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)

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

We considered that a moderate reduction of the central blood volume (CBV) may activate the coagulation system. Lower body negative pressure (LBNP) is a non-invasive means of reducing CBV and, thereby, simulates haemorrhage. We tested the hypothesis that coagulation markers would increase following moderate hypovolemia by exposing 10 healthy male volunteers to 10 min of 30 mmHg LBNP. Thoracic electrical impedance increased during LBNP (by 2.6 +/- 0.7 Omega, mean +/- SD; P < 0.001), signifying a reduced CBV. Heart rate was unchanged during LBNP, while mean arterial pressure decreased (84 +/- 5 to 80 +/- 6 mmHg; P < 0.001) along with stroke volume (114 +/- 22 to 96 +/- 19 ml min(-1); P < 0.001) and cardiac output (6.4 +/- 2.0 to 5.5 +/- 1.7 l min(-1); P < 0.01). Plasma thrombin-antithrombin III complexes increased (TAT, 5 +/- 6 to 19 +/- 20 microg l(-1); P < 0.05), indicating that LBNP activated the thrombin generating part of the coagulation system, while plasma D-dimer was unchanged, signifying that the increased thrombin generation did not cause further intravascular clot formation. The plasma pancreatic polypeptide level decreased (13 +/- 11 to 6 +/- 8 pmol l(-1); P < 0.05), reflecting reduced vagal activity. In conclusion, thrombin generation was activated by a modest decrease in CBV by LBNP in healthy humans independent of the vagal activity.
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PMID:Early activation of the coagulation system during lower body negative pressure. 1965 65