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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thoracic aortae of normal rabbits were perfused with pancreatic elastase in vitro at 37 degrees C and 70 mm Hg pressure in the presence or absence of elastin ligands previously shown to stimulate or inhibit the enzymatic degradation of elastin. Perfusion with elastase results in an average of 3.6 lamellae degraded, whereas addition of sodium linoleate before and during the perfusion with elastase increases this value to 7.9 (P less than 0.001). Conversely, perfusion with the cationic detergent, dodecyltrimethylammonium chloride, completely prevents the degradation of elastic lamellae by elastase. These effects do not reflect alterations of the intrinsic catalytic activity of elastase, but apparently indicate the formation of complexes between the elastin ligands and arterial elastic lamellae, as is consistent with prior studies indicating such interactions between fatty acids or detergents and purified elastin. These studies suggest that agents such as fatty acids may significantly alter the metabolic susceptibility of elastin in vivo and possibly contribute to the degradation of elastic lamellae seen in arteries with advanced atherosclerosis.
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PMID:A possible role for elastin ligands in the proteolytic degradation of arterial elastic lamellae in the rabbit. 75 37

Simultaneous measurements of thoracic duct lymph flow and small intestinal lymph flow were carried out in mongrel dogs after the administration of mannitol, ethacrynic acid, furosemide and chlorothiazide. Thoracic duct lymph flow increased only after injection of mannitol. Intestinal lymph flow increased after injection of all diuretics except chlorothiazide. Furthermore, mannitol produced simultaneous increases in thoracic duct and intestinal lymph flows. The durations of response of the increased lymph flows from each lymph channel produced by mannitol were statistically identical. The durations of increased intestinal lymph flows observed with each drug were: 40+/-3 (S.E.), 43+/-2 and 38+/-2 minutes for mannitol, ethacrynic acid and furosemide, respectively. Mean arterial blood pressures and inferior vena cava pressures did not change from the control to the experimental state in any animal studied. Similarly measurements of serum and lymph sodium, potassium and protein concentrations were unchanged from the control to the experimental state. These studies demonstrate that mannitol simultaneously increases thoracic duct lymph flow as well as intestinal lymph flow. Secondly, the results suggest that the increases in thoracic duct lymph flow after ethacrynic acid and furosemide administration, observed in previous studies arose primarily from the small intestine.
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PMID:Diuretics and small intestinal lymph flow in the dog. 83 66

Pregnancy is associated with decreases of blood pressure and vascular sensitivity to vasopressor agents. We have hypothesized that the increased liberation of endogenous vasodilator(s) by the vascular endothelium or other structures could mediate these blunted responses. Thoracic aorta rings of nonpregnant, 21 days pregnant, and first day post partum rats respond similarly to acetylcholine, an endothelium-dependent vasorelaxant. In contrast, the potency of the response to sodium nitroprusside, an endothelium-independent vasorelaxant, is unchanged in tissues of pregnant rats and increased (p less than 0.05) in those of post partum animals. In the presence of indomethacin (10 mumol/L) the three groups of tissues show a decreased potency. The effects of phenylephrine on aortic rings of both nonpregnant and pregnant rats are markedly increased in the presence of Ng-monomethyl-L-arginine. Indeed, the concentration producing 50% of the maximum response of phenylephrine decreases (p less than 0.001) from 50.7 to 8.02, from 93.8 to 37.6, and from 60.4 to 5.97 nmol/L with the use of Ng-monomethyl-L-arginine (0.1 mmol/L) in rings from nonpregnant, pregnant, and postpartum rats, respectively. Simultaneously, the maximum response to phenylephrine increases markedly in the three groups of tissues. In the presence of Ng-monomethyl-L-arginine, indomethacin does not influence the response to phenylephrine. Our results do not support the possible involvement of an endogenous vasodilator (prostaglandin-like or endothelium-derived) in the blunted responses to vasoconstrictors during pregnancy.
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PMID:Prostaglandin- or endothelium-mediated vasodilation is not involved in the blunted responses of blood vessels to vasoconstrictors in pregnant rats. 153 53

Thoracic aortic cross-clamping causes proximal aortic hypertension. Theoretically, the method used to treat hypertension can influence spinal cord perfusion pressure and neurologic outcome. Phlebotomy was compared to sodium nitroprusside/isoflurane in terms of ability to treat increased proximal mean aortic pressure (MAPp) after thoracic aortic cross-clamping in dogs. Dogs were assigned randomly to one of three groups depending on the method used to treat hypertension after cross clamping: 1) phlebotomy (n = 10); 2) sodium nitroprusside/isoflurane (n = 11); and 3) control (no treatment) (n = 8). In each dog, anesthesia was maintained with isoflurane in oxygen, 1.4% end-tidal. The thoracic aorta was occluded 2.5 cm distal to the left subclavian artery for 50 min and then was released. Hemodynamics, cerebrospinal fluid pressure (CSFP), and regional blood flows by the radioactive microsphere technique, were measured at 1) baseline; 2) 2 min after aortic cross-clamping; 3) after treatment of proximal aortic hypertension; 4) 5 min after aortic unclamping; and 5) 30 min after resuscitation. At 24 h, a neurologic assessment was performed. Thoracic aortic cross-clamping increased MAPp, decreased distal MAP (MAPd), and reduced lumbar spinal cord perfusion pressure (SCPPl), [SCPPl = MAPd - CSFP], in all three groups. Control of increased MAPp necessitated removal of 36 +/- 9 ml/kg of blood in the phlebotomy group. In the sodium nitroprusside/isoflurane group, sodium nitroprusside (16 micrograms.kg-1.min-1) was infused and end-tidal isoflurane concentration increased to 2.5 +/- 0.7%, restoring MAPp to baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of proximal aortic hypertension after thoracic aortic cross-clamping in dogs. Phlebotomy versus sodium nitroprusside/isoflurane. 164 54

A postal survey of selected general practitioners from Brisbane, Melbourne, Sydney and rural New South Wales was conducted to compare general practitioners' self-reported asthma management practices with the Asthma Management Plan (1989) of the Thoracic Society of Australia and New Zealand. The results suggest that most general practitioners know and practise appropriate asthma management. Room for improvement, however, was detected in the following areas: 1. appropriate understanding of the use of theophyllines, 2. the use of preventive medications such as inhaled steroid and sodium cromoglycate, 3. use of crisis planning for severe asthma attacks, 4. lung function measurement.
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PMID:Asthma management in general practice. 168 25

We compared the cardiovascular and renal actions of the neutral endopeptidase (NEP) inhibitor, SQ 28,603, in normal rats and in rats with healed myocardial infarcts. The infarcted rats were studied in the conscious state 8 weeks after ligation of the left main coronary artery and 4 h after placement of cardiovascular and renal catheters. Infarct size was 39 +/- 1.2% of left ventricle circumference; right ventricle and lung weight to body weight ratios were twice those of normal rats. These postmortem values were shown to be associated with elevated left ventricular end diastolic pressure and high plasma atrial natriuretic peptide (ANP) concentration in separate groups of rats. SQ 28,603 at 100 mumol/kg intravenously (i.v.) caused urine volume and sodium excretion to increase by 79 +/- 11 microliters/min and 8.2 +/- 1.4 microEq/min, respectively, 20 min after injection in infarcted rats; these changes were significantly greater than those in normal rats (12 +/- 5 microliters/min and 1.6 microEq/min, respectively). Thoracic venous pressure decreased by 1.9 +/- 0.4 mm Hg 80 min after SQ 28,603 in infarcted rats and by only 0.1 +/- 0.1 mm Hg in normal rats (p less than 0.05 vs. infarcted rats). SQ 28,603 had no effects on mean arterial pressure (MAP), cardiac output (CO), or glomerular filtration rate (GFR). The observation that NEP inhibition has more pronounced effects in animals with high ambient ANP level than in those with normal ANP is consistent with previous studies in a variety of animal models and supports the concept that NEP inhibition potentiates endogenous ANP.
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PMID:Heart failure augments the cardiovascular and renal effects of neutral endopeptidase inhibition in rats. 172 Aug 29

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

1. Recent evidence has suggested that the impairment of endothelium-dependent cholinergic relaxation in vitro, which is seen in atherosclerotic large arteries of animals and man, could be part of a general deleterious effect to the endothelium of hypercholesterolaemia. 2. This possibility has been investigated in vitro by measuring the response to acetylcholine, sodium nitroprusside, 5-hydroxytryptamine and noradrenaline in segments of aorta and of femoral, mesenteric and cerebral small arteries (internal diameter approximately 200 microns) from control rabbits (n = 12) and from rabbits fed a 1% (w/w) cholesterol and 3% (w/w) coconut oil diet (n = 12) for 12 weeks. 3. Thoracic aorta segments from the control rabbits exhibited a maximal relaxation in response to acetylcholine of 64 +/- 11% compared with 10 +/- 5% (P less than 0.01) for thoracic segments from cholesterol-fed animals. Cerebral, femoral and mesenteric small arteries exposed to acetylcholine (10(-9)-10(-4) mol/l) relaxed to the same degree as arteries from control rabbits. The responses to sodium nitroprusside and bradykinin of the small arteries from the cholesterol-fed rabbits remained unaffected. 5-Hydroxytryptamine evoked comparable contractions in the small arteries, while the sensitivity to noradrenaline of the femoral small arteries was significantly decreased and the response of cerebral small arteries to noradrenaline in cholesterol-fed rabbits slightly increased compared with control rabbits. 4. Aorta from the cholesterol-fed rabbits had extensive atheromatous lesions. Morphological measurements and histological examination showed unchanged thickness and light microscopic appearance of intima and media of small arteries from cholesterol-fed animals compared with control animals. 5. The present study indicates that hypercholesterolaemia in this rabbit model is followed by atherosclerotic lesions and changed function of large arteries, but that both function and structure of systemic small arteries are largely unaffected.
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PMID:Functional properties in vitro of systemic small arteries from rabbits fed a cholesterol-rich diet for 12 weeks. 184 63

Virtually every blood vessel in the body is surrounded to some degree by adipose tissue. A potential role for perivascular adipose tissue as a neurohumoral regulator of vascular responsiveness was studied. Thoracic aortae obtained from male Sprague-Dawley rats were cut into rings for use in a standard in vitro smooth muscle bath set-up. The vessels were either cleaned of surrounding adipose tissue or left intact. Contractile responses to KCl and phenylephrine as well as relaxation responses to acetylcholine, isoproterenol and sodium nitroprusside were not different between cleaned and intact tissues. However, a significant decrease in the sensitivity to norepinephrine was observed in intact vessels. This altered response was corrected by prior treatment with desipramine plus deoxycorticosterone. Contractile responses of aortic ring preparations to tyramine and a potassium-free physiological solution were significantly greater in intact tissues. Electrical stimulation resulted in no response in cleaned tissues, however, a frequency-dependent contraction was elicited in intact vessels. Phentolamine blocked the contractile responses generated by these manipulations which activate the sympathetic neuroeffector system. Responses evoked by electrical stimulation in intact vascular preparations were significantly attenuated by prior exposure to the selective angiotensin II (AII) antagonist SarI-Ile8-AII. These observations demonstrate that perivascular adipose tissue significantly influences vascular responsiveness in the in vitro setting.
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PMID:Influence of perivascular adipose tissue on rat aortic smooth muscle responsiveness. 206 67

Vascular relaxation by the organic (nitroglycerin) and inorganic (sodium nitroprusside) nitrovasodilators and the endothelium-dependent vasodilators (acetylcholine and histamine) has been associated with cyclic GMP accumulation. Tolerance to vasodilation by nitroglycerin commonly occurs following prolonged exposure to nitroglycerin. This study investigates the effects of in vivo nitroglycerin therapy on vascular relaxation and cyclic GMP accumulation induced by the nitrovasodilators and the endothelium-dependent vasodilators. Rats were injected with nitroglycerin or the propylene glycol diluent control for 4-7 days. Thoracic aortas from the nitroglycerin-treated rats were 750-fold less sensitive to the relaxant effects of nitroglycerin. In contrast, these aortas were only threefold less sensitive to the relaxant effects of sodium nitroprusside, while the maximum relaxation to acetylcholine and histamine was depressed by 50 and 41%, respectively. Desensitization to relaxation was associated with reduced cyclic GMP elevations to all the vasodilators. Relaxation to 8-bromo cyclic GMP, dibutyryl cyclic AMP, or diltiazem was unaffected by nitroglycerin therapy. Tolerance was also associated with an increased sensitivity to the contractile effects of low concentrations of norepinephrine. This increased sensitivity to norepinephrine was associated with a decrease in cyclic GMP levels. The present results suggest that: (1) desensitization to nitroglycerin, sodium nitroprusside, acetylcholine, and histamine by nitroglycerin therapy may be at the level of cyclic GMP accumulation; (2) cyclic GMP is the common mediator of relaxation induced by the nitro- and endothelium-dependent vasodilators; (3) the mechanisms involved in the activation of guanylate cyclase and relaxation by sodium nitroprusside, acetylcholine, and histamine are probably different than those of nitroglycerin; and (4) cyclic GMP may be acting as a physiological negative feedback signal in agonist-induced contraction.
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PMID:Effect of in vivo nitroglycerin therapy on endothelium-dependent and independent vascular relaxation and cyclic GMP accumulation in rat aorta. 244 89


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