bioimpedance, blood composition, and hemodynamic dose-responses during different angles of passive orthostatic loading (head-up tilt, HUT) ranging from 12 degrees to 70 degrees. Measurements were performed with 20 min supine (pre-HUT), 30 min upright (HUT-12 degrees, HUT-30 degrees, HUT-53 degrees, or HUT-70 degrees), and 20 min supine (post-HUT); or supine only (HUT-0 degree, rest control). Norepinephrine increased above rest control by 19, 44, 80 and 102%; epinephrine 30, 41, 64, and 68%; aldosterone 29, 62, 139, and 165%; plasma renin activity n. s., 41, 91, and 89%; vasopressin n. s., 27, 47, and 59%; thoracic bioimpedance n. s., 8, 13, and 16%; heart rate n. s., 5, 26, and 45%, and mean arterial pressure n. s., 5, 7, and 10%; respectively, at min 27 of HUT-12 degrees, -30 degrees, -53 degrees, and -70 degrees. Pulse pressure narrowed with HUT-53 degrees and -70 degrees by 4 and 10%. Hematocrit increased 0.2, 1.7, 6.3, and 7.2%, respectively. Blood density increased by 2.3 and 3.0 g/l, plasma density by 1.7 and 1.8 g/l with HUT-53 degrees and -70 degrees. After finishing HUT, heart rate fell to values which stayed below pre-HUT, and also below rest control levels for > or = 5 min ("post-orthostatic bradycardia") even after the lowest orthostatic load (HUT-12 degrees). Thoracic bioimpedance and arterial blood pressure stayed increased after finishing HUT-30 degrees, -53 degrees, and -70 degrees. In summary, passive orthostasis of different degree produces specific dose-responses of different magnitude within endocrine, blood concentration, thoracic bioimpedance, and hemodynamic variables. Heart rate is depressed even after HUT-12 degrees, while arterial blood pressure and thoracic bioimpedance exceed pre-stimulus levels after HUT of higher degree, indicating altered cardiovascular state after passive orthostasis.
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PMID:[Cardiovascular and humoral adaptation with passive orthostasis in men]. 1137 90