Biomedical subjects

R J Gelpi

Publications and source records attributed to R J Gelpi.

At least 19 recordsLinked to original sources

PubMed2006

Doctor-patient sexual relationships in medical oaths.

BACKGROUND: Doctor-patient sexual relationship is considered to be unfair because the first party would be abusing the second party's vulnerability. The prohibition of this relationship is noted in the Hippocratic oath. Currently, a reprise of the use of oaths in medical schools can be observed. AIM: To determine whether the prohibition has been maintained and how its expression has varied in the oaths during different periods. METHODS: 50 oaths were studied: 13 ancient-medieval and 37 modern-contemporary. Of the 50 texts, 19 were versions of the original oaths. The oaths that pointed out the prohibited doctor-patient relationship referred to any sexual aspect or included paragraphs that began as the Hippocratic oath does were noted. RESULTS: Of the 24 (48%) texts that expressed the prohibition, 8 (62%) were ancient-medieval and 16 (43%) were modern-contemporary. Some expressly call it Hippocratic oath, many use general terminology (corruption or vice) and others describe it in association with other commitments (abortion and euthanasia). CONCLUSIONS: The clause on the prohibition of the doctor-patient sexual relationship in Hippocratic oath was included to be for legal, economic and social reasons at the time. That the clause is found mostly in the ancient-medieval oaths can be attributed to the influence of the original. This commitment is generalised and associated with others by contemporary formulas. Currently, sexual relationships are the subject of legal and ethical analysis and their inclusion in the oaths is being debated.

Codes of Ethics↗

PubMed2001

[The activation of A1 adenosine receptors attenuates myocardial stunning in the rabbit].

Hearts exposed to a prolonged period of ischemia (> or = 30 minutes) present smaller infarct size when reperfused in the presence of adenosine. However, when the period of ischemia is shorter, the infarct areas are not very significant, but a postischemic ventricular dysfunction persists. The objective of this study was to determine the effect of adenosine, (administered only during reperfusion) on systolic and diastolic alterations present in postischemic ventricular dysfunction, as well as to determine whether A1 receptors participate in this effect. Isolated isovolumic rabbit hearts were subjected to 15 minutes of global ischemia followed by 30 minutes of reperfusion. Before ischemia and during reperfusion ventricular function was evaluated. In the control group, the left ventricular developed pressure (LVDP) reached 56 +/- 2% of recovery at 30 minutes of reperfusion. The administration of adenosine improved LVDP 75 +/- 3% (P < 0.05 vs. control). However, when adenosine was given in presence of an A1 receptor selective antagonist (DPCPX), LVDP reached 50 +/- 2% (P < 0.05 vs. control). In the control group, left ventricular end diastolic pressure (LVEDP) (diastolic stiffness), increased 293 +/- 4%, at 30 minutes of reperfusion. Only a 15 +/- 8% (P < 0.05 vs. control) increase in LVEDP was observed with adenosine. Reperfusion with adenosine plus DPCPX did not attenuate an increase of 493 +/- 9% (P < 0.05 vs. control) in diastolic stiffness. Adenosine administered from the beginning of reperfusion attenuated both systolic alterations and diastolic stiffness in postischemic dysfunction. This effect was abolished by DPCPX, suggesting an important role for the A1 receptors in adenosine protection.

Adenosine↗

PubMed2001

[Time course of the myocardial infarction in the rabbit].

The histopathologic evolution of myocardial infarct and of areas distant from infarct in rabbit hearts was studied. The left coronary artery of 55 rabbits was ligated, and rabbits were sacrificed at 2, 4, 6, 8, 12, 14, 16, 18, 26, 35 and 56 days post-ligature (n = 5 per group). Two rabbits were used as control and two were sham operated. The hearts were excised, cut in slices and stained with hematoxilin-eosin, Masson's trichrome and picrosirius red. Histological evaluation was semi-quantitative (scale: 0 to +++). At day 2, presence of neutrophils was +++, disappearing completely at day 6. Fibroblast proliferation increased from day 4 to day 14 post-occlusion. Coagulation necrosis in medial myocardium during the first week was +++. Subendocardic myocytolysis was evident from day 2 up to day 56 post-infarction. During the second week, proliferation of lymphocytes and macrophages (+++), granulation tissue formation (+++), and incipient traces of fibrosis that peaked at day 35 were observed. Cicatrization was complete at day 56 (+++). In areas far from infarction (right ventricle and septum), proliferation of fibroblasts was observed at day 2, and perivascular, interstitial and endocardic fibrosis at day 16. In conclusion, myocardial infarction in rabbits, unlike myocardial infarction in human beings, is characterized by early presence of fibroblasts and subendocardic fibrosis, and quick increase and precocious disappearance of neutrophils. An interesting finding was the early proliferation of fibroblasts in normal areas far from infarct.

Animals↗

PubMed2000

[Confidentiality in medical oaths: (When the white crow becomes gray...)].

Confidentiality, together with the ethical principles of beneficence and non-maleficence, is the most important rule in Medical Oaths at the present time. However, the scientific-technical advances in medicine have made this rule one of the most controversial ones because of its exceptions. In consequence, the aim of the present paper is to comparatively analyze the rule of confidentiality in Medical Oaths of different places, times, origins and in different versions of the Hippocratic Oath in order to determine what should be kept a secret and with what degree of commitment (absolute or "prima facie"). Of the thirty six analyzed Oaths, twenty-seven manifest this rule and nine do not. No relation was found between the manifestation of this rule and the place, time, origin and different versions of the Hippocratic Oath. Most pledges suggest not to reveal what has been seen or heard during the medical act, the same as in the Hippocratic Oath. Seven texts point out that confidentiality should be absolute and four give exceptions in connection with beneficence and justice principles and the moral duty of causing no damage to third parties. Two pledges specify protection of privacy. In conclusion, today confidentiality is considered to be a moral duty for the benefit of the patient and out of consideration for his autonomy; however, at the present time in medicine the duty of keeping absolute secrecy is being reconsidered.

Confidentiality↗

PubMed1999

[Exogenous adenosine and postischemic dysfunction in the isolated rabbit heart].

It is recognized that adenosine lessens the systolic alterations of the postischemic ventricular dysfunction ("stunned myocardium"), but little is known about the drug's effects on the diastolic phase of the cardiac cycle. The aim of this work was to determine the effect of adenosine when it was administered: a) before ischemia and during reperfusion, and b) from the early reperfusion period to the end of the experiment on the systolic and diastolic function of the "stunned myocardium". An additional objective was to determine whether adenosine modifies the release of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), in the "stunned myocardium". Rabbit isolated isovolumic hearts were perfused according to Langendorff's technique, and subjected to 15 minutes global ischemia and 30 minutes reperfusion. A small latex balloon was inserted into the left ventricle via the left atrium which allowed to measure the ventricular end-diastolic pressure (diastolic stiffness) and calculate the developed pressure, the maximal rate of pressure generation and maximal rate of pressure decay (+dP/dtmax and -dP/dtmax), the ratio between these two variables (+P/-P), and the time constant of isovolumic relaxation (tau, Tau). The adenosine administered both before the ischemia period, and at the beginning of reperfusion, attenuated the systolic and diastolic stiffness alterations without modifying the isovolumic relaxation. The administration of adenosine did not diminish the CPK and LDH release significantly when it was given before the ischemia period or the beginning of reperfusion.

Adenosine↗

PubMed1998

[Effect of enalaprilat on postischemic systolic and diastolic dysfunction (stunned myocardium) on the isolated rabbit heart].

The aim was to determine: 1) whether Enalaprilat (0.08 mg/kg/min) administration: a) before ischemia or b) at the beginning of reperfusion improved the postischemic systolic and diastolic dysfunction ("stunned myocardium") and attenuated the "hyperfunction" phase at the beginning of reperfusion; and 2) whether creatine kinase (CPK), and lactate dehydrogenase (LDH) activities, and lactate release are involved in the protective effects of Enalaprilat. An isolated isovolumic rabbit heart preparation was used as experimental model and subjected to 15 minutes of ischemia followed by 30 minutes of reperfusion, without (group 1), and with Enalaprilat before the ischemia (group 2) and at the beginning of reperfusion (group 3). Left ventricular developed pressure, and end diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (t, Tau) and the ratio between +dP/dtmax and -dP/dtmax were calculated. For the determinations of lactate release and CPK and LDH activities in the perfusate, samples were taken from the coronary effluent for spectrophotometrical measurements. In comparison to the stunned group (group 1) both Enalaprilat preischemia (group 2) and postischemia (group 3) exerted a significant protective effect on the postischemic recovery of contractile state and diastolic stiffness, and attenuated the "hypercontractile" phase in both groups. However Enalaprilat failed to improve myocardial relaxation. Lactate release was also attenuated, but the enzyme activities were not modified.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

[Analysis of the ethical principles in medical oaths used by medical schools of Argentina in relation to the Hippocratic Oath].

Medical oaths have consulted the source of all Medical Ethics through centuries. Since the 60s a new consensus on ethics was sought to apply to the new medical problems. The consensus was on the basic principles: beneficence, non-maleficence, justice and respect for the patient's autonomy with its two rules of confidentiality and veracity. The Hippocratic Oath specifies the principles of beneficence and non-maleficence and the rule of confidentiality. They are included in the texts used in different Medical Schools of the United States, Canada and the United Kingdom. The purpose of this analysis is to determine which of those ethical principles are included in the Argentinian Medical Oaths. At present, out of the ten Faculties of Medicine that use a formula, six choose the Declaration of Geneva and the rest use their own texts. No schools use the Hippocratic Oath. Neither of the five different Oaths include the four principles. The rule of confidentiality is the one most frequently mentioned followed by the principles of beneficence and justice. The principles of non-maleficence and of respect for the patient's autonomy, in general, and the rule of veracity, in particular, are not indicated. Revision of the Medical Oaths used in Argentina, is basically for the ethical revision suggested, in order to include all the ethical principles strongly agreed upon.

Argentina↗

PubMed1998

Comparison of the effects of ACE inhibition with those of angiotensin II receptor antagonism on systolic and diastolic myocardial stunning in isolated rabbit heart.

The aim was to determine whether enalaprilat (0.08 mg/kg/min) or losartan (0.01 mg/kg/min) administration before ischemia can improve postischemic systolic and diastolic dysfunction ('stunned myocardium') and attenuate the 'hyperfunction' phase at the beginning of reperfusion. An isolated isovolumic rabbit heart preparation was subjected to 15 min of ischemia followed by 30 min of reperfusion without (group 1) or with pretreatment with enalaprilat (group 2) or losartan (group 3). Left ventricular developed pressure and end-diastolic pressure (diastolic stiffness) were measured and the time constant of isovolumic relaxation (T, Tau) and the ratio between +dP/dt and -dP/dt were calculated. In comparison to the stunned group (group 1) both enalaprilat (group 2) and losartan (group 3) exerted a significant protective effect on postischemic recovery of contractile state and diastolic stiffness. Only enalaprilat attenuated the 'hypercontractile' phase. However, both enalaprilat and losartan failed to improve myocardial relaxation. In summary, these data strongly suggest a direct deleterious action of the local renin-angiotensin system on ischemic myocardium and diminution of myocardial stunning with its successful blockade. Although, we can not exclude the possibility that bradykinin has some cardioprotective effect, these data suggest that angiotensin exacerbates myocardial injury.

Angiotensin II↗

PubMed1998

Is stunning prevented by ischemic preconditioning?

In a model of global ischemia in the isolated perfused rat heart, a 20 min ischemic period followed by 30 min of reperfusion induces a decrease in isovolumic developed pressure (LVDP) and +dP/dtmax to 61+/-6% and 61+/-7% of baseline, respectively. Left ventricular end-diastolic pressure (LVEDP) increases to 36+/-4 mmHg at the end of the reperfusion period. No significant necrotic area as assessed by triphenyltetrazolium chloride (TTC) was detected at the end of the reperfusion period. By an immunohistochemical method using antiactin monoclonal antibodies 10.8+/-1.9% of unstained cells were detected in the stunned hearts and 10.3+/-1.2% in control hearts. Preceding the ischemic episode with a cycle of 5 min of ischemia followed by 10 min of reperfusion (ischemic preconditioning) protected contractile function. LVDP and +dP/dtmax now stabilized at 89+/-5% and 94+/-5% of baseline respectively. LVEDP was 20+/-2 mmHg at the end of the reperfusion period. The protection of contractile dysfunction after 20 min of ischemia was achieved also by early reperfusion of low Ca2+-low pH perfusate. With this intervention LVDP stabilized at 87+/-5% of baseline. LVEDP was 12+/-2 mmHg at the end of the reperfusion period. A positive inotropic intervention induced by a modified postextrasystolic potentiation protocol at the end of the reperfusion period increases LVDP to levels higher than baseline in the stunned hearts. However, these values were less than those obtained in control hearts. Ischemic preconditioning significantly increased the maximal inotropic response. Therefore, ischemic preconditioning diminishes the contractile dysfunction of early stunning.

Animals↗

PubMed1994

Chronic administration of nicardipine attenuates myocardial stunning in isolated rabbit hearts.

The purpose of this study was to evaluate the effects of the chronic administration of a calcium channel blocker, nicardipine, on systolic and diastolic alterations occurring during myocardial stunning in isolated rabbit hearts. Rabbits were pretreated with nicardipine 20 mg (O.I.D.) for 30 days. Then hearts were isolated (group II) and compared with control hearts (group I) in their response to 20 min of global ischemia and 30 min of reperfusion. Coronary flow and heart rate were kept constant. Left ventricular isovolumic developed pressure (LVDP), its first derivative (dP/dt), and end diastolic pressure (LVEDP) were measured. After isolation, no statistically significant changes were detected in LVDP, +dP/dtmax, LVEDP, or coronary resistance in hearts of rabbits with or without the pharmacological intervention. Early after the onset of reperfusion, LVDP and +dP/dtmax partially recovered in a similar way in groups I and II. Late in reperfusion LVDP stabilized at 48 +/- 7% in group I and 71 +/- 6% in group II (P < 0.05) and +dP/dtmax stabilized at 56 +/- 7% and 79 +/- 6% (P < 0.05), respectively. Diastolic dysfunction was manifested by a 217 +/- 39% increase in LVEDP (P < 0.05) in group I, and 140 +/- 31% in group II (P < 0.05). The isovolumic relaxation time constant (tau, tau) increased from 70 +/- 5 to 151 +/- 27 ms (P < 0.05), and from 66 +/- 6 to 97 +/- 10 ms. (NS) in groups I and II, respectively at 5 min of reperfusion. This relaxation parameter returned to normal values in the late reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Adenosine and dipyridamole mimic the effects of ischemic preconditioning.

The effects of preconditioning, adenosine and dipyridamole in protecting the systolic and diastolic alterations of myocardial stunning in rabbit hearts were studied. Isovolumic left ventricular developed pressure (LVDP), and end diastolic pressure (LVEDP) were measured. The time constant of relaxation (T) was calculated. Isolated rabbit hearts were subject to 15 min of global ischemia (37 degrees C) followed by 30 min of reperfusion. LVDP and LVEDP stabilized to 55 +/- 5% and 320 +/- 28% of control values respectively (stunned group) T increased early in reperfusion (from 48.2 +/- 3.9 to 97.2 +/- 10 ms P < 0.05) but returned to control value late in reperfusion. When hearts were preconditioned by a single cycle of 5 min of ischemia LVDP and LVEDP stabilized at 89 +/- 3% and 162 +/- 34% of preischemic values respectively (P < 0.05 with respect to stunned group). The change in T was attenuated (62 +/- 6 ms at 5 min of reperfusion, P < 0.05 with respect to stunned group). Hearts treated either with adenosine (800 micrograms/min) or the nucleoside transport blocker dipyridamole (4 micrograms/min) previously to the ischemia, recovered their LVDP to 86 +/- 1% and 82 +/- 3% of preischemic values, respectively (P < 0.05 with respect to stunned group). Adenosine and dipyridamole also attenuated the increase in LVEDP (195 +/- 12% and 197 +/- 10% respectively, P < 0.05 with respect to stunned group).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1993

Dissociation between myocardial relaxation and diastolic stiffness in the stunned heart: its prevention by ischemic preconditioning.

The effects of myocardial stunning and ischemic preconditioning on left-ventricular developed pressure and end-diastolic pressure (diastolic stiffness) as well as on coronary-perfusion pressure were examined in isolated isovolumic rabbit hearts. The isovolumic relaxation was evaluated, and the time constant of pressure decay during the isovolumic period was calculated. Our experimental protocol comprised: 1) myocardial stunning-global ischemia (15 min) followed by reperfusion (30 min); 2) myocardial stunning-global ischemia (20 min) followed by reperfusion (30 min); and 3) ischemic preconditioning--a single cycle of brief global ischemia and reperfusion (5 min each), before a second ischemic period, of 20-min duration. There was no effect upon systolic and diastolic parameters when 15 and 20 minutes of ischemia were evaluated. In both stunned groups the left ventricular developed pressure first recovered to near control values, but then stabilized at only 60% of the control values. Whereas the isovolumic relaxation time constant was increased after 5 min of reperfusion, and return to control values at late reperfusion, the end diastolic pressure remained elevated during the entire period. Values of dP/dV calculated at common pressure levels, were used as a second index of diastolic stiffness. They were increased after stunning, as also was the coronary perfusion pressure. When the heart was preconditioned with a single episode of ischemia, the systolic and diastolic alterations were completely abolished. We thus concluded that diastolic abnormalities incurred by myocardial stunning consist in both an increase in diastolic stiffness and an early impairment of isovolumic relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Inotropic response to norepinephrine is augmented early and maintained late in conscious dogs with perinephritic hypertension.

We studied the inotropic responses to intravenous infusions of norepinephrine in nine conscious chronically instrumented dogs before and early (2-4 weeks) in the development of perinephritic hypertension; seven conscious dogs were studied later (approximately 14 weeks), during a more stable phase of hypertension. perinephritic hypertension was associated with a 24% increase in left ventricular (LV) mass during developing hypertension; no further increase was seen during the stable hypertension phase. LV end-systolic stress was increased early (p less than 0.01) but was normalized later. The LV end-systolic stress-volume relation demonstrated an enhanced contractile response to norepinephrine during developing hypertension, which returned toward control later in the course of stable hypertension. The LV dP/dt responses to norepinephrine (0.4 microgram/kg/min) were significantly greater during developing hypertension (7,509 +/- 337 mm Hg/sec, p less than 0.05) compared with the control period (4,737 +/- 286 mm Hg/sec) and returned toward the control value during stable hypertension (5,168 +/- 465 mm Hg/sec). The enhanced inotropic responses to norepinephrine in developing hypertension were preserved in the presence of ganglionic blockade, suggesting that the augmentation was not mediated via reflex mechanisms. These physiological responses were associated with an increase in beta-adrenergic receptor density, but no significant change in basal or maximal adenylate cyclase stimulation occurred during developing hypertension. Thus, in contrast to prior studies in anesthetized animals, the inotropic response to beta-adrenergic stimulation is not depressed in conscious dogs but is enhanced selectively during the development of hypertension and maintained during stable hypertension.

Animals↗

PubMed1991

Changes in diastolic cardiac function in developing and stable perinephritic hypertension in conscious dogs.

The effects of developing perinephritic hypertension (2-3 weeks) and a more stable period of perinephritic hypertension (approximately 14 weeks) were examined on indexes of left ventricular (LV) diastolic function in conscious, chronically instrumented dogs. The complete period of diastole was studied using indexes of isovolumic relaxation (tau), early filling (LV +dD/dt), and stiffness (myocardial stiffness and chamber stress/diameter ratio). During developing hypertension, increased LV end-diastolic pressure, LV end-diastolic stress, peak filling rate, myocardial stiffness, and the stress/diameter ratio increased (p less than 0.05); the time constant tau was not changed. These changes were associated with preserved baseline levels of coronary blood flow (radioactive microspheres) but an impaired coronary vasodilator response to adenosine. Acute administration of phenylephrine in the normotensive dogs caused increases in systolic and diastolic stress and resulted in increases in myocardial stiffness and in the stress/diameter ratio similar to values observed in developing hypertension. During stable hypertension, LV end-diastolic stress, peak filling rate, and both parameters of late-diastolic function (myocardial stiffness and stress/diameter ratio) returned toward control values, but the isovolumic relaxation time constant was increased. Quantitative histological evaluation revealed no increase in stainable connective tissue in dogs with stable hypertension compared with control dogs, and hydroxyproline concentration was not increased in the subendomyocardium, midmyocardium, or subepimyocardium of the dogs with chronic perinephritic hypertension. Thus, in developing hypertension, major alterations in diastolic function were observed that were not structurally related, since these changes 1) could be induced in normal dogs by increasing preload and afterload acutely with phenylephrine and 2) were improved during the ensuing stable period of hypertension.

Adenosine↗

PubMed1991

[Effects of calcium on left ventricular diastolic function in anesthetized dogs].

The effects of extracellular calcium concentration on isovolumic relaxation, rapid filling phase, and passive properties of left ventricle, were studied in open chest dogs instrumented with ultrasonic crystals, and a miniature pressure transducer. A single dose of calcium chloride (0.025 mEq/kg/m) was administered to each dog. In another experimental group beta-adrenergic blockade (propranolol 2 mg/kg) was induced before calcium administration. Diastolic function was evaluated using the time constant of the isovolumic relaxation (tau), the ratios between both +dP/dtmax and -dP/dtmax, and +dP/dt and -dP/dT at the common pressure of 35 mmHg, +dD/dtmax (as an equivalent of peak filling rate) and the chamber stiffness constant (Kc). To avoid the problem that rapid filling phase includes a portion of isovolumic relaxation, the concept of passive pressure for calculation of Kc was used. Calcium produced more increase in +dP/dtmax than in -dP/dtmax. The ratio between both maximal velocities was increased. When both velocities were examined at the common pressure of 35 mmHg, the ratio between them was not changed. tau was not changed but the asymptotic value was decreased. +dD/dtmax was increased, and Kc did not change. The same results on diastolic function of left ventricle were obtained after beta-adrenergic blockade. These data suggest that increased extracellular calcium did not alter the relaxation rate and chamber stiffness, but increased the peak filling rate and decreased the value towards left ventricular pressure decays.

Animals↗

PubMed1990

The effects of Bay K 8644 on diastolic function in the dog heart.

The effects of increased cytosolic calcium on cardiac mechanics were studied in open chest dogs instrumented with ultrasonic crystals and a miniature pressure transducer. Calcium was increased either by promoting calcium influx with Bay K 8644 (Bay K) or by increasing extracellular calcium concentration. A single dose of Bay K (10 micrograms/kg/min) was administered to each dog. Bay K increased LV systolic pressure, maximal rate of rise of LV pressure (LV + dP/dt), mean velocity of circumferential fiber shortening (Vcf), and calculated LV end-systolic wall stress. The time constant of isovolumic pressure decay (T) was calculated following two different methods: (a) a semilogarithmic method (Tz), and (b) using the linear relation between LV - dP/dt vs LV pressure (T1). Whereas Tz decreased from 31.7 +/- 2.6 to 26.7 +/- 1.7 ms (P less than 0.05), no changes were detected in T1 (46.3 +/- 4.4 vs 50.9 +/- 4.0 ms N.S.) The asymptote value (PB) decreased after Bay K from -9 +/- 2.8 to -22.5 +/- 4.2 mmHg (P less than 0.05). The same results were obtained when the changes in the loading conditions of the heart produced by Bay K were controlled by mechanical manoeuvers or after beta-blockade with propranolol. When calcium chloride was administered in amounts that will produce equal contractile changes as Bay K, a decrease in PB was also observed (from -14.7 +/- 1.6 to -27.7 +/- 6.1 mmHg (P less than 0.05]. Tz decreased from 29.6 +/- 3.6 to 22.5 +/- 2.9 ms (P less than 0.05) and no changes in T1 (52.5 +/- 5 vs 52.4 +/- 7.3 ms, N.S.) were detected. The decrease in the asymptote reported herein could induce a false decrease in the time constant if the altered values of PB are not considered, or another method of calculation of the time constant is used. Neither Bay K nor elevated extracellular calcium concentration modified the diastolic compliance. Changes in loading conditions or a cAMP pathway can be ruled out as a cause of the decrease in PB, since the results were reproduced under controlled loading conditions and beta blockade. These data suggest that increasing cytosolic calcium does not alter either the relaxation rate or the diastolic compliance but does decrease the value toward left ventricular pressure decays.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1990

Application of the systolic stiffness concept to assess myocardial function in developing hypertension.

The concept of end-systolic myocardial stiffness permits the quantification of preload effects on fiber shortening and changes in the slope (max Eav) of the end-systolic stress-strain relation, which, if linear, reflect changes in the inotropic state. As an application of this new concept, the end-systolic stress-strain and shortening-afterload relations were evaluated on the basis of data from dogs studied during development of perinephritic hypertension. End-systolic stress-strain relations were linear before and 2 weeks after the induction of hypertension and the end-systolic pressure-diameter relations were not always linear. The shortening-afterload relations obtained directly from raw data points displayed enhanced contractility in the hypertensive state under beta-adrenergic receptor blockade. However, the preload-corrected shortening-afterload relations demonstrated that contractility was unchanged in hypertension. Hypertensive hearts operated at higher preload than normotensive hearts at any afterload levels. This discrepancy between the conventional method without preload-correction and the preload-corrected analysis indicates the importance of preload-correction on shortening-afterload relations in hypertension.

Animals↗

PubMed1990

[Effect of nifedipine on cardiac chronotropism in conscious dogs].

The effect of nifedipine (NIF) was studied in intact conscious dogs with and without autonomic blockade. Maximal decrease of systolic arterial pressure (delta P, in mmHg), maximal increase of heart rate (delta F, in beats/min), the ratio delta F/delta P, and the time elapsed between delta F and delta P (delta t) were measured after the acute administration of the drug. Two intravenous doses of NIF (50 and 150 micrograms/kg) were administered either alone or after sympathetic and parasympathetic blockade. Group Ia: 50 micrograms/kg of NIF alone. The delta F/delta P and delta T were 3.8 +/- 0.4 and 11.3 +/- 2.2 sec respectively. Group Ib: 150 micrograms/kg of NIF alone. The delta F/delta P and delta T were 2.4 +/- 0.2 and 15 +/- 3 sec respectively. Group IIa: 2 mg/kg of propranolol + 150 micrograms/kg of NIF. The delta F/delta P and delta T were 0.84 +/- 0.4 and 16 +/- 5 sec respectively. Group IIIa: 0.2 mg/kg of atropine + 2 mg/kg of propranolol + 50 micrograms/kg of NIF. In this group left systolic ventricular pressure decreased about 14 mmHg, but the heart rate (HR) was not modified. Group IIIb: 0.2 mg/kg of atropine + 2 mg/kg of propranolol + 150 micrograms/kg of NIF. In this group, left systolic ventricular pressure decreased about 18 mmHg but the HR was not modified. We conclude that acute administration of NIF decreases systolic ventricular pressure and increases HR. The reflex tachycardia is partially abolished by 2 mg/kg of propranolol, and completely abolished by sympathetic and parasympathetic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗