Biomedical subjects

W Durante

Publications and source records attributed to W Durante.

41 records · Page 3Linked to original sources

PubMed1989

Alterations in atrial reactivity in a strain of spontaneously diabetic rats.

1. The present study examined the reactivity of atria from control and spontaneously diabetic rats to various adrenoceptor agonists and to adenosine. 2. Isoprenaline (1.5 nM-1500 nM) produced concentration-dependent increases in inotropy which were unchanged in diabetic atria. However, the sensitivity to isoprenaline-induced changes in chronotropy was reduced in diabetic preparations. 3. In the presence of propranolol (2 microM), phenylephrine (0.2 microM-100 microM) produced concentration-dependent increases in both inotropy and chronotropy; however, atria from diabetic rats exhibited a much greater maximal response. The diabetic state did not alter the sensitivity to phenylephrine. 4. Adenosine (0.15 microM-300 microM) produced concentration-dependent decreases in both inotropy and chronotropy which were unchanged in diabetic atria. 5. Radioligand binding studies revealed that both alpha 1- and beta-adrenoceptor populations were substantially reduced in atria from diabetic rats. However, there was no change in receptor affinity for either adrenoceptor. 6. These results show that diabetes leads to an alteration in atrial reactivity to adrenoceptor stimulation. Future studies examining steps following hormone-receptor coupling are required in order to characterize this defect.

Adenosine↗

PubMed1988

Impairment of endothelium-dependent relaxation in aortae from spontaneously diabetic rats.

1. Diabetes mellitus is known to produce alterations in vascular reactivity. The present study examined the effects of endothelium-dependent and endothelium-independent relaxing substances on thoracic aorta from control and spontaneously diabetic rats. 2. Endothelium-dependent relaxation produced by acetylcholine or the calcium ionophore, A23187, in aortic rings precontracted with phenylephrine was significantly attenuated in diabetic vessels. 3. Relaxations produced by sodium nitroprusside or adenosine in diabetic preparations were comparable to those in control vessels. 4. The results show that diabetes leads to a specific impairment of endothelial-dependent relaxation.

Acetylcholine↗

PubMed1987

Cardiovascular effects of high frequency ventilation--the possible involvement of thromboxane.

Recent studies with high frequency ventilation (HFV) have noted that HFV-induced increases in mean airway pressure leads to a marked cardiovascular depression, especially in cardiac output (CO). Aside from mechanical events a negative inotropic agent possibly prostaglandin in nature may also be involved. This study examined the possible involvement of thromboxane A2 (TXA2) in the HFV-induced cardiovascular deterioration. Chloralose-anesthetized mechanically-ventilated dogs were subjected to HFV 4, 10, and 20 mm Hg for 30 min. Some animals were also treated with imidazole (25 mg/Kg/hr) prior to HFV. Arterial levels of TXB2 (stable metabolite of TXA2) where monitored by radioimmunoassay. During HFV, tracheal pressure-related decreases in both CO and stroke volume (SV) were noted. Imidazole treatment significantly reduced the decrement in SV. Application of HFV resulted in variable changes in circulating TXB2 levels. Overall, application of HFV did not result in a significant change from baseline levels. Furthermore there was no correlation between changes in CO and SV with changes in arterial TXB2 concentration. These results do not support the hypothesis that hyperexpansion of the lungs during HFV causes the release of a cardiodepressant prostanoid.

Animals↗

PubMed1986

The possible involvement of PGI2 in the PEEP-induced changes in cardiac output and blood pressure.

Ventilation with positive end-expiratory pressure (PEEP) is employed in clinical and aviation medicine. The widespread application of PEEP, however, is limited principally because of its adverse effect on cardiac output (CO) and systemic arterial blood pressure (BP). Recently, it has been suggested that this PEEP-induced cardiovascular depression may be mediated by vasoactive agents, possibly prostaglandin in nature. This study examined the possible involvement of PGI2 in the PEEP-induced decreases in CO and BP. Chloralose-anesthetized mechanically ventilated dogs were subjected to brief intervals (75 s) of PEEP 10 or 20 mm Hg. Arterial levels of 6-keto-PGF1 alpha (stable metabolite of PGI2) were monitored by radioimmunoassay. These parameters were compared before and during PEEP application. During PEEP, tracheal pressure-related decreases in both CO and BP were noted. Application of either PEEP 10 or 20 mm Hg resulted in an increase in circulating 6-keto-PGF1 alpha levels in three animals while a decrease was noted in two others. Overall, application of PEEP did not result in a significant change from baseline levels. Furthermore, there was no correlation between changes in either CO or BP with changes in arterial 6-keto-PGF1 alpha levels. These results do not support the hypothesis that the short term PEEP-induced changes in CO or BP are mediated by endogenously released PGI2.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells.

Experiments were designed to determine whether the omega 3-unsaturated fatty acid eicosapentaenoic acid affects the production of nitric oxide evoked by interleukin-1 beta in cultured vascular smooth muscle cells. Incubation of cultured rat or human aortic smooth muscle cells with interleukin-1 beta evoked a time- and concentration-dependent release of nitrite, an oxidation product of nitric oxide. The exposure of cells to interleukin-1 beta in combination with eicosapentaenoic acid caused a significantly larger production of nitrite than that evoked by the cytokine alone. The potentiation by eicosapentaenoic acid was concentration-dependent. The production of nitrite evoked by equieffective concentrations of interleukin-1 beta in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L-arginine (an inhibitor of nitric oxide synthase), transforming growth factor beta 1, platelet-derived growth factorAB and thrombin. The addition of interleukin-1 beta-activated smooth muscle cells to suspensions of washed and indomethacin-treated platelets inhibited the aggregation caused by thrombin. The inhibitory effect was enhanced when the smooth muscle cells were exposed to the cytokine in the presence of eicosapentaenoic acid prior to the experiment. Smooth muscle cells exposed to interleukin-1 beta and eicosapentaenoic acid did not affect platelet aggregation in the presence of oxyhemoglobin or methylene blue. Untreated cells or cells exposed to the fatty acid alone did not have such effects. These observations suggest that eicosapentaenoic acid potentiates the production of nitric oxide evoked by interleukin-1 beta in vascular smooth muscle.

Animals↗