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Biomedical subjects

R J Gelpi

Publications and source records attributed to R J Gelpi.

36 records · Page 2Linked to original sources
PubMed1989

Subendomyocardial exhaustion of blood flow reserve and increased fibrosis in conscious dogs with heart failure.

The effects of near-maximal coronary vasodilation were examined in conscious dogs with left ventricular (LV) failure after pressure overload hypertrophy induced by either aortic banding alone or aortic banding plus a peripheral arteriovenous shunt. The findings were compared with results in littermates with compensated LV hypertrophy and with a third group of normal dogs. At rest, there was a marked difference in the intramyocardial distribution of coronary flow, measured with radiolabeled microspheres. The endocardial/epicardial (endo/epi) flow ratio in the LV failure dogs was 0.96 +/- 0.08 as compared with control dogs (1.28 +/- 0.06, p less than 0.05) or dogs with compensated LV hypertrophy (1.23 +/- 0.08, p less than 0.05). During near-maximal coronary vasodilation with adenosine, all groups showed similar increases in subepimyocardial (epi) flow. While significant increases in subendomyocardial (endo) flow during adenosine infusion were seen in the control group (0.88 +/- 0.10 to 3.53 +/- 0.24 ml/min/g) and in dogs with compensated LV hypertrophy (1.12 +/- 0.14 to 3.60 +/- 0.16 ml/min/g), there was no change in endo flow in the LV failure dogs (1.55 +/- 0.20 to 1.71 +/- 0.47 ml/min/g) and a further significant reduction in the endo/epi flow ratio was observed (0.30 +/- 0.06, p less than 0.01). These hemodynamic changes were associated with chronic multifocal interstitial or discrete areas of fibrosis observed preferentially in endo layers. Thus, endo flow reserve is nearly exhausted in dogs with decompensated pressure overload LV hypertrophy, which may induced periodic episodes of endo ischemia resulting in myocyte necrosis and fibrosis, which in turn results in exacerbation of LV failure.

Adenosine↗
PubMed1988

Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs.

To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P less than 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (Vcf) and rate of change of LV short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, Vcf, LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or beta-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

Animals↗
PubMed1988

Systolic and diastolic dysfunction during atrial pacing in conscious dogs with left ventricular hypertrophy.

To determine the extent to which the hypertrophied left ventricle responds to the chronotropic stress induced by graded atrial pacing rates, we studied conscious, chronically instrumented dogs with severe compensated pressure overload left ventricular (LV) hypertrophy induced by aortic banding in puppies 8-10 weeks of age. At 1-2 years, dogs with severe LV hypertrophy (LV free wall/body wt ratio 6.8 +/- 0.6 g/kg) and sham-operated littermates (LV free wall/body wt ratio 4.0 +/- 0.3 g/kg) were instrumented with ultrasonic dimension crystals to measure LV short axis internal diameter and wall thickness, miniature LV pressure transducers, and aortic and LV catheters. During atrial pacing (240 beats/min) in eight control dogs, LV pressure did not change from 119 +/- 2 mm Hg, and mean velocity of circumferential fiber shortening (VCF) did not change from 1.25 +/- 0.09/sec. In seven dogs with LV hypertrophy, atrial pacing (240 beats/min) decreased systolic LV function; that is, LV systolic pressure decreased (p less than 0.01) by 65 +/- 12 from 254 +/- 14 mm Hg, and VCF decreased (p less than 0.01) by 0.19 +/- 0.03 from 0.97 +/- 0.15/sec. Diastolic dysfunction was also observed in the dogs with LV hypertrophy. In the control dogs during atrial pacing (240 beats/min), LV end-diastolic pressure decreased (p less than 0.01) by 8 +/- 1 from 9 +/- 1 mm Hg, end-diastolic stress decreased (p less than 0.01) by 18 +/- 2 from 22 +/- 2 g/cm2, and the radial myocardial stiffness constant did not change from 5.6 +/- 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Comparative cardiovascular effects of nifedipine in anesthetized dogs].

"In vitro" experiments in our laboratory, using coronary conductance arteries, showed that nifedipine produced selective relaxant action. The aim of the present experiments was to demonstrate if this selective vasodilating effect was also detected on coronary resistance vessels of the whole animal. The experiments were performed in anesthetized dogs. In one of the groups a dose-response curve to nifedipine was obtained. In the other group a single dose was infused to each dog. The doses used were: 0.5, 1, 5 and 10 micrograms x kg-1 x min-1. The following parameters were measured: systolic, diastolic (DAP) and mean arterial pressure (MAP); systolic, diastolic (DCF), and mean coronary blood flow; developed tension (DT), heart rate (HR) and cardiac output (CO). Diastolic coronary resistance (DCR) was calculated as the ratio of DAP and DCF. Systemic resistance (SR) was calculated as the ratio of MAP and CO. DAP, MAP, DT and HR remained unchanged with the lowest doses used (0.5 and 1 micrograms x kg-1 x min-1). DCF increased 28 +/- 7% (P less than 0.05) with 0.5 microgram x kg-1 x min-1 and 49 +/- 11% (P less than 0.05) with 1 microgram x kg-1 x min-1. CO increased 13 +/- 3% (P less than 0.05) and 20 +/- 6% (P less than 0.05) respectively. DCR decreased 31 +/- 4% (P less than 0.05) with 0.5 microgram x kg-1 x min-1 and 36 +/- 6% (P less than 0.05) with 1 microgram x kg-1 x min-1. SR decreased 19.5 +/- 5% (P less than 0.05) and 19 +/- 7% (P less than 0.05) respectively. With 5 micrograms x kg-1 x min-1 DAP, MAP and DT decreased 31 +/- 2% (P less than 0.05), 26 +/- 4% (P less than 0.05), and 15 +/- 4% (P less than 0.05) respectively. HR remained unchanged. DCF and CO increased 39 +/- 13% (P less than 0.05) and 35 +/- 11% (P less than 0.05) respectively. DCR and SR decreased 49 +/- 5% (P less than 0.05) and 43 +/- 5% (P less than 0.05) respectively. DAP, MAP and DT decreased 34 +/- 3% (P less than 0.05), 29 +/- 1% and 31 +/- 5% (P less than 0.05) respectively, with 10 micrograms x kg-1 x min-1. HR decreased 9 +/- 3% (P less than 0.05). DCF and CO remained unchanged. DCR and SR decreased 47 +/- 9% (P less than 0.05) and 36 +/- 6% (P less than 0.05) respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia↗
PubMed1985

[Substituted sydnonimines: hemodynamic effects and distribution of coronary blood flow in normal and ischemic myocardium].

Some aspects of hemodynamic effects and distribution of coronary flow of molsidomine were evaluated in anesthetized dogs with open chest. Three experimental groups were performed: In groups I and II 100 micrograms/kg and 200 micrograms/kg of molsidomine were administered respectively. Cardiac output (CO), end diastolic pressure (EDP), mean arterial pressure (MAP), heart rate (HR), systolic left ventricular pressure (SLVP), their maximal rates of development and fall (+P and -P, respectively), developed tension (DT), their maximal contraction (+T) and relaxation (-T) rates, were measured. Peripheral resistance (PR) and the ratios +P/-P and +T/-T were calculated. In group III 100 micrograms/kg of molsidomine were administered after the ligature of the anterior descendent artery (AD) was performed. In this group the distribution of coronary flow was measured through radioactive microspheres injection in the circumflex area (CX) (normal area) and in the AD area (ischemic area). After injecting the microspheres and following its effects for one hour, the maximum effect was determined in 30 minutes. Heart rate did not show any statistically significant variation at any of the doses used. MAP fell from 92 +/- 3 mmHg to 77 +/- 5 mmHg (P less than 0.05) in group I and from 87 +/- 3 mmHg to 69 +/- 4 mmHg in group II. Cardiac output fell from 1.63 +/- 0.13 1/min to 1.22 +/- 0.12 1/min (P less than 0.05) in group I and from 1.60 +/- 0.19 1/min to 1.13 +/- 0.18 1/min (P less than 0.05) in group II. PR did not show any significant change in any of the groups. +P decreased 13 +/- 6% (P less than 0.05) in group I and 13 +/- 5% (P less than 0.05) in group II. The decrease of -P was of 17 +/- 5% (P less than 0.05) in both groups. EDP decreased from 6.0 +/- 1.0 mmHg to 3.9 +/- 0.9 mmHg (P less than 0.05) and from 5.5 +/- 0.5 mmHg to 2.9 +/- 0.8 mmHg (P less than 0.05) in groups I and II, respectively. DT, +T, -T, +T/-T and +P/-P did not show any significant change. EDP fell from 8 +/- 1 mmHg to 4.1 +/- 1.3 mmHg (P less than 0.05); MAP fell from 82 +/- 4 mmHg to 62 +/- 6 mmHg (P less than 0.05) and CO fell from 2.05 +/- 0.27 1/min to 1.30 +/- 0.14 1/min in group III. HR and PR did not show any significant change in group III.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

[Hemodynamic effects of changes in the heart rate].

The effects of the variations in heart rate (HR) within the range of 80 and 180 beats/min were studied in open-chest dogs with complete AV block. Left ventricular systolic pressure (LVSP) and the maximal velocities of development (+P) and fall (-P), left ventricular end diastolic pressure (LVEDP), cardiac output (CO) and duration of ejection (DE) were recorded and analyzed. Contractility was assessed by the force developed by an isometric segment of the left ventricular wall (DT) and the maximal velocities of rise (+T) and fall (-T). Stroke volume (SV), stroke work (SW), stroke power (SP), +P/-P and +T/-T ratios, the time constant of LV pressure fall during isovolumic relaxation (T tau), and mean rate of ejection of left ventricle (MRE) were calculated from the precedent data. LVSP, LVEDP and -P did not show any statistically significant difference, while +P fell by 10 +/- 5% and 16 +/- 4% at 160 and 180 beats/min, respectively. +P/-P ratios were 1.25 +/- 0.07 at 80 beats/min; 1.08 +/- 0.06 at 140 beats/min (P less than 0.01); 1.03 +/- 0.05 at 160 beats/min (P less than 0.01) and 1.02 +/- 0.06 at 180 beats/min (P less than 0.01). CO remained unchanged and due to this SV fell significantly when HR increased. DT, +T, -T, +T/-T and T (tau) were unchanged. DE fell significantly at 120, 140, 160 and 180 beats/min with respect to the initial HR. SW fell significantly at every HR studied. MRE was 147 +/- 13 ml/sec at 80 beats/min and 100 +/- 8 and 93 +/- 7 ml/sec at 160 and 180 beats/min, respectively (P less than 0.01 with respect to control). SP was 161.7 +/- 19.3 g X m X sec-1 at 80 beats/min, and 122.3 +/- 13.2 and 103.8 +/- 9.2 g X m X sec-1 at 160 and 180 beats/min, respectively (P less than 0.01 with respect to control). We may come to the following conclusions: 1) When HR changed in our experimental conditions, CO remained unchanged and due to this the SV fell significantly, showing the difficulty of the heart pump to regulate the CO by itself. 2) The process of relaxation is not affected within the used HR range. 3) In our experiments the inotropic effect due to increments of heart rate ("Bowditch staircase phenomenon") was not detected. However, it might become evident in preparations with more depressed contractility.

Animals↗
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↗
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↗
PubMedDate not supplied

[Analysis of the ethical principles of beneficence and no harm in medical oaths in relation with the Hippocratic one].

The principles of beneficence and no-maleficence, already set forth in the Hippocratic Oath, have been the foundation of medical ethics for the last twenty-five centuries. The principle of beneficence is currently maintained in most wordings of the pledges of medical schools of the United States, Canada and Argentina; it is not the same with the principle of non-maleficence. The aim of this paper is to determine whether these principles are described in medical oaths at different times. These principles did not remain in an oaths. Of twenty-nine analyzed texts, nine describe both principles simultaneously, eleven only mention beneficence; three only express non-maleficence, and six indicate neither of them. Most wordings that describe these principles are modifications of the Hippocratic Oath. Two contemporary wordings describe the achievement of the greatest benefit with minimum harm. Two current wording also subordinate the principle of beneficence to the principle of respect for the patient's autonomy, and eight wordings indicate not only patients' benefit in particular but that of society in general. It is not possible to ignore that it is no enough to fulfill only these two principles. Physicians should encourage the development of patients' responsibility in managing their own health and respect their autonomy.

Ethics, Medical↗