Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of buprenorphine-diazepam-N2O (60%)-O2 anesthesia in open heart surgery was investigated. The authors examined the hemodynamic changes produced and the response of stress hormones. Twenty adult patients with atrial septal defects undergoing surgical correction were studied in two groups of 10, receiving either 6 micrograms/kg of buprenorphine (B6) or 12 micrograms/kg of buprenorphine (B12) for the induction of anesthesia. Both groups received a subsequent dose of 6 micrograms/kg of buprenorphine with the commencement of extracorporeal circulation (ECC). With surgery, mean arterial pressure showed a transient increase in both groups and thereafter was stable. Heart rate in the B6 group was increased from the onset of surgery to the day after, while the B12 group showed no significant change. Filling pressures showed no change in either group. Plasma catecholamine concentrations in the B6 group, in contrast to the B12 group, increased significantly from midoperation to after completion of the operation (ECC 10 minutes, B6 group v B12 group: plasma norepinephrine 616 +/- 231 v 195 +/- 38 pg/mL, plasma epinephrine 1385 +/- 392 v 572 +/- 132 pg/mL, P less than 0.05). Plasma ADH levels in both groups rose with the commencement of surgery, reaching a peak at ECC 10 minutes (B6 group 88.1 +/- 8.4 v B12 group 124.4 +/- 27.2 pg/mL). However, in contrast to plasma catecholamines, the antidiuretic hormone (ADH) levels in the B12 group remained higher until the first postoperative day. Therefore, patients who received the larger dose of buprenorphine had better control of hemodynamics and catecholamines, but a greater elevation of plasma ADH levels.
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PMID:Variations in hemodynamic and stress hormonal responses in open heart surgery with buprenorphine/diazepam anesthesia. 252 Sep 12

We have previously reported that the potent tumor-promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA) and a factor from fetal calf serum (FCS) markedly enhance the transformation of mouse C3H 10T1/2 and Rat 6 fibroblasts, when added to cultures following transfection with plasmid pT24 DNA that contains an activated c-Ha-ras oncogene. In the present study, we examined possible enhancing or inhibiting effects of various chemicals on the transformation of Rat 6 fibroblasts by T24 DNA when tested in the presence of calf serum, calf serum plus TPA or FCS. We found that, like TPA, the chemicals mezerein, 1-oleoyl-2-acetylglycerol, and phospholipase C increased the yield of T24-induced foci, thus further implicating protein kinase C as a critical constituent in this process. Low concentrations (10(-6)-10(-7)M) of retinoic acid (both trans and 13-cis) also stimulated cell transformation. Several compounds inhibited T24-induced transformation. These included nontoxic concentrations of the calcium ionophore A23187, indomethacin, and epsilon-amino-n-caproic acid. Compounds that failed to exert a significant reproducible effect included vasopressin, vitamin D3, selenium, antipain, Bowman-Birk inhibitor, vitamin B12, epidermal growth factor, platelet-derived growth factor, insulin, and transferrin. These findings suggest that this simple in vitro system might be useful for detecting enhancers and inhibitors of ras oncogene-induced cell transformation and also elucidating their mechanisms of action.
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PMID:Effects of various chemical agents on the transformation of rat fibroblasts by an activated c-Ha-ras oncogene. 266 19

The present study investigated how variations in coronary vascular resistance and metabolic demand affected myocardial capillary diffusion capacity. Hearts from Wistar rats were perfused with Krebs-Henseleit-albumin buffer in a Langendorff preparation, where heart rate (HR), contractility (dP/dtmax) and myocardial oxygen consumption (MVO2) were recorded continuously. Myocardial capillary diffusion capacity was measured as the permeability surface area product (PS) for Cr-EDTA and vitamin B12 by the single injection colorimetric indicator dilution method. After base-line recordings without drugs, angiotensin II+Arginine-vasopressin was infused, which increased coronary vascular resistance by 90%, stimulated HR by 11%, decreased dP/dtmax by 21% and reduced MVO2 by 4%. PSCr-EDTA and PSB12 decreased by 24 and 27%, respectively, leaving the ratio PSCr-EDTA/PSB12 unchanged indicating unaltered capillary permeability. Moreover, the reductions in MVO2 and PS correlated significantly. During vasodilation: (1) nitroprusside-NA stimulated HR by 7% and decreased dP/dtmax by 14%; (2) adenosine reduced dP/dtmax by 37% and decreased MVO2 by 9%; and (3) isoproterenol increased HR, dP/dtmax and MVO2 by 53, 76 and 9%, respectively. However, all three vasodilators reduced PSCr-EDTA and PSB12 in parallel by 7-25% leaving PSCR-EDTA/PSB12 unchanged. Thus, maximal estimated diffusion capacities were obtained during spontaneous coronary vascular tone, most likely reflecting maximal capillary recruitment in the Krebs-Henseleit-albumin perfused heart. The derecruiting effects of the vasoconstrictors were partly overridden by metabolic factors, while the reductions of PS after vasodilation more likely were due to increased heterogeneity in coronary flow.
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PMID:Changes in myocardial capillary diffusion capacity during infusion of vasoactive drugs. 845 41