Biomedical subjects

R Heckel

Publications and source records attributed to R Heckel.

6 recordsLinked to original sources

PubMed1991

[Orienting toxicologic studies in Wistar rats for the evaluation of knotgrass--(Polygonum convolvulus)--seed].

Black bindweed seed (Polygonum convolvulus) from the 1987 harvest was tested for possible toxicity in a 38-day range-finding test with Wistar rats which received feed rations on the basis of VDT-1 standard feedstuff and components of 5 or 20%. Histological liver findings as well as parameters recorded from laboratory diagnosis (plasma activities of ALAT, ASAT, and gamma GT as well as total protein and albumin levels in plasma) were indicative of incipient impairment of liver metabolism. More detailed and comprehensive chemico-analytical investigations are recommended, with due consideration of the unity between high-value primary components, on the one hand, and possibly toxic secondary constituent substances, on the other.

Animal Feed↗

PubMed1983

A factor analytic study of screening scales of adjudicated delinquent males and females.

Obtained a factor analysis of demographic and behavioral variables from self-ratings and observations of trained raters on a sample of 200 incarcerated delinquents, which resulted in eight identifiable factors with eigenvalues over 1.0. These were described as: The undersized youthful offender with emotional problems, the aggressive threatening offender, the drug subculture repeat offender, the neurotic polyabuse offender, the institutionally unadjusted offender, the bright offender, the immature neurotic offender, and the "established" psychopathic offender. Results provide understanding of the relationships and disparities between self-ratings, the ratings of others, and demographic variables.

Adolescent↗

PubMed1981

Significance of hypotension preceding fatal ventricular tachyarrhythmias in post-coronary obstruction sudden death.

While sudden death after acute myocardial infarction or ischemia most commonly occurs in the first few minutes, usually from tachyarrhythmias, little is known of associated hemodynamics. We monitored hemodynamics for 15 minutes following coronary embolization with mercury in 31 awake dogs. In 17 nonsurvivors, mean arterial pressure (MAP) fell 7 mm Hg at 15 seconds, 15 mm Hg by 45 seconds, 27 mm Hg at 120 seconds, and continued falling until ventricular fibrillation (VF) occurred. In contrast, in 14 survivors, MAP was unchanged at 15 seconds, fell 8 mm Hg at 45 seconds, 15 mm Hg at 120 seconds, and than returned toward control. The decline in MAP was significantly greater and earlier in nonsurvivors. Heart rate increased at 15 seconds in nonsurvivors (21 bpm) but not until 75 seconds in survivors (33 bpm). Cardiac output fell significantly only in nonsurvivors. Ventricular ectopics (greater than 5 beats/15 sec) first appeared after hemodynamic changes in both groups; at 68 seconds in survivors and at 45 seconds in non survivors. While such ectopy persisted at the same frequency thereafter in both groups, VF occurred only in the more hypotensive dogs at 177 seconds. In a second series of 26 dogs, hypotension was randomly treated by intra-aortic balloon. All nine nonhypotensive dogs survived, whereas five of six untreated hypotensive dogs died compared to 2 of 11 treated ones (p less than 0.02). We conclude that significant hemodynamic changes precede ectopy, and VF and sudden coronary death occurs usually after persistence of hypotension.

Animals↗

PubMed1981

Effect of inhibition of platelet function with carbenicillin or aspirin on experimental canine sudden death.

The role of blood platelets in the pathogenesis of experimental sudden death was evaluated in dogs. Coronary artery embolization resulted in acute myocardial ischemia that was followed by sudden death (death within 15 min of embolization) in 51% of anesthetized control animals. Pretreatment with carbenicillin, which markedly inhibited platelet aggregation or estradiol cypionate, which induced severe thrombocytopenia, significantly reduced the incidence of sudden death to 9% and zero, respectively. Pretreatment with aspirin, which uniformly inhibited platelet aggregation, was associated with a reduced incidence of sudden death (25%), but the difference between aspirin-treated and control animals lacked statistical significance. Drug treatment did not prevent myocardial infarction, and the sizes of myocardial infarcts observed in animals that survived 30 days were not different from those of control animals. Sudden death was preceded by a significantly greater fall in mean arterial pressure than that observed in survivors, but the frequency of ventricular ectopic beats did not differ in survivors and nonsurvivors. These studies suggest that (1) platelets play an important role in experimental sudden death which follows acute coronary embolization and (2) inhibition of platelet function protects against experimental sudden death by a mechanism that prevents severe hypotension but is not antiarrhythmic. Drug-induced platelet dysfunction and thrombocytopenia may protect against experimental sudden death by preventing intravascular platelet aggregation and embolization.

Animals↗

PubMed1980

Progressive myocardial dysfunction associated with increased vascular resistance.

To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 +/- 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 +/- 8.5 to 84.0 +/- 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 +/- 0.8 mmHg at control and rose to 11.8 +/- 1.4 mmHg at 1 mo and 14.9 +/- 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 +/- 0.1 at control to 3.8 +/- 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.

Animals↗

PubMed1978

Left and right ventricular dimensions during ventricular fibrillation in the dog.

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.

Animals↗