PubMed Health⌕ Search

Biomedical subjects

S M Mosca

Publications and source records attributed to S M Mosca.

28 records · Page 2Linked to original sources
PubMed1983

Effect of calcium antagonism on contractile behavior of canine hearts.

The cardiovascular effects of prenylamine (P), verapamil (V), and nifedipine (N) were studied in open-chest, anesthetized dogs and in isolated, isovolumic dog hearts perfused at constant coronary blood flow (CBF). These drugs significantly decreased left ventricular pressure (LVP) and its maximal rates of rise (+P) and fall (-P). The tension developed by an isometric segment of the left ventricle and its maximal rates of rise (+T) and fall (-T) also decreased, whereas heart rate (HR) did not show statistically significant differences. Maximal rates of fall (-P and -T) were proportionally more depressed than maximal rates of rise (+P and +T), producing significant increments in the ratios between both maximal velocities (+P/-P and +T/-T). The time constant of LVP isovolumic decay tau was significantly prolonged, either in the whole animal or in isolated perfused hearts. The afterload reduction produced by the compounds can account in part for the increase in +P/-P but not for the increase in +T/-T or for the prolongation of tau. These relaxation indices remained unchanged after comparable myocardial depressions elicited by d,l-propranolol or pentobarbital sodium. It is concluded that calcium antagonist compounds are characterized by an "antirelaxant" effect, not explained by changes in HR, CBF, or loading conditions, and independent from their negative inotropic action.

Animals↗
PubMed1981

Myocardial flow distribution. II : Empty beating heart, ventricular fibrillation and cardiac arrest.

Myocardial oxygen consumption (MVO2) and coronary blood flow (CBF) distribution were studied in 21 isolated, metabolically supported dog hearts. Measurements of MVO2 and CBF distribution were carried out in three different experimental conditions : empty beating heart (EBH), ventricular fibrillation (VF) and high potassium-induced cardiac arrest (CA). MVO2 was approximately the same in EBH and VF (4.09 +/- 0.77 and 4.28 +/- 0.68 ml O2 min-1 100 g-1 respectively), and significantly lower in the group with CA (2.40 +/- 0.18 ml O2 min-1 100 g-1, P less than 0.05). Total CBF showed no significant differences among the three groups (84 +/- 7 ml/min in EBH; 78 +/- 7 ml/min in VF and 83 +/- 7 ml/min in CA). Subendocardial CBF per unit of tissue mass was significantly lower in hearts with VF (0.43 +/- 0.01 ml/min-1 g-1, P less than 0.05) when tested against the other two groups of experiments (0.69 +/- 0.03 ml min-1 g-1 in EBH and 0.65 +/- +/- 0.04 ml min-1 g-1 in CA). This was also reflected in the endo/epi ratio, that was significantly lower in VF (1.41 +/- 0.07, P less than 0.05) with respect to the other two groups (2 +/- 0.09 in EBH and 2.21 +/- 0.07 in CA). From data presented here we can conclude that cardioplegia, even in absence of hypothermia, is a method that will assure myocardial protection providing : (1) a lower subendocardial MVO2; (2) a higher subendocardial CBF, which helps for a prompt recovery during reperfusion.

Animals↗
PubMed1977

[Effects of acute hypercapnia upon the myocardium: contractility, coronary resistance, oxygen consumption and potassium balance (author's transl)].

In the isolated perfused dog heart, at constant coronary blood flow and heart rate, we studied the effect of altering CO2 in the gas mixture from 5 to 15% on contractility, coronary resistance, myocardial O2 consumption and K balance. Contractility, assessed by the developed force, and its derivative through a strain-gauge arch sewed to the left ventricle decreased to 54 +/- 7% (p less than 0.01) and 59 +/- 6% (p less than 0.01), respectively from control values. Coronary resistance decreased to 79 +/- 3% of control ( less than 0.01). The negative inotropic effect of hypercapnia was accompanied by a decrease in myocardial O2 consumption to 68 +/- 11% (p less than 0.01) of control value and a net uptake of K by the heart. The possibility of an exchange of H+ by K+ is suggested as a possible mechanism involved in the negative inotropic effect of hypercapnia.

Animals↗
PubMedDate not supplied

Biphasic changes in relaxation following reperfusion after myocardial ischemia.

The present study provides evidences of left ventricular diastolic alterations following reperfusion in a model of global ischemia. Isolated perfused rabbit and rat hearts, were subjected to ischemia for 15 and 20 min respectively, followed by 30 min of reperfusion. In rabbit heart at the end of the reperfusion period, isovolumic left ventricular developed pressure (LVDP) and +dP/dtmax stabilized at 55 +/- 3% and 60 +/- 2% of preischemic values respectively and, in rat heart LVDP = 61 +/- 8% and +dP/dtmax = 57 +/- 9% of preischemic values. Stunned heart was then obtained from both species. Left ventricular end diastolic pressure (LVEDP) values stabilized at the end of reperfusion period at values higher than preischemic conditions in both species (38.9 +/- 4.4 mmHg and 30.3 +/- 3.1 mmHg in rabbit and rat respectively). The time constant of relaxation (T) increased early in reperfusion in both species, but then decreased and stabilized at the end of reperfusion period at values lower than preischemic values. The ratio between both maximal velocities (+P/-P), also showed a transitory impairment in relaxation, followed by normalization and stabilization at values lower than preischemic values. This biphasic pattern in relaxation was detected in both species. The changes in relaxation were dissociated from the diastolic compliance and could be the result of a transitory calcium overload and/or sarcoplasmic reticulum dysfunction. The faster myocardial relaxation at the end of reperfusion period is consistent with the decreased myofilament sensitivity, which characterizes the stunned myocardium.

Animals↗
PubMedDate not supplied

The effects of hypocapnic alkalosis on the myocardial contractility of isovolumic perfused rabbit hearts.

During acute respiratory alkalosis myocardial contractility first increases but then decreases towards control levels. The mechanism of this response was investigated in isovolumic perfused rabbit hearts. Developed pressure (DP) and its first derivative (dP/dt) were measured before, during and after hypocapnia induced by equilibrating the perfusate with 2% CO2 rather than the 5% used in control. pH of the perfusate (pHo) changed from 7.36 +/- .02 to 7.71 +/- .01. After about 20 s, an increase in DP of about 20% was detected. This increase in contractility is followed by a partial recovery towards control levels. After the partial recovery a new mechanical steady state is reached in about 2 min. Neither 5-[N-ethyl-N-isopropyl]amiloride (EIPA) 10(-6) M, a blocker of the Na+/H+ exchanger, nor 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid (SITS) 10(-4) M, or 5-[aminosulfonyl]-4-chloro-2-[(2-furanylmethyl)-amino] benzoic acid (furosemide) 10(-4) M, blockers of Cl-/HCO3- exchanger, abolished the recovery in contractility towards control levels. The recovery was not abolished by replacing 50% of extracellular Cl- concentration by either sulfate or gluconate. The lack of blockade of this mechanical recovery in spite of the intervention performed suggests a mechanism other than the exchangers as the cause of the biphasic changes.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗