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)

To determine whether or not the blockade of sympathetic efferents by epidural anaesthesia blunts the normal increase in plasma renin activity in response to hypotension, we assessed the effect of hypotensive thoracic epidural anaesthesia with widespread sympathetic blockade on plasma renin activity. Plasma renin activity and vasopressin concentration, arterial pressure, and serum osmolality were measured in 17 patients before and after random epidural injection of either 6.7 ml of 0.75% bupivacaine (n = 7) or the same volume of saline (n = 10). As an indicator for efferent sympathetic drive, skin temperatures were measured on the hand and foot. A decrease in mean arterial pressure by more than 25% of baseline values was prospectively defined as hypotension requiring intervention. Thoracic epidural anaesthesia induced a decrease in mean arterial pressure of 24 mmHg (range 16-47) from 101 mmHg to 77 mmHg (P less than 0.001 vs. saline). Despite hypotension, plasma renin activity remained unchanged [medians 2.9 ng ml-1 h-1 (0-9.1) vs. 3.4 ng ml-1 h-1 (0-13.8)]. In contrast, vasopressin concentrations increased from a median of 3.8 pg ml-1 (0.5-8.2) to 6.0 pg ml-1 (4.2-33.6; P = 0.025). Both hand and foot skin temperatures increased significantly indicating widespread extent of sympathetic blockade. Serum osmolality did not change. With epidural saline, variables remained unchanged. Thus, during hypotension induced by widespread attenuation of efferent sympathetic drive through thoracic epidural anaesthesia, renin activity did not change, whilst vasopressin concentrations increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic blockade by thoracic epidural anaesthesia suppresses renin release in response to hypotension, but activates the vasopressin system. 173 99

Thoracic shifts of blood stimulate diuresis and natriuresis during spaceflight. The available literature is not conclusive as to whether thoracic afferent neurons are essential for this response. Possibly, an acute elevation in cerebrospinal fluid pressure (CSF-p) activates central compensatory mechanisms. This is because central venous pressure is elevated by thoracic blood shifts and may reduce the pressure gradient for drainage of CSF into the venous sinuses. We tested whether rats with constriction of the venous return at the level of the heart (0.4 mm maximum diameter) had CSF-p different from sham-operated controls. CSF-p in the immediate postoperative period, as well as 1 and 10 days after surgery, were within normal limits and did not differ (p greater than 0.05). Blood collected at the end of the experiment showed no group differences (p greater than 0.05) in the hematocrit, or concentrations of sodium, potassium or vasopressin. Thus, changes in CSF-p, per se, appear to be insufficient to explain the cardiovascular or salt/water balance readjustments observed in spaceflight. It is likely that compensatory systems are highly redundant.
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PMID:Cerebrospinal fluid pressure of conscious rats after venous constriction at the right atrium. 177 18

Cardiovascular and hormonal responses to anaphylactic shock were evaluated in anaesthetized pigs sensitized by natural exposure to Ascaris suum as verified by antibodies. In six animals with such antibodies, Ascaris antigen injection produced a plasma histamine increase of 52 (42-196) fold (median and range; P < 0.05), while four pigs without such antibodies served as controls with only insignificant increases in histamine. In the anaphylactic group, two of the animals died during the investigation due to cardiovascular collapse. In the sensitized pigs resting heart rate (HR), 104 (86-118) beats min-1, increased to 204 (164-240) beats min-1 as mean arterial pressure (MAP) decreased from 94 (83-102) to 45 (31-90) mmHg (P < 0.05). In contrast, the non-sensitized pigs maintained the resting HR of 101 (79-113) beats min-1, as MAP decreased to 50 (41-97) mmHg (P < 0.05). In the sensitized group systemic vascular resistance (SVR) fell from 1114 (843-1811) to 990 (588-1173) dyne s-1 cm-5 and then increased to 3617 (2593-4166) dyne s-1 cm-5, while in the control group there was only a reduction to a minimum value of 730 (458-1307) dyne s-1 cm-5 (P < 0.05). Thoracic electrical impedance increased only in the sensitized group [from 28.3 (24.7-31.4) to 29.9 (24.0-31.4)], indicating central volume depletion. Plasma catecholamines increased markedly only in the sensitized pigs, and plasma pancreatic polypeptide, vasopressin, aldosterone and renin responses confirmed to those established during central hypovolaemia. During anaphylaxis, this study demonstrated cardiovascular responses similar to those established during a major blood loss. However, as indicated by plasma catecholamines, sympathetic activity was many times that previously demonstrated during haemorrhage, and sympathoactivation may explain the marked vasoconstriction noted in the sensitized pigs.
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PMID:Cardiovascular and hormonal responses to anaphylactic shock in the pig. 771 95

In healthy humans, the increase in arterial blood pressure seen in patients with autonomic dysfunction in response to exogenous vasopressin (AVP) is abolished. We tested the hypothesis that redistribution of blood from the intra- to the extrathoracic vascular compartment might contribute to this buffer response. Regional distribution of 99mTc labeled autologous red cells was assessed in healthy supine volunteers (n = 7) during arginine-vasopressin administration (1 ng.kg-1 bolus i.v. followed by a 14-min infusion of 3 ng.kg-1 x min-1), along with arterial and central venous pressures, and heart rate. Exogenous vasopressin increased plasma vasopressin concentration from 4.0 +/- 1.4 SEM to 91 pg.ml-1 +/- 12. Thoracic counts increased slightly but significantly by 2.2% +/- 0.9, while global abdominal counts remained unchanged. Most surprisingly, counts in the liver markedly increased (+8.1% +/- 1.8, p = 0.02), but significantly decreased in the spleen (-3.1% +/- 1.4). Intestinal (-2.5% +/- 2.4) and limb counts did not change significantly. Consistent with the increase in thoracic counts central venous pressure increased from 3.6 mmHg +/- 1 to 4.7 +/- 1 (p = 0.02), while arterial pressure and heart rate did not change. All changes reversed towards baseline when vasopressin administration ceased. Thus, in humans with an intact autonomic system, vasopressin, at concentrations observed during hypotension, increases liver and, albeit to a small extent, also thoracic blood volume, but decreases splenic blood content. These results: 1) are incompatible with the hypothesis that AVP induces a shift of blood from intra- to extrathoracic capacitance vessels, and 2) show that AVP increases rather than decreases central blood volume.
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PMID:Effects of arginine-vasopressin on regional blood volume distribution in supine humans. 821 79

In the etiological diagnosis of ACTH-dependent Cushing's syndrome, it may be difficult to distinguish pituitary disease from ectopic ACTH production, specially when this is due to a benign neuroendocrine tumor. We describe a patient with partial dexamethasone suppression consistent with Cushing's disease, an absent response to CRH suggesting ectopic ACTH production and an atypical, apparent circadian rhythm. Bilateral cavernous sinus catheterization suggested a nonpituitary source of ACTH and, in the search of an ectopic tumor, somatostatin receptor scintigraphy, abdominal CT scan, and duodenopancreatic endoscopic echography were performed and failed to reveal any abnormality. Thoracic CT scan disclosed a tiny right lung nodule that showed a definite tracer uptake on MIBG scintigraphy. After resection, the nodule proved to be an 8-mm typical pulmonary carcinoid, with positive immunostaining for the classical neuroendocrine markers and for ACTH, and showing tissue expression of the POMC gene. However, the CRH receptor gene was not expressed, explaining the absent CRH response in vivo, whereas the V3 vasopressin receptor gene was expressed in the tumor tissue. The latter feature appears to be characteristic of benign carcinoids and may contribute to explaining the CRH-independent circadian rhythm observed in this case.
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PMID:Ectopic ACTH Cushing's syndrome: V3 vasopressin receptor but not CRH receptor gene expression in a pulmonary carcinoid tumor. 983 45

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

A 62-year-old man presented in June 2006 with right thoracic pain, cough, and weight loss, which had persisted for 3 months. Chest X-ray showed a mass-like shadow in the right pulmonary apex, suggesting a stage IIIb adenocarcinoma which was confirmed by biopsy. We gave a total radiation dose of 60 Gy, after this which general malaise and weakness were noted. The results of endocrinological examinations suggested syndrome of inappropriate antidiuretic hormone secretion (SIADH). Thoracic CT showed ground-glass opacity (GGO) in both lungs, and we could not rule out pulmonary tuberculosis. A sputum was positive for acid-fast stain and PCR-Tb, suggesting that SIADH was associated with pulmonary tuberculosis. Water restriction, i.v. physiological saline, and antituberculosis therapy relieved hyponatremia and the symptoms.
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PMID:[A patient who sufferred pulmonary tuberculosis with syndrome of inappropriate secretion of antidiuretic hormone, after radiotherapy for pulmonary adenocarcinoma]. 1818 40

Small cell lung cancer accounts for approximately 15% of bronchogenic carcinomas. It is the cancer most commonly associated with various paraneoplastic syndromes, including the syndrome of inappropriate antidiuretic hormone secretion, paraneoplastic cerebellar degeneration, and Lambert-Eaton myasthenic syndrome. Because of the high propensity of small cell lung cancer to metastasize early, surgery has a limited role as primary therapy. Although the disease is highly sensitive to chemotherapy and radiation, cure is difficult to achieve. The combination of platinum and etoposide is the accepted standard chemotherapeutic regimen. It is also the accepted standard therapy in combination with thoracic radiotherapy (TRT) for limited-stage disease. Adding TRT increases absolute survival by approximately 5% over chemotherapy alone. Thoracic radiotherapy administered concurrently with chemotherapy is more efficacious than sequential therapy. Furthermore, the survival benefit is greater if TRT is given early rather than late in the course of chemotherapy. Regardless of disease stage, no relevant survival benefit results from increased chemotherapy dose intensity or dose density, altered mode of administration (eg, alternating or sequential administration) of various chemotherapeutic agents, or maintenance chemotherapy. Prophylactic cranial radiation prevents central nervous system recurrence and can improve survival. In Japan and some other Asian countries, the combination of irinotecan and cisplatin is the standard chemotherapeutic regimen. Clinical trials using thalidomide, gefitinib, imatinib, temsirolimus, and farnesyltransferase inhibitors have not shown clinical benefit. Other novel agents such as bevacizumab have shown promising early results and are being evaluated in larger trials.
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PMID:Small cell lung cancer. 1831 5

An 11-year-old spayed female domestic shorthair cat was evaluated for anorexia, lethargy and weight loss of 6 days' duration. Bilateral mydriasis, absent menace response, slow-to-absent pupillary light reflexes, bilateral retinal detachment, intermittent horizontal nystagmus, intermittent ventral strabismus and systemic hypertension were present. Biochemical analysis revealed severe hyponatremia, severe hypochloremia and mild hypokalemia. Multifocal central nervous system disease was suspected based on optic, trigeminal sensory (ophthalmic branch), vestibulocochlear and possible oculomotor nerve dysfunction. Thoracic radiographs showed mild cardiomegaly without evidence of congestive heart failure. Ultrasound revealed mild pleural and peritoneal effusion. A cause of the severe hyponatremia was not identified, and it persisted despite fluid therapy. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) was suspected as the cause of hyponatremia. Humane euthanasia was elected owing to continued clinical decline. Serum hyposmolality, urine hyperosmolality, natriuresis and lack of confirmed renal, thyroid and pulmonary disease aided in the presumed diagnosis of SIADH. Post-mortem histopathology of the brain revealed degeneration of the hypothalamus and optic tracts, along with a prominent fluid-filled craniopharyngeal duct (putative Rathke's cleft cyst) separating the pars distalis and the pars intermedius. The hypothalamic degeneration, possibly secondary to a Rathke's cleft cyst, was hypothesized to be the cause of presumptive SIADH in the patient. Although rare in occurrence, Rathke's cleft cyst should be included as a differential diagnosis in dogs and cats with signs of pituitary dysfunction.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion in a cat with a putative Rathke's cleft cyst. 2465 77


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