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Biomedical subjects

J Spadaro

Publications and source records attributed to J Spadaro.

At least 19 recordsLinked to original sources
PubMed2000

Early rather than delayed administration of lisinopril protects the heart after myocardial infarction in rats.

BACKGROUND: ACE inhibitors have shown beneficial results in several studies after myocardial infarction (MI). However, these studies have shown conflicting results about the ideal starting time of the ACE inhibitors administration after MI and the importance of infarct size. OBJECTIVES: This study was designed to assess the long-term effects of lisinopril on mortality, cardiac function, and ventricular fibrosis after MI, in rats. METHODS: Lisinopril (20 mg/kg/day) was given on day 1 or 21 days after coronary occlusion in small or large infarctions. RESULTS: The mortality rate was reduced by 39 % in early treatment and 30 % in delayed treatment in comparison to the untreated rats. Early treatment reduced cardiac dysfunction in small MIs; however, delayed treatment did not. No statistical difference was observed among the groups for large MIs. No statistical difference was observed among the groups with large or small MIs on myocardial hydroxyproline concentration. CONCLUSIONS: Both early and delayed treatments with lisinopril increased survival. Treatment exerts no marked effects on fibrosis; early treatment has exerted beneficial influences on cardiac function whereas delayed treatment had no consistent effects. The protective effect of lisinopril is detectable only in small (< 40 % of LV) MIs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Combination therapy with angiotensin converting enzyme inhibition and AT1 receptor inhibitor on ventricular remodeling after myocardial infarction in rats.

BACKGROUND: There are limited data regarding the effects of angiotensin II receptor blockade after myocardial infarction (MI). In addition, whether combined angiotensin converting enzyme (ACE) inhibitor and angiotensin II type I (AT(1)) receptor antagonist may be superior to either drug alone on ventricular remodeling remains unclear. The goal of this study was to determine if the cardiac effects of the combined administration of an ACE inhibitor and AT(1) receptor antagonist are greater than those produced by either of these agents administered individually after MI. METHODS AND RESULTS: After MI, rats were divided into 4 groups: 1) untreated animals, 2) lisinopril treatment (20 mg/kg/day), 3) losartan treatment (20 mg/kg/day), and 4) lisinopril plus losartan treatment. After 3 months, the cardiac parameters studied were: mortality, fibrosis (hydroxyproline), hypertrophy (ventricular weight/body weight ratio [VW/BW]), left ventricular enlargement (volume at end-diastolic pressure equaled zero/body weight ratio [V0/BW]), and ventricular function (isovolumetric developed pressure, dp/dt, -dp/dt). A lowest mortality rate in the animals treated with the combination of both ACE inhibitor and AT(1) receptor antagonist was observed. Although lisinopril and losartan significantly decreased VW/BW ratio, when administered concomitantly, VW/BW ratio was lower than when either agent was administered individually. There were no differences in right ventricle hydroxyproline concentration. Only combination therapy decreased V0/BW ratio. The treatment with lisinopril plus losartan resulted in increases in the development of pressure versus untreated group; without alteration in dp/dt and -dp/dt. CONCLUSIONS: The combination of the AT(1) receptor blockade and ACE inhibitor is more effective than individual treatment on ventricular remodeling and survival after MI in rats.

Angiotensin Receptor Antagonists↗
PubMed2000

Effects of losartan on ventricular remodeling in experimental infarction in rats.

OBJECTIVE: To evaluate the effects of losartan on ventricular remodeling and on survival after myocardial infarction in rats. METHODS: After surgical occlusion of left coronary artery, 84 surviving male Wistar rats were divided into two groups: LO treated with losartan (20mg/kg/day, n=33 ) and NT (n=51 ), without medication. After 3 months, we analyzed mortality; ventricular to body mass ratio (VM /BM ); myocardial hydroxyproline concentration (HOP); isovolumetric pressure, +dp/dt , -dp/dt , and diastolic volume/left ventricle mass ratio (VO/LV ). RESULTS: Mortality was: LO = 22 % , and NT = 47 % (p<0.05). Ventricular mass,(VM/BM , mg/g ) was 4.14 +/- 0.76 and 3.54+/-0.48, in the NT and LO groups, respectively (p<0.05). HOP (median) was 4.92 upsilong/mg in the LO and 5.54 upsilong/g in the NT group (p>0.05). The V0/LV values (median) were 0.24 mL/g in group LO and 0.31 mL/g in group NT (p<0.05) compared to NT group. There were no differences between the groups for +dp/dt and -dp/dt parameters. CONCLUSION: 1. The use of losartan myocardial infarction causes an attenuation of ventricular remodeling, bringing about an increased survival, an attenuation of ventricular hypertrophy and dilation, and an improvement of the isovolumetric pressure; 2. the treatment does not modify the myocardial collagen concentration.

Animals↗
PubMed1999

Effects of lisinopril on experimental ischemia in rats. Influence of infarct size.

OBJECTIVE - Angiotensin-converting enzyme inhibitors (ACEIs) have gained importance in preventing or attenuating the process of ventricular remodeling after myocardial infarction. The significance of infarct size in regard to the response to ACEIs, however, is controversial. This study aimed to analyze the effects of lisinopril on mortality rate, cardiac function, degree of cardiac hypertrophy and fibrosis in rats with different infarct sizes. METHODS - Lisinopril (20 mg/kg/day) dissolved in drinking water was administered to rats immediately after coronary artery occlusion. After being sacrificed, the infarcted animals were divided into two groups: one group of animals with small infarcts (< 40% of the left ventricle) and another group of animals with large infarcts (> 40% of the left ventricle). RESULTS - The mortality rate was 31.7% in treated rats and 47% in the untreated rats. There was no statistical difference between the groups with small and large infarcts in regard to myocardial concentration of hydroxyproline. In small infarcts, the treatment attenuated the heart dysfunction characterized by lower levels of blood pressure and lower values of the first derivative of pressure and of the negative derivative of pressure. The degree of hypertrophy was also attenuated in small infarcts. In regard to large infarcts, no differences between the groups were observed. CONCLUSION - Treatment with the ACEIs had no effect on mortality rate and on the amount of fibrosis. The protective effect of lisinopril on heart function and on the degree of hypertrophy could only be detected in small infarcts

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

[Effect of lisinopril on cardiac parameters and mortality after myocardial infarction in rats].

PURPOSE: To analyse the effect of early (< 24h) administration of lisinopril on ventricular remodeling and mortality after myocardial infarction (MI) in rats. METHODS: Wistar rats weighing 200-250 g were submitted to ligation of the left coronary artery (LCA) and divided into three groups: SHAM (S, n = 9); infarcted and lisinopril (20mg/kg/day) treated rats (L, n = 38); infarcted and non-treated animals (NT, n = 24). Three months later, the cardiac function was studied in isolated heart preparation according to the Langendorff technique. Starling curves were constructed using fluid injection in the left ventricular balloon, which permitted to alter the diastolic pressure range from 0 to 30mmHg by means of pressure increments of 5mmHg. Body weight (BW), right ventricular weight (RVW), and RVW/BW were also determined. RESULTS: Three months after the surgery, the comparative mortality rate among groups was: S = 0; L = 34.4% and NT = 54.4% (p > 0.05, for L vs NT). In infarctions < 40% of the left ventricle (LV), the RVW/BW relation was S = L < NT (p < 0.05); the left ventricular systolic pressure was S > L > NT (p < 0.05). In infarctions > 40% of LV, the RVW/BW relation was S < L = NT (p < 0.05). For the Starling curves, the results were S > L > NT (p < 0.05). CONCLUSION: In our model lisinopril did not interfere with post-infarction mortality of rats, although decreasing the mortality risk in 49%, in the treated group. The drug also altered the remodeling process, preventing hypertrophy and systolic disfunction after MI, mainly in infarctions < 40% of LV.

Analysis of Variance↗
PubMed1989

Morphometric evaluation of the time course of right ventricular hypertrophy after left coronary artery ligation in rats.

1. In order to describe the time course of compensatory right ventricular hypertrophy after infarction, rats submitted to left coronary obstruction and sham-operated controls were compared in terms of heart weight, chamber weight and right ventricular fiber diameter 1, 8 and 21 days after surgery. 2. One day after infarction, only the left ventricle weight increased (0.583 +/- 0.045 g vs 0.698 +/- 0.062 g, P less than 0.05), while right ventricular weight and fiber diameter suffered no change. 3. Eight days after infarction, heart weight (0.781 +/- 0.127 g vs 0.856 +/- 0.100 g, P greater than 0.05) as well as right ventricular fiber diameter (16.5 +/- 1.0 microns vs 17.5 +/- 2.1 microns, P greater than 0.05) and left ventricular weight did not differ between sham-operated animals and animals with left coronary obstruction. However, a significant increase in right ventricular weight was observed in infarcted animals (0.168 +/- 0.026 g vs 0.242 +/- 0.017 g, P less than 0.05). 4. Twenty-one days after infarction, right ventricular weight (0.198 +/- 0.034 g vs 0.316 +/- 0.118 g, P less than 0.05), heart weight (0.864 +/- 0.095 g vs 0.985 +/- 0.105 g, P less than 0.05) and right ventricular fiber diameter (15.0 +/- 1.8 microns vs 21.3 +/- 2.3 microns, P less than 0.05) were significantly increased in infarcted animals, whereas left ventricular weight (0.665 +/- 0.065 g vs 0.669 +/- 0.039 g, P greater than 0.05) was unchanged. 5. We conclude that hypertrophy occurs in the right ventricle of randomized infarcted rats 21 days after infarction, and that this phenomenon precedes the increase in fiber diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Does the oxygen tension of coronary sinus blood reflect myocardial oxygen tension?

Coronary sinus blood oxygen tension (CSpO2) and myocardial oxygen tension (MpO2) were measured simultaneously during cardiac ischemia and reperfusion. Oxygen tension was measured using a polarographic method. Myocardial ischemia caused a reduction (5 +/- 1.5%; P less than 0.05) in CSpO2 and a decrease (56.5 +/- 10.1%; P less than 0.001) in MpO2. Reperfusion induced a rapid but transient increase (35.9 +/- 4.3%; P less than 0.001) in CSpO2 above the basal state while MpO2 returned gradually to the basal state. These results indicate that CSpO2 is of little value for the detection of changes in myocardial oxygen metabolism during the initial phase (seconds) of cardiac reperfusion.

Animals↗
PubMed1988

Is coronary sinus blood oxygen tension behavior determined by myocardial oxygen tension variation during cardiac reperfusion?

The relationship between coronary sinus blood oxygen tension (CSPO2) and myocardial oxygen tension (MPO2) variations during cardiac ischemia and reperfusion was studied in anesthetized open-chest dogs. Oxygen tension was measured by a polarographic method. Ischemia resulted in a slightly decreased CSPO2 and a more pronounced reduction of MPO2. After reperfusion the CSPO2 rose rapidly and transiently before it returned gradually to the control level. By contrast, during the recovery period, the MPO2 increased slowly, with recovery occurring long after the peak of CSPO2. These data suggest that during the reperfusion phase, the CSPO2 variation is probably due to opening of the myocardial arteriovenous shunts instead of an increase of flow through the myocardial capillary bed.

Animals↗
PubMed1988

Changes in myocardial and coronary sinus blood oxygen tension induced by asphyxia and reoxygenation.

1. This study analyzes variations of oxygen tension induced by asphyxia in the myocardium (MpO2) and coronary sinus blood (CSpO2) of the anesthetized open-chest dog. Oxygen tension was measured polarographically and arterial blood pressure and coronary blood flow were recorded simultaneously. 2. Asphyxia increased arterial pressure and coronary blood flow but decreased both MpO2 and CSpO2. 3. During the reoxygenation phase, arterial pressure and coronary flow decreased gradually. Reoxygenation induced a rapid but transient increase in CSpO2 above control levels. In contrast, MpO2 returned gradually to the basal state. 4. The mechanism(s) involved in the differential effects of asphyxia followed by reoxygenation on MpO2 and CSpO2 remain to be elucidated.

Animals↗
PubMed1984

Length dependence of activation studied in the isovolumic blood-perfused dog heart.

In studies utilizing the isolated isovolumic blood-perfused canine heart, left ventricular pressure was measured following a sudden expansion of ventricular volume. An increase in performance occurred in two phases: first, there was an instantaneous rise of developed pressure simultaneous with ventricular distension; in the second phase, developed pressure continued to increase for several minutes until a final steady state was reached. The immediate increase in developed pressure occurred with a prolongation of the time-to-peak pressure, and there was no further change of time-to-peak pressure during the time-dependent increase of developed pressure. In another series of experiments, systolic pressure was elevated without changing resting volume, and mechanical performance changed in a different manner: after an increase in systolic load, there was a modest and transient decrease of developed pressure; thereafter, ventricular pressure recovered only to original values. The influence of different degrees of ventricular expansion, calcium, and verapamil were studied. Under higher ventricular dilations the immediate as well as the slow increase of contraction were heightened and the time to reach half of the slow increase was shortened. When ventricular dilation was induced during an infusion of calcium chloride, higher values for the immediate pressure increase were observed, whereas the time-dependent increase and the time to reach half of the slow increase did not change in comparison with control studies. Verapamil decreased the immediate and the time-dependent enhancement of contraction. The time-dependent increase in developed pressure occurs more slowly with verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of dopamine on the pulmonary circulation of the dog.

The effects of dopamine infusion (10 and 20 micrograms kg-1 min-1) on pulmonary arterial pressure (PAP) and pulmonary arterial resistance (PAR) were studied. Experiments were carried out on 60 anesthetized dogs using two different models: model A, with mechanical perfusion of pulmonary circulation and constant left ventricular output, and model B, with physiologic pulmonary perfusion and non-fixed ventricular output. When pulmonary blood flow was constant, dopamine did not change PAP or PAR at either dose. When cardiac output (CO) was allowed to increase, PAP increased with dopamine at both doses, whereas PAR did not change with 20 micrograms kg-1 min-1 dopamine and was reduced by the 10 micrograms kg-1 min-1 dose. We conclude that the increase in PAP could not be explained solely by the rise in CO, but was probably related to an inhibitory effect of dopamine on pulmonary vascular accommodation and to increases in CO, especially when the drug was utilized at higher doses.

Animals↗
PubMed1982

Independent protection provided by red blood cells during cardioplegia.

Isolated, blood-perfused dog hearts were subjected to 2 hours of arrest at 27 degrees C and perfused at 15-minute intervals with either a potassium crystalloid cardioplegic solution (KCC) or an identical solution to which washed red blood cells were added (KrbcC). After reperfusion, hearts protected with KCC were easily defibrillated and systolic pressure returned to 62% of prearrest values 90 minutes after reperfusion. In hearts protected with KrbcC, systolic pressures recovered to 103% of prearrest values 15 minutes after reperfusion. Metabolic variables recovered more quickly in hearts perfused with KrbcC. Adenosine triphosphate did not decline with arrest in either group. Creatine phosphate values decreased with KCC and increased with KrbcC. The pH of the myocardial effluent fell to 6.48 during arrest with KCC and to 7.19 with KrbcC (p less than 0.001). Carbon dioxide tension increased with KCC, but decreased with KrbcC (p less than 0.001). Thus, marked improvement in recovery after 2 hours of arrest is seen with KrbcC. Protection beyond that provided by KCC appears solely due to the washed red cells, and may be the result of the buffering action of the red cell improved oxygen delivery.

Adenosine Triphosphate↗