Influence of desoxycorticosterone on the response of coronary artery segments to adrenaline in the presence of pyrogallol

The effect of desoxycorticosterone on the adrenaline-induced relaxation of coronary arteries was studied in vitro, after a known inhibitor of COMT, pyrogallol. Relaxation induced by adrenaline was enhanced by desoxycorticosterone. Relaxation in response to adrenaline was increased by desoxycorticosterone. Pyrogallol potentiated the responses of coronary strips to adrenaline and also reduced or abolished the enhancing effects of desoxycorticosterone. It is concluded that desoxycorticosterone enhances the response of coronary smooth muscle to adrenaline by inhibiting an enzymatic pathway for the inactivation of catecholamines.     

Response of isolated coronary artery strips to noradrenaline in the presence of desoxycorticosterone

The effect of desoxycorticosterone on the noradrenaline-induced relaxation of coronary arteries was studied "in vitro". It resulted that the effect of noradrenaline was enhanced by desoxycorticosterone. It is concluded that desoxycorticosterone potentiates the effects of noradrenaline by inhibiting its inactivation by Catechol-O-methyltransferase.     

Influence of dexamethasone on the responses of isolated coronary arteries to adrenaline

The effect of Dexamethasone on the adrenaline-induced relaxation was studied in vitro. Relaxation of response to adrenaline increased by Dexamethasone. We suggest that the Dexamethasone influence depends on inhibition of Catecol-O-methyl transferase (COMT).     

Influence of 6-methylprednisolone on responses of isolated coronary arteries to adrenaline

The effect of 6-Methylprednisolone on the adrenaline-induced relaxation was studied in vitro. Relaxation of response to adrenaline increased by 6-Methylprednisolone. We suggest that the 6-Methylprednisolone influence influence depends on inhibition of Catecol-O-methyl transferase (COMT).     

Influence of desoxycorticosterone on the reaction of isolated segments of coronary arteries to noradrenaline in the presence of pyrogallol

The effect of the desoxycorticosterone on the noradrenaline-induced relaxation of coronary arteries waw studied in vitro, after a known inhibitor of COMT, pyrogallol. Relaxation induced by noradrenaline was enhanced by desoxycorticosterone. Relaxation in response to noradrenaline was increased by desoxycorticosterone. Pyrogallol potentiated the responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of desoxycorticosterone. It is concluded that desoxycorticosterone enhances the reponse of coronary smooth muscle to noradrenaline by inhibiting and enzymatic pathway for the inactivation of catecolamines.     

Effects of statins on myocardial and coronary artery response to ischemia-reperfusion

This study tested the hypotheses that (i) lipophilic statins (atorvastatin and simvastatin) impair ventricular recovery from myocardial ischemia-reperfusion, owing to their greater myocyte permeability, compared with a hydrophilic statin (pravastatin), and (ii) statins enhance endothelium-dependent vasodilation of isolated coronary arteries from the ischemic region. Farm pigs consumed chow supplemented with atorvastatin (2.5 mg.kg(-1).d(-1); n=6), pravastatin (10 (n=3) or 20 (n=2) mg.kg(-1).d(-1)), simvastatin (5 mg.kg(-1).d(-1); n=6), or no statin (control; n=6) for 3 weeks. Animals were anesthetized and instrumented to measure regional (% segment shortening) and global (dP/dt max) left ventricular (LV) function during coronary artery occlusion (10 min) and reperfusion (30 min). Coronary resistance (i.d. = 119 +/- 3 microm) and conductance (i.d. = 487 +/- 11 microm) arteries were isolated from the ischemic region to measure receptor-dependent (acetylcholine (ACh)) and -independent (KCl) vasoconstriction, and endothelium-dependent (bradykinin (BK)) and -independent (sodium nitroprusside (SNP)) vasodilation. At 30 min reperfusion, neither percent recovery of regional ventricular function (atorvastatin, 24% +/- 15%; pravastatin, 36% +/- 13%; simvastatin, 29% +/- 13%; control, 36% +/- 13%) nor percent recovery of global LV cardiac function differed among groups. However, BK-induced vasorelaxation of coronary conductance vessels was greater (P<0.05) in statins versus controls, and ACh-induced vasoconstriction was less in simvastatin-treated animals, suggesting the potential for enhanced coronary arterial blood flow to the jeopardized region. In conclusion, our data suggest that ischemia-induced myocardial stunning is similar among pigs treated for 3 weeks with atorvastatin, pravastatin, or simvastatin, even though statin treatment appears to augment endothelium-dependent vasodilation of conductance, but not resistance, vessels subjected to ischemia-reperfusion.     

Influence of bioflavonoid (4-methylesculetin) on the reaction of isolated calf hepatic artery to serotonin

The effect of 4-metilesculetin on strips of calf hepatic arteries was investigated. 4-metilesculetin antagonizes the contraction induced by 5-HT probably through activation of the synthesis of vasodilator prostaglandins.     

The effect of afterload on the cardiodepressor reflex response to coronary artery occlusion in dogs

The acute hemodynamic responses to anterior and posterior wall ischemia were examined at different afterloads in 30 open-chest anaesthetized dogs. Regional and global left ventricular responses to acute ischemia were also measured before and following bilateral cervical vagotomy in 18 dogs. As the preocclusion afterload (mean aortic pressure) was progressively raised with intravenous methoxamine, a significant decrease in stroke volume occurred following circumflex artery occlusion, whereas no change in stroke volume occurred following occlusion of the left anterior descending artery. Bilateral cervical vagotomy completely inhibited the decrease in stroke volume during circumflex occlusion at high afterload. Vagotomy had no effect on the hemodynamic response to acute anterior wall ischemia. Reversible cold vagal block in paced hearts at high afterload unmasked compensatory inotropy in the nonischemic anterior myocardial segment during circumflex occlusion. Restoring vagal tone by rewarming attenuated the fractional shortening of the nonischemic segment. The results indicate that a relationship exists between myocardial wall tension and reflex cardioinhibition during acute posterior wall but not anterior wall ischemia in dogs.     

Influence of coronary artery diameter on eNOS protein content

The purpose of this study was to test the hypothesis that the content of endothelial nitric oxide synthase (eNOS) protein (eNOS protein/g total artery protein) increases with decreasing artery diameter in the coronary arterial tree. Content of eNOS protein was determined in porcine coronary arteries with immunoblot analysis. Arteries were isolated in six size categories from each heart: large arteries [301- to 2,500-microm internal diameter (ID)], small arteries (201- to 300-microm ID), resistance arteries (151- to 200-microm ID), large arterioles (101- to 150-microm ID), intermediate arterioles (51- to 100-microm ID), and small arterioles(<50-microm ID). To obtain sufficient protein for analysis from small- and intermediate-sized arterioles, five to seven arterioles 1-2 mm in length were pooled into one sample for each animal. Results establish that the number of smooth muscle cells per endothelial cell decreases from a number of 10 to 15 in large coronary arteries to 1 in the smallest arterioles. Immunohistochemistry revealed that eNOS is located only in endothelial cells in all sizes of coronary artery and in coronary capillaries. Contrary to our hypothesis, eNOS protein content did not increase with decreasing size of coronary artery. Indeed, the smallest coronary arterioles had less eNOS protein per gram of total protein than the large coronary arteries. These results indicate that eNOS protein content is greater in the endothelial cells of conduit arteries, resistance arteries, and large arterioles than in small coronary arterioles.     

Influence of group B streptococci on piglet pulmonary artery response to bradykinin

To study whether a sepsis-induced increase indes-Arg⁹-bradykinin(des-Arg⁹-BK) and bradykinin (BK)B₁-receptor activity participatesin the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays ofpulmonary artery (PA) rings were studied, after 4-h exposure to eitherKrebs or GBS, by using the following protocols:1) BK dose-response curve,2) vascular response to BK withN^G-nitro-L-arginine methyl ester(L-NAME), and3) response todes-Arg⁹-BK (BK metabolite andB₁ agonist). PA rings exposed toBK resulted in contraction in the GBS group and a decrease in restingtension in the Control group (P = 0.034) at a concentration of10⁵ M. GBS-treated PA ringscontracted more to des-Arg⁹-BKthan did Controls (P < 0.001). BK(10⁶ M) relaxedpreconstricted PA rings incubated in GBS less than BK relaxed Controls(P < 0.001), and preincubation withL-NAME decreased relaxation inboth. These results suggest that GBS decreased endothelium-dependent BKrelaxation and increased contractile response todes-Arg⁹-BK. We speculate thatthis occurs secondary to upregulation of B₁ receptors reflected byB₁-agonist-mediated PA contraction.