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

Recent data from this laboratory indicate that insulin resistant obese Zucker rats exhibit hypertension associated with exaggerated in vitro vascular reactivity to phenylephrine, serotonin, and KCl, and we have found insulin to attenuate vascular reactivity responses to these agonists. Accordingly, in the present study we evaluated the possibility that exaggerated vascular reactivity responses in obese Zucker rats may result from insulin resistance and a consequent failure of insulin to attenuate vasoactive responses. Thoracic aortae were isolated from male 16 week old lean and obese Zucker rats, and replicate helical strips from each animal were suspended in a muscle bath under a resting tension of 1.4 g in the presence or absence of insulin (0.1 mU/mL) for 1 h. The insulin was then washed out, and vascular reactivity responses to phenylephrine were determined. The obese rats exhibited greater reactivity to phenylephrine (ED50:1.10 +/- 90 X 10(-8) v 7.57 +/- 0.88 X 10(-10) mol/L in lean and obese rats, respectively, P less than .025). Insulin caused a significant attenuation of the contractile response in both the lean and obese aortae. However, lean rats exhibited a markedly greater attenuation than the obese rats (46.0 +/- 17.0 v 17.8 +/- 7.5% attenuation in the lean and obese rats, respectively, P less than .01). These data suggest that increased vascular reactivity responses in obese Zucker rats may result from their insulin resistant state and, consequently, a diminished ability of insulin to attenuate vasoconstrictor responses.
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PMID:Insulin attenuation of vasoconstrictor responses to phenylephrine in Zucker lean and obese rats. 187 6

Experiments were designed to investigate the phenomenon of endothelium-dependent relaxation (EDR) to acetylcholine in two animal models of insulin dependent diabetes mellitus. Thoracic aortas obtained from streptozotocin diabetic rats and genetically diabetic biobreeding rats (BB rats) were used in this study. Concentration-effect curves to acetylcholine were carried out on aortic rings under isometric tension. Following the induction of diabetes with streptozotocin, half of the animals were treated with daily intermediate acting insulin and the other half maintained without insulin for a period of 12 weeks before the experiment. The diabetic BB rats were also maintained on insulin. The EDR to acetylcholine was not impaired in the aortas of streptozotocin diabetic rats (insulin treated as well as untreated) compared to nondiabetic controls. The scanning electron microscopic (SEM) appearances of the aortic endothelium did not differ among the three groups of animals. However, the EDR to acetylcholine was found to be impaired in the aortas of diabetic BB rats. (Maximum relaxation: 25.3 +/- 5.0% of the contraction to norepinephrine compared to 52.2 +/- 5.3% in controls.) The SEM appearances of the aortic endothelium in the diabetic BB rats were found to be abnormal with edema and loss of definition of cell margins compared to nondiabetic controls. The differences in EDR to acetylcholine seen between the two animal models of diabetes may be related to the different aetiologies of diabetes in the animals.
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PMID:Endothelium-dependent relaxation to acetylcholine in the aorta of streptozotocin induced diabetic-rat and the BB-diabetic rat. 252 76

Influence of various hormones on the induction of cellular retinoic acid binding protein (CRABP) was investigated in the mouse mammary gland organ cultures. Thoracic pairs of mammary glands from the BALB/c mice were cultured for seven days in the presence of various hormones in CMRL medium at 37 degrees C under 50% O2, 5% CO2 and 45% N2 atmosphere. There was a modest increase of mammary CRABP by insulin (I) + prolactin (P), however, addition of progesterone (Pg) or estrogen (E) + Pg to the medium resulted in a dramatic increase in the CRABP. Aldosterone (A) + hydrocortisone (F), in addition to I + P, which promotes differentiation to an extent similar to that of I + P + E + Pg did not have any influence on the induction of CRABP. These results indicate that prolactin and/or Pg in the medium can increase the concentration of CRABP in the mammary gland in vitro. From the results presented in this report, as well as previous work by other investigators, it is concluded that the biological response to retinoids in the mammary tissues cannot be correlated with the absolute concentration of CRABP in the cells. However, the biological response may be dependent upon both the ability of the target organ cells to metabolize the retinoid and to have minimal concentration of CRABP for binding to the active metabolite. The functional significance of hormone-induced CRABP is presently unknown.
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PMID:Role of hormones on the induction of retinoic acid binding protein in mouse mammary gland organ culture. 299 Jul 55

Human arterial endothelial cells were cultured in vitro for up to 40 cumulative population doublings. Culture conditions similar to those required for long-term propagation of human umbilical vein endothelial cells were employed. These included fibronectin-coated culture vessels, 5 to 20% fetal bovine serum, endothelial cell growth factor, and heparin. Thoracic aorta endothelial cells were larger than iliac artery endothelial cells. Both cell types stained positively for Factor VIII antigen by immunofluorescence. A decrease in confluent density as a function of population doubling level was correlated with the appearance of large, senescent cells in the cultures. Serum growth factors to which the arterial endothelial cells responded included insulin, transferrin, epidermal growth factor, thrombin, and somatomedins. The effect of thrombin did not require the availability of the active site of the protease. The effect of the somatomedins was only seen in the presence of heparin. Neither platelet-derived growth factor nor hydrocortisone induced arterial endothelial cell proliferation. These growth factor responses were also observed on the part of human umbilical vein endothelial cells.
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PMID:Growth factor responses of human arterial endothelial cells in vitro. 375 96

Mouse mammary gland organ culture technique was utilized to determine the effects of retinoids on the prolactin-induced structural differentiation of the mammary gland. Thoracic glands from BALB/c mice pretreated with steroids differentiate in 6 days into alveolar structures in presence of insulin and prolactin. All-trans-retinoic acid and N-(-4-hydroxyphenyl)retinamide inhibit prolactin-induced structural changes in the glands. Retinyl acetate, which is effective against mammary carcinogenesis in the rat, but is ineffective against mouse mammary carcinogenesis, failed to inhibit such proliferation. These results were correlated with inhibition of [3H]thymidine incorporation into DNA in a dose related manner by retinoids effective in inhibiting mammary development.
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PMID:Retinoids inhibit prolactin-induced development of the mammary gland in vitro. 682 85

Prior attempts at in vivo reversible vagal denervation of the gastrointestinal tract have been limited to cervical cooling techniques that also denervate both sympathetic and vagal pulmonary and cardiac branches. Denervation of vagal efferent fibers at this level has produced results that are inconsistent with those obtained after surgical truncal vagotomy. We have, therefore, developed a technique to provide reversible vagal denervation below the pulmonary and cardiac branches for the study of gastric motility. Five dogs, previously equipped with gastric strain gages and electrodes, underwent implantation of a tubular cooling jacket around a distal thoracic vagal trunk with contralateral vagotomy (4 dogs), or around both vagal trunks (1 dog). The jacket was made of stainless steel tubing in a "J" design. Its inside channel was lined with a sterling silver sheet, and a thermistor was attached to record temperature change. Silicone tubing coursed externally to a pump and flask to which 95% ethanol at -70 degrees C was circulated at variable speeds. Thoracic vagal cooling, extending up to 5 h, reversibly blocked gastric contractions induced by insulin hypoglycemia. Contractile waves were terminated at device temperatures of 2 degrees-6 degrees C but promptly returned with warming. Dogs were tranquil during denervation, and enclosed nerves remained functional for greater than 40 days.
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PMID:Reversible truncal vagotomy in conscious dogs. 687 4

A 40-year-old man with a 3-year history of uncontrolled NIDDM, 2-pack/month cigarette smoking habit and alcohol abuse, was admitted to our university hospital. He presented with severe back pain, persistent cough and fever. A left lung infiltrate was noted on chest X-ray film. Staphylococcus aureus was isolated from arterial blood. Thoracic bone destruction with pleural mass lesion confirmed by computed tomography (CT) and magnetic resonance image (MRI). These findings mislead our diagnosis to pyogenic osteomyelitis associated with NIDDM. An absence of marked clinical and roentgenological improvement after antibiotic therapy and strict glycemic control with insulin was noted. This suggested to us the need for needle biopsy of the osteolytic and mass lesions confirmed by imaging techniques. This resulted in making the diagnosis of metastasis of small cell carcinoma from the left lung. The correlation between NIDDM and pulmonary small cell carcinoma possibly induced by genetic abnormality remains to be resolved. By making the most of imaging techniques and needle biopsy, the possibility of pulmonary small cell carcinoma complicating NIDDM can be appropriately evaluated.
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PMID:Vertebral bone metastasis of small cell carcinoma of lung in a diabetic patient, initially diagnosed as pyogenic vertebral osteomyelitis. 807 45

We previously reported a striking similarity between the dynamics of both glucose turnover and thoracic duct lymph insulin during euglycemic clamps (J Clin Invest 84:1620, 1989), which suggested that transendothelial insulin transport (TET) is rate-limiting for insulin action in vivo. Thoracic duct lymph, however, is primarily derived from insulin-insensitive tissues, which raises questions as to the physiological significance of this relationship. The relationship between glucose turnover and TET was thus examined in insulin-sensitive tissues by the simultaneous measurement of insulin in plasma, thoracic duct lymph, and hindlimb lymph during euglycemic clamps in normal anesthetized dogs (n = 8). Clamps consisted of two 3-h phases: a 0.6 mU.min-1.kg-1 insulin infusion (activation phase) followed by termination of the insulin infusion (deactivation phase). Lymph insulin was less than plasma insulin during both phases (P < 0.01) with steady-state hindlimb (120 +/- 12 pM) and thoracic duct lymph insulin (138 +/- 12 pM) 38 and 45%, respectively, lower than steady-state plasma insulin (222 +/- 24 pM) at the end of the activation phase (P < 0.05). Also, the rate of increase of lymph insulin was slower than plasma insulin during hormone infusion; half-time to steady-state was 8.8 +/- 2.0 min for plasma insulin, but longer for thoracic (25.8 +/- 3.5) and hindlimb lymph insulin (40.7 +/- 5.7 min). A very close relationship was observed during activation between the rate of increase of glucose uptake (Rd) and the increase in hindlimb lymph insulin (r2 = 0.92); this relationship was weaker for thoracic lymph (r2 = 0.74) and much weaker between glucose uptake and plasma insulin (r2 = 0.35). These data support the concept that interstitial insulin (represented by hindlimb lymph) is the signal that determines glucose uptake by insulin-sensitive tissues and that the rate of increase of glucose uptake is determined by transendothelial insulin transport into insulin-sensitive tissue. Also, during activation, hindlimb lymph insulin was a very strong predictor of the rate of suppression of hepatic glucose output (HGO) (r2 = 0.96), and the correlation with HGO was stronger than that for thoracic lymph (r2 = 0.85). The evidence that the rate of increase of Rd and the rate of suppression of HGO during insulin infusion are very strongly predicted by the time course of insulin in hindlimb lymph is consistent with the single-gateway hypothesis: the insulin transport rate across endothelium in insulin-sensitive tissue (skeletal muscle) determines the rate of glucose utilization and the suppression of hepatic glucose output.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dynamics of glucose production and uptake are more closely related to insulin in hindlimb lymph than in thoracic duct lymph. 828 41

We have previously shown that insulin attenuates vasoconstrictor responses to pressor agonists and accelerates vascular smooth muscle cell (VSMC) Ca(2+)-ATPase mediated Ca2+ efflux and vascular relaxation. We have now sought to determine if VSMC from insulin resistant (Zucker Obese, ZO) rats manifest exaggerated [Ca2+]i responses to pressor agonists and impaired [Ca2+]i recovery (rate of [Ca2+]i return to baseline) compared to their lean controls (ZL). Thoracic aortae from ZO and ZL were enzymatically digested to release VSMC (n = 16 animals/group and 8 determinations/group). Freshly dispersed cells were washed, counted, and loaded with Fura-2-AM. The [Ca2+]i responses to and rate of recovery from angiotensin II (AII; 200 nmol/L) and arginine vasopressin (AVP; 10 mumol/L) were studied fluorometrically in stirred suspension (10(6) cells/mL). Peak [Ca2+]i responses to AVP were not significantly different in ZO v ZL, while responses to AII were higher in ZL ([Ca2+]i, 180 +/- 7 v 160 +/- 4% of baseline in ZL and ZO, P < .02). Since we have recently shown insulin to increase AII-releasable Ca2+ stores in sarcoplasmic reticulum, this increase in peak [Ca2+]i response to AII in ZL may reflect relative VSMC insulin resistance in ZO. Despite their increased peak AII response, ZL exhibited a more rapid recovery from both the AII-stimulated load (recovery rate, 66.1 +/- 8.9 v 42.1 +/- 9.0 nmol/L/min in ZL and ZO, P < .02) and the AVP-stimulated [Ca2+]i load (22.2 +/- 2.3 v 18.4 +/- 4.6 nmol/L/min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired recovery of vascular smooth muscle intracellular calcium following agonist stimulation in insulin resistant (Zucker obese) rats. 834 33

We report on eight patients with diabetic thoracoabdominal neuropathy in whom careful evaluation of peripheral and autonomic nervous system function was performed. All patients had non insulin-dependent diabetes mellitus of 10.5 +/- 6.7 years mean (+/- SD) known duration with poor glycemic control. Thoracic (n = 7) or abdominal (n = 1) pain of sudden onset involved several adjacent dermatomal segments and was bilateral and asymmetrical in 7/8 patients. Four patients had hypoesthesia in the painful zone and six presented with significant weight loss (6.2 +/- 4.3 kg) which reversed after the relief of pain. Truncal electromyogram was abnormal in 7/7 patients. Nerve damage was not limited to thoracic nerves since electrophysiological studies evidenced distal polyneuropathy in all patients. The autonomic nervous system was also involved. Sympathetic skin response was abnormal in 7/7 patients and autonomic cardiovascular function tests demonstrated cardiac denervation in 5/5 patients. In 4/4 patients a marked relief of pain was noted within one week with amitriptyline treatment. This report confirms the characteristic clinical presentation of diabetic thoracoabdominal neuropathy. Moreover, it suggests that this neuropathy is part of a diffuse damage that also involves peripheral nerves of the limbs and autonomic nervous system.
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PMID:[Diabetic thoracoabdominal neuropathy. Clinical and electrophysiological study with evaluation of the autonomic nervous system]. 851 Nov 33


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