Disease relevance of Intensain

• Systemic and coronary haemodynamic effects of carbochromen (0.125 mg kg-1 min-1 for 40 min i.v.) and dipyridamole (0.05 mg kg-1 min-1 for 10 min i.v.) were investigated in 18 patients without detectable heart disease [1].
• Atrial fibrillation plus chromonar abolished reactive hyperaemia in both the sinus node artery and the right ventricular branch vessel [2].
• This paper describes the effect of carbocromene pretreatment on the functional recovery of the isolated rat heart submitted to ischemic cardiac arrest and reperfused [3].
• In the present work, carbocromene-pretreated hearts are submitted to 30 minutes of normothermic no-flow ischemia after being arrested by a 2 min high potassium, substrate-free perfusion, containing 2 mg/l carbocromene (cardioplegic solution) [3].
• In a previous study we showed that hearts isolated from rats which had been pretreated for 8 days with a daily oral administration of carbocromene at 15 mg/kg body weight, exhibit higher mechanical performances (aortic output, coronary flow, cardiac work) than hearts isolated from untreated animals [3].

High impact information on Intensain

• Collateral blood flow was quantified during chromonar-induced maximal vasodilation and expressed as a collateral zone/normal zone (CZ/NZ) ratio [4].
• Chromonar increased coronary blood flow 2.8 times in the control animals, but did not significantly increase flow or decrease vascular resistance in the rabbits given 1-thyroxine [5].
• Dipyridamole induced a significant increase in myocardial oxygen consumption by 46% (P less than 0.001); after application of carbochromen myocardial oxygen consumption remained unchanged [1].
• Reactive hyperaemic responses were measured using Doppler crystals fixed to the sinus node artery and to an adjacent right ventricular branch artery during sinus rhythm, after 20 minutes of atrial fibrillation, and after systemic administration of chromonar (a potent coronary dilator) during atrial fibrillation [2].
• The ratio of subendocardial to subepicardial flow remained normal with or without the pericardium, at low and high diastolic ventricular pressure, and before and after pharmacological vasodilation with chromonar [6].

Chemical compound and disease context of Intensain

• The phosphodiesterase inhibitors papaverine, carbocromene, theophylline and caffeine caused hypertension and tachycardia which increased with the dose while the phosphodiesterase activator imidazole exerted opposite effects [7].
• We studied the effects of carbocromene (4 mg/kg plus 40 micrograms/kg/min i.v.) and molsidomine (0.1 mg/kg plus 2 micrograms/kg/min i.v.) on arrhythmias occurring during 90-min occlusion and 30-min reperfusion of the left anterior descending coronary artery in anesthetized dogs [8].
• The effects of carbocromene, 4 mg/kg intravenously, prior to coronary artery occlusion plus 40 microgram/kg/min during coronary artery occlusion and reperfusion on ventricular fibrillation threshold (VFT) were studied in pentobarbital-anesthetized open-chest dogs and compared to controls receiving saline [9].
• Systolic, diastolic, and mean coronary blood flow after addition of chromonar (8 mg/kg iv), adenosine triphosphate (400 micrograms/min intracoronary), or adenosine (500 micrograms/min intracoronary) exceeded the respective flow at the peak of reactive hyperemia (90-s occlusion period) [10].
• Blood flow and high energy phosphate (HEP) content were determined simultaneously in multiple microregions of the left ventricular subendocardium in 49 anaesthetized open-chest rabbits, to determine the relationship between the parameters during high O2 supply with hypercapnia and chromonar treatment [11].

Biological context of Intensain

• Carbocromene, in a dose of 3.0 mg/(kg x min) i.v., infused for 5 min, raised coronary blood flow from 6.2 +/- 0.6 to 15.6 +/- 0.1 ml/(min x g); heart rate and blood pressure were only slightly changed [12].
• Different degrees of vasodilation in nonischemic myocardium were produced by the selective coronary dilator, chromonar, at a constant heart rate and aortic blood pressure [13].
• Carbocromene possibly exerts metabolic effects on the heart, in addition to its coronary dilating properties, which confer the cardioprotective effects observed in acute canine experiments [14].
• Platelet aggregation and adhesiveness as well as blood lipids level in dogs treated with di-(1-isoquinolinyl)-di-(pyridyl-2')-butane and carbocromen [15].
• Carbochromen increases coronary flow and cardiac output [16].

Anatomical context of Intensain

• Ultrastructural modifications of the platelet plasma membrane in vascular diseases and the effect of a carbochromen derivative as studied by freeze-fracture and computer measurement [17].
• Effects of oral carbocromene pretreatment on infarct size following experimental coronary artery occlusion [18].
• When criteria 1 and 2 were used to identify ischemic myocardium, chromonar (5 and 7.5 mg/kg, i.v.) produced no change in ischemic blood flow [13].
• Density of plasma-perfused capillaries in the rat heart during carbocromene-induced vasodilation [12].
• The carbochromene derivative AD6 reduces the TxB2/6-keto-PGF1 alpha ratio in cerebral cortex during hypoxia and recovery and leukotriene synthesis in brain tissue, in the rat [19].

Associations of Intensain with other chemical compounds

• From these data it can be concluded that for the evaluation of coronary dilatory capacity carbochromen may be more suitable than dipyridamole because (1) maximal coronary vasodilation is induced without changes in myocardial oxygen consumption and (2) no systemic effects occur [1].
• Studies on the characteristics of carbochromen hydrochloride crystals. II. Polymorphism and cracking in the tablets [20].
• Adenosine or chromonar vasodilated more than did hypoperfusion alone in all layers of the heart at perfusion pressures as low as 30 mmHg (P less than 0.05) [21].
• The effect of di-(1-isoquinolinyl)-di-(pyridyl-2')-butane (S-147) on platelet aggregation and adhesiveness as well as on blood lipids level (total lipids, triglycerides, total cholesterol) was tested in mongrel dogs, in comparison with carbocromen [15].

Gene context of Intensain

• Normothermic Ischemic Cardiac Arrest and Reperfusion of the Isolated Working Rat Heart: Effect of Carbocromene Pretreatment on Functional and Metabolic Recovery [3].

Analytical, diagnostic and therapeutic context of Intensain

• The first set of 10 dogs had CT and microsphere measurements before and after chromonar-induced increases in myocardial blood flow [22].
• Normothermic ischemic cardiac arrest and reperfusion of the isolated working rat heart: effect of carbocromene pretreatment on functional and metabolic recovery [3].
• In 19 dogs, we measured left ventricular pressure with a catheter tip transducer and dimensions with an epicardial echo transducer and, during each experiment, compared the diastolic pressure-dimension relationship during two states of coronary blood flow: control and maximal vasodilation (induced by intravenous chromonar) [23].
• Carbocromene led to only slight pressure and rate alterations after ligation and reperfusion whereas untreated animals gave evidence of significant changes in these parameters [14].
• Furthermore, contractility remained unaffected by carbocromene but was significantly augmented in the control group after both experimental procedures [14].

References