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A Genovese

Publications and source records attributed to A Genovese.

At least 73 records · Page 4Linked to original sources

Dilazep-induced reduction of ischemic necrosis in rats with coronary artery occlusion.

To assess whether dilazep reduces myocardial necrosis we assigned 72 rats that survived coronary artery occlusion to 3 groups. The first control group (n = 26) received coronary occlusion and was untreated. The second group (n = 21) received coronary occlusion and was treated with dilazep (150 micrograms/kg s.c.) every 8 hours for 48 hours. The third group (n = 25) was sham-operated. Forty-eight hours later the creatine-kinase activity of the left ventricle was measured. The calculated left ventricular fraction that survived the occlusion was larger in dilazep-treated rats (44.5 +/- 4.1% of left ventricle) than in controls (31.2 +/- 3.2%; P less than 0.05). Twenty-six more rats also underwent coronary occlusion; 12 were controls and the remaining 14 were treated with dilazep at the same time and dose as before and killed 21 days after occlusion. Infarct size was evaluated on histological sections of the hearts by planimetry. The amount of left ventricle preserved from necrosis was larger in dilazep-treated rats, 82.1 +/- 0.9%, compared to controls 69.5 +/- 1.4% (P less than 0.05). Dilazep seems effective in preserving myocardial tissue from ischemic necrosis, and its beneficial effects are long-lasting, producing permanent reduction of infarct size.

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Bilateral ventricular hypertrophy in rats exposed to acute or chronic hypobaric hypoxia.

Development of bilateral ventricular hypertrophy in animals exposed to sustained hypoxia is demonstrated. Female Sprague-Dawley rats (180-200 g) were subjected to acute (0.40 atm/24 h) or chronic intermittent (0.40 atm/18 h/day/7days) hypobaric hypoxia. Control animals were maintained at room pressure. The changes in ventricular mass (right ventricle and left ventricle including the septum) were evaluated on the basis of the dry weight values immediately at the end of hypoxic stimulus. Data show that both acute and chronic hypobaric hypoxia allow rate to develop a significantly degree of hypertrophy in the left as well as in the right ventricle. The factors involved in the genesis of the left ventricular hypertrophy in hypoxic conditions are presented.

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Quantitative assessment of infarct size in isoproterenol-infarcted rats.

The authors performed a number of experiments aiming at quantifying the infarct size in Sprague-Dawley male rats. The experimental model employed was isoproterenol (ISP) induced, infarctlike myocardial lesions. In quantifying the extent of the infarct area they compared the cross reliability of enzymatic and histological methods. ISP was administered in two subcutaneous injections (50 mg/100 Gm body weight) at a 24 hour interval. At the peak of the necrotic process (48 hrs after the first injection), the heart was subjected to enzymatic or histological studies. Thus, a group of infarcted animals (n = 25) and their controls (n = 15) underwent the assessment of creatine kinase (CK) content in the homogenate of the myocardium. Another group of animals (n = 15) was used for histological observations, including measurement of infarct size by planimetry from histological sections. A good relationship was observed between the percentage of necrotic tissue calculated on the basis of CK values (69.11 +/- 2.39%) and the infarction area assessed by planimetry (72.37 +/- 2.69%) (mean +/- standard error of the mean [SEM]). Thus, the present study confirms that ISP-induced myocardial lesions are a simple and reliable model for experimental infarct. Moreover, the assessment of the CK content in the heart is correlated with histological studies by planimetry, and is suggested as a direct enzymatic method to quantify the extent of myocardial necrosis.

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[Influence of myocardial infarct on ventricular arrhythmias during the exercise test. Study in patients with stable angina of effort].

The incidence of ventricular arrhythmias observed during exercise (EVA) was correlated with the presence of previous myocardial infarction (IM) and angiographic severity of coronary artery disease (CAD) in 162 patients (pts.) with stable angina on effort, who had a positive stress test and greater than 70% stenosis of a major coronary artery. Our study population was divided in two groups: the first was composed of 95 pts. with previous MI, the second of 67 pts. without previous MI. Pts. of both groups were subdivided according to severity of CAD and to presence and degree of abnormal segmental wall motion (ASWM). In the MI group only 11.5% of pts. had single vessel disease, and 86.3% had ASWM. In pts. without MI 28.6% had single vessel disease; ASWM was found in 59.7% (p less than 0.001 vs MI pts.). Pts. with MI showed a higher incidence of EVA than pts. without MI (60% vs 32.8%, p less than 0.001). In both groups EVA were more frequent among pts. with double, triple vessel and main left CAD, than in pts with single vessel disease, but the difference was not significant. In general, EVA were found to correlate better with the number of areas with ASWM: in both groups significant differences of EVA frequency were found when pts. with normal left ventricular function were compared to those with more severe ASWM, while no difference was found between pts with and without MI who had the same degree of CAD. The most severe EVA (Tilkian's classification), were found in pts with a previous MI and a high ASWM score. In conclusion, our results show that a previous MI affects the development of EVA in pts. with stable effort angina. However EVA seem to be better correlated with the severity of LV impairment than with the extent of CAD.

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Development of cardiac hypertrophy in rats exposed to acute hypobaric hypoxia. - Studies with protein synthesis inhibitors.

The study is based on the experimental model of myocardial hypertrophy in rats. Male Sprague-Dawley adult rats were exposed to acute hypoxia in a hypobaric chamber (0.40 atmospheres of air for 24 hours). Myocardial hypertrophy was detected by wet and dry heart weight values when calculated on the basis of total body weight; i.e., ratio heart weight in mg to body weight in 100 g. The behaviour of myocardial hypertrophy was assessed after treatment of intact animals with Puromycin (10 mg/rat i.p.) or Actinomycin-D (100 micrograms/rat i.p.). The experimental results showed the following dry heart weight values (mean +/- SEM): room pressure 60.5 +/- 1.5; hypoxia 69.2 +/- 0.9; Actinomycin-D + hypoxia 63.5 +/- 0.6; Puromycin + hypoxia 62.4 +/- 1.5, (P less than 0.001). From the comparison of data reveals that inhibitors of protein synthesis completely inhibit the myocardial hypertrophy due to hypoxia. Thus it is documented that acute hypobaric hypoxia is able to induce in the rat an actual myocardial hypertrophy condition as expressed of the enhanced protein synthesis.

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[Coronary artery disease (CAD) in females. Coronary arteriographic findings in 34 women and comparison with 184 males with cad].

We studied the clinical, hemodynamic and angiographic findings of 34 women (W) and of 184 men (M) with significant (greater than or equal 50%) CAD. W, compared to M, presented a higher incidence of systemic hypertension (p less than .025), while less frequent were among W smoking habits (p less than .001), history of old myocardial infarction (MI) (p less than .005), and patients in III-IV NYHA class (p less than .025). Left ventricular (LV) dP/dt was higher in W than in M (p less than .005). At coronary arteriography, single vessel disease (SVD) was more frequently found in W than in M (70% vs 23%, respectively, p less than .001); this findings was more evident in patients under 50 years of age (100% vs 30%, respectively, p less than .055). Prevalence of left anterior descending (LAD) over right (RCA) and circumflex (Cx) coronary artery stenoses was more marked in W than in M, especially in patients under 50 years of age (SVD of the LAD in 67% and of RCA in 33% of young W). Poor angiographic run-off of LAD was found in 21% of W, and only in 10% of M. In 2 of the 3 W with poor run-off of LAD operated on, a coronary bypass on the distal LAD was no technically feasible. At left ventriculography, a lower frequency of LV segmental wall motion abnormalities was found in W than in M, especially in patients with no history of MI (p less than .001). In summary, W with significant CAD, compared to age matched M, presented in our experience with a higher frequency of SVD and of LAD stenoses, and with a better LV contractile performance at left ventriculography. Furthermore, in W LAD more frequently showed a poor angiographic run-off. Such findings may bear important implications on the indication and results of coronary surgery in W with CAD.

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Myocardial hypertrophy in the rat. Correlation between two experimental models.

Two different conditions responsible for cardiac hypertrophy in the rat were investigated: the first one is isoproterenol-induced myocardial infarct, the second is exposure to hypoxia (0.42 atmospheres/24 h) in hypobaric chamber. To demonstrate that in both experimental models stimulation of protein synthesis is an absolute requirement to induce cardiac hypertrophy, a variety of techniques were employed including: evaluation of dry heart weight value, concentration of radiothallium (201T1) in the heart and effects of inhibitors of protein synthesis (Puromycin). Experimental results have showed: (A) a significant increase (p<0.001 as compared to control group) of dry heart weight values both in isoproterenol-treated and hypoxic rats; (B) a significant increase over control group (p<0.001) in myocardial 201T1 concentration in isoproterenol-treated rats; (C) total inhibition of cardiac hypertrophy in Puromycin treated group subjected to hypoxia. Finally, on the basis of different mortality observed in infarcted (85.0%) or hypoxic (5.0%) rats treated with Puromycin (40 mg/Kg body weight i.p.) a different role of cardiac hypertrophy in 2 experimental conditions is postulated: in the case of infarct-like lesions the cardiac hypertrophy has compensatory significance; under hypoxic stimulus is only due to increased cardiac work.

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