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Biomedical subjects

A C Cicogna

Publications and source records attributed to A C Cicogna.

At least 19 recordsLinked to original sources

Comparative mechanical study of isolated papillary muscle from Wistar-Kyoto and Wistar rats.

Isolated papillary muscles have often been used in myocardial mechanical function studies. The objective of the present study was to compare the mechanical function of papillary muscle isolated from left ventricle between Wistar (W) and Wistar-Kyoto (WKY) rats of different ages (1, 3, 6 and 12 months), in order to examine whether there is a difference in intrinsic mechanical properties of muscle between the two rat strains. Muscles were perfused with Krebs-Henseleit solution at 28 degrees C and studied isometrically and isotonically at a stimulation rate of 0.2 Hz. The W and WKY showed statistically significant differences during both isometric and isotonic contractions. During isometric contraction, (1) the peak developed tension (DT) and +dT/dt were lower in WKY rats in the 1 mo groups, (2) the resting tension (RT) was greater in WKY at 3, 6 and 12 mo, (3) time to peak tension (TPT) was greater in WKY at 3 and 12 mo, (4) time for tension to fall from peak to 50% of peak tension (RT 1/2) was greater in WKY at 3 mo and (5)-dT/dt was lower in WKY at 1 and 3 mo. During isotonic contraction, (1) the peak shortening (PS) and--dL/dt were lower in WKY at 12 mo, (2) the time to peak shortening (TPS) was greater in WKY at 3 and 12 mo; (3) +dL/dt was lower in WKY at 3, 6, and 12 mo and (4) the relative variation of length (Lmax-PS)/Lmax was greater in WKY at 6 and 12 mo. These data showed a difference in mechanical behaviour of the papillary muscle between Wistar and Wistar-Kyoto rats of different age.

Aging

Protective effects of diltiazem on the mechanical performance of the hypoxic myocardium.

1. To determine whether diltiazem protects the hypoxic myocardium by reducing contractile work, we have compared the effects of diltiazem and quiescence on left ventricular (LV) papillary muscle subjected to hypoxia. Papillary muscles were obtained from male Charles River CD rats weighing 150-250 g. 2. Four groups of muscles were studied: control (N = 6), non-stimulation (N = 10), diltiazem 10(-4) M (N = 6) and diltiazem 10(-4) M plus non-stimulation (N = 10). 3. Isolated rat LV papillary muscles were studied in Krebs-Henseleit solution with a calcium concentration of 2.52 mM at 28 degrees C while contracting isometrically at a stimulation rate of 0.2 Hz. Resting tension and active isometric tension were measured. 4. Both diltiazem and quiescence significantly attenuated contracture tension during hypoxia (0.91 +/- 0.10 vs 2.26 +/- 0.49 g/mm2 for diltiazem vs control, and 0.55 +/- 0.18 vs 2.26 +/- 0.49 g/mm2 for quiescence vs control). Recovery of active tension was improved in the diltiazem groups during reoxygenation (4.16 +/- 0.42 vs 3.75 +/- 0.51, 3.53 +/- 0.15 vs 2.90 +/- 0.13, 5.84 +/- 0.33 vs 6.48 +/- 0.29 and 5.98 +/- 0.90 vs 7.67 +/- 0.68 g/mm2 for diltiazem, diltiazem non-stimulation, non-stimulation and control groups). 5. The results suggest that the protective effect of diltiazem during hypoxia was due to the reduction in energy demand of the myocardium.

Animals

[Effects of aging on mechanical performance of Wistar rat papillary muscles].

PURPOSE: To evaluate the effects of age on mechanical performance of rat myocardium. METHODS: Left ventricular papillary muscles were isolated from male Wistar rats at 1, 3, 6 and 12 months of age. Muscles were studied isometrically and isotonically, stimulated at 0.2 Hz, perfused with Krebs-Henseleit solution having an external calcium concentration of 2.52 mM, and maintained at 28 degrees C. RESULTS: Peak isometric developed tension was significantly higher in 1 month than 3, 6 and 12 months. Peak rate of isometric tension rise decreased substantially between 1, 3 and 12 months. Time to peak isometric developed tension showed a significant increase of both 3 and 12 months of age. Time to half relaxation increased significantly from 3 to 6 and from 3 to 12 months. Maximum rate of tension decline decreased from 3 to 6 and from 3 to 12 months. No difference in resting tension was noted among any group. Isotonically, peak shortening and time to peak shortening increased from 1 to 3 months of age. Time to half re-lengthening increased from 3 to 6 and from 3 to 12 months of age. No difference in peak shortening velocity, peak relaxation velocity and relative change in muscle length was noted among any groups. CONCLUSION: The maturation affects the mechanical performance of cardiac muscle.

Aging

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

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

[Effect of anesthesia and/or decapitation on the mechanical behavior of papillary muscles isolated from the left ventricle of the rat].

The mechanical performance of isometrically contracting papillary muscle was studied in rats sacrificed by decapitation or anesthetized with sodium pentobarbital or chloralose before decapitation. The purpose was to evaluate which maneuver would be the more adequate to ve used, when performance of papillary muscle mechanics must be evaluated later. The data suggest that either anesthetic agents used in this experiment and/or decapitation have the same effects on isolated muscle performance in the three groups. The results may be a consequence of the time elapsed between animal decapitation and the recording of cardiac parameters: this fact would attenuate the many factors that could promote mechanical performance dysfunction or isolated papillary muscles.

Analysis of Variance

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

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

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

Inversion of cardiac inotropism response to carotid arteries occlusion in dogs treated with propranolol.

The effect of beta-adrenergic blockade achieved by propranolol (0.5-1.0 mg/kg) on the inotropic alterations induced by adrenergic hyperactivity resulting from bilateral carotid occlusion (BCO) was analysed in 25 dogs anesthetized with morphine (2 mg/kg) and sodium pentobarbital (20 mg/kg). The heart rate was kept unchanged by means of a pace-maker. The first derivative of ventricular pressure (dp/dt) was considered as contractility index. Because BCO is followed by increase of left ventricle end-diastolic pressure (LVEDP) and of blood pressure (BP), to avoid the influence of these variables on dp/dt, we have reduced preload and afterload by means of hemorrhage (group A) and alpha-adrenergic blocker administration--phentolamine (group B). The carotid occlusion promoted similar variations in hemodynamic parameters in the two groups--there was a significant increase of blood pressure and LVEDP. BCO did not produce alteration in dp/dt values in both groups; when BP and LVEDP in group A were reduced, there was a significant reduction of dp/dt (2 927 +/- 139 to 2 066 +/- 95 mmHg/s; p less than 0.01). However there was no dp/dt alteration in group B (2 559 +/- 239 to 2 512 +/- 285 mmHg/s). These results suggest that during increase of sympathetic activity, anesthetized dogs under beta-adrenergic blockade show contractility depression. This could be related to secondary myocardic hypoxia and coronary vasoconstriction due to coronary alpha-adrenergic hyperactivity, once cardiac inotropism response can be alleviated by alpha-adrenergic blockers.

Animals