Graded experimental myocardial contusion in rabbits: antemortem and postmortem diagnosis

A controlled animal model was used to clarify the role of serum total creatine phosphokinase [CPK] and creatine phosphokinase-MB [CPK-MB] fraction in the diagnosis of myocardial contusion in patients, as well as, the role of cardiac tissue levels of creatine phosphate [CP] and adenosine triphosphate [ATP] in the diagnosis of fatal myocardial injury on autopsy. Graded myocardial contusion was produced by a single blow with a weight pendulum in two groups of rabbits [group I received a moderate impact, 78 +/- 5 m Joules/g, group II received a major impact, 87 +/- 7 m Joules/g]. Gross and microscopic examinations on autopsy showed a minor pathologic entity in group I, while in group II a distinct pathological entity could be identified. 20 minutes after the impact, a very highly significant [p <0.001] increase in the serum total CPK appeared in both groups. CPK-MB fraction was not detected in the serum of control animals [uninjuried group], but its level and percentage were 10.9 +/- 0.80 IU/L, 6.98% in group I and 29.7 +/- 1.23 IU/L, 8.18% in group II. Cardiac tissue levels of CP and ATP, 25 minutes after impact, revealed a very highly significant [p <0.001] reduction in both groups. It is clear that, the increase in the serum enzyme and the decrease in the cardiac tissue levels of high-energy phosphates were proportional to the severity of the blow. These results suggested that the serum total CPK and CPK-MB fraction are most reliable indicators of myocardial contusion following blunt chest trauma. The cardiac tissue CP and ATP levels, also can be used as diagnostic criteria for a suspected fatal cardiac injury and clearly apparent on autopsy

Influence of ethanol on potentiation of the response to blunt cardiac trauma in rabbits

Acute changes in mechanical performance [spontaneous rate and contractile force of the hearts] were followed after blunt cardiac trauma, ethanol infusion, and ethanol infusion with blunt cardiac trauma in 40 anesthetized male rabbits. Impact was delivered to the whole anterior pericardium by a single blow with a weighted pendulum. Energy delivered, which was calculated as kinetic energy, was 67 +/- 7 m Joules/g. Impact alone caused complete cardiac arrest, followed by sequential ventricular recovery, atrial recovery with atrioventricular [A-V] block, transient normal sinus rhythm, tachycardia and normal sinus rhythm. These transient cardiac dysfunctions were accompanied with significant reductions in the spontaneous rate and contractile force, except the height of auricular contraction during A-V block which showed a significant rise. All animals survived impact and regained nearly normal mechanical performance within 10 minutes after impact. Intravenous infusion of ethanol [average blood alcohol concentration, 65 +/- 1 mg%], resulted in nonsignificant decrease in the mechanical performance, but, when combined with trauma, caused a mortality rate of 75%. All animals died from complete and persistent cardiac arrest after marked slowdown in the spontaneous rate and severe weakness in the contractile force. It is concluded that even low blood alcohol concentrations can significantly reduce cardiac performance in the presence of otherwise nonfatal cardiac injury

Histopathological and serum enzyme changes in fatal electric shock

Thirty adult albino rats were killed by electrocution, Using alternating house-hold current, of 220 volts, They were divided to three groups, each consisted of 10 rats. The electrodes were connected to either forelimb hindlimb [gr. II], both forelimbs [gr. II], or head-hindlimb [gr. Ill]. Ten animals served as control of the study [Group IV]. The gross and histopathological changes of the main vital organs [heart, lungs, and brain] and the big blood vessels involved in the electric circuits were studied. Congestion, dilatation, intravascular thrombotic aggregates, and rupture with perivascular hemorrhages' were frequently observed. Degenerative and necrotic cellular damage of the myocardium and cerebral neurons, could be detected. The extent of damage varied according to the direction of the current. There were a significant rise in both STDH and SGOT while SGPT and SALP enzymes showed non significant changes

Experimental evaluation of hydrofluoric acid and hypocalcemia

Experimental evaluation of the effect of hydrofluoric acid exposures on serum calcium has been achieved in male rats. Five concentration levels [10, 20, 30, 40, 50 percent] of hydrofluoric acid were used in this study; whereas for each concentration, two groups of animals were subjected to either skin or inhalation exposure. Hydrofluoric acid induced hypocalcaemia, in a concentration- related manner, either by skin or inhalation exposure as shown by the significant [P< 0.05, P<0.01 P< 0.001] decrease in serum calcium, except the group subjected to inhalation exposure of 10 percent hydrofluoric acid vapor which revealed non - significant diminution. These results suggest that proper treatment of hydrofluoric acid burns must include administration of intravenous calcium, to replenish the biologically active calcium and to prevent death from hypocalcaemia

Effect of female sex steroid hormones on lipid metabolism

In the present study we demonstrated the effects of female sex steroid hormones [estrogen and / or progesterone] on lipid metabolism in female. Female albino rats were used for this study. After ovariectomy, we injected either estrogen and/ or progesterone every day for 14 days, then all animals were decapitated, blood taken and serum analyzed for total cholesterol, triglycerides, phospholipids, high density lipoprotein cholesterol [HDL.C] and low density lipoprotein cholesterol [LDL.C]. We found that estrogen induced significant rise in HDL.C and significant decrease in total cholesterol and LDL.C, while no changes in triglycerides or phospholipids were observed. Progesterone injection resulted in insignificant changes in lipid profile. Combined estrogen and progesterone injection resulted in significant rise in HDL.C and decrease in total cholesterol, LDL.C and insignificant changes in triglycerides or phospholipids. These data may indicate that cyclic fluctuations in lipid levels do occur under the influence of female sex hormones and estrogen use in postmenopausal women is associated with increase HDL.C, which reduces risk factors for coronary artery disease

Bacterial translocation from the gut complicating hemorrhagic shock

To determine whether hemorrhagic shock would promote bacterial translocation from the gut to visceral organs, rabbits were subjected to a model of hemorrhagic shock [mean pressure, 30 mm/Hg]. Twenty- four hours after being subjected to sham-shock, or 90 minutes of shock, rabbits were sacrificed and their organs quantitatively cultured for translocating bacteria. There was a direct relationship between the duration of hemorrhagic shock and the 24-hours mortality rate. Bacteria did not translocate from the gut in the sham-shock rabbits, but translocated to the mesenteric lymph nodes, livers and spleens of the rabbits subjected to hemorrhagic shock. Rabbits subjected to 90 minutes of shock exhibited a greater degree of bacterial translocation than rabbits receiving 30 or 60 minutes of shock; whereas the incidences of translocation were significantly [P < 0.01 and P < 0.001] increased with the increase of duration of hemorrhagic shock. The most common translocating bacteria were Escherichia coli and Enterococcus. Hemorrhagic shock produced subepithelial edema and focal areas of necrosis in the ileum, vacuolization of the renal epithelial cells with cellular debris within the renal tubules, and hepatic centrilobular venous congestion. Thus hemorrhagic shock followed by reinfusion of shed blood disrupts the gut barrier and allows indigenous bacteria normally contained within the gut to cause systemic infections

Influence of ketonic and ketogenic compounds on potential of carbon tetrachloride hepatotoxicity: Role of ketone bodies

The smallest dosage needed to potentiate CCI4 hepatotoxicity was estimated to be between 5.5-11 mm mol/kg/day for BD and 0.95-1.9m mol/kg for MnBk. BD or MnBk also, resulted in a dose dependent metabolic ketosis in the plasma observable at the same dosages which produced potentiation of CCI4 -induced liver injury. This ketonic state was due to an increase in B-hydroxybutyrate [BOHB], while acetoacetate [Ac-Ac] remained at its basal levels. The potentiated response appeared to be related to severity of the metabolic ketosis produced by BD or MnBk. These results suggest that plasma B- hydroxybutyrate concentrations might be useful for predicting possible potentiation of the hepatotoxic effect of CCI4 by BD or MnBk

Influence of short-term starvation on reproductive hormones secretion in male rats

The effects of short-term starvation [6 days] on the pituitary testicular function of adult male rats were studied, while the serum reproductive hormone levels were measured at the end of the study. Fasting decreased body weights by 19.83% [P< 0.001], testicular weights by 6.16% [P< 0.05] and those of seminal vesicles by 51.28% [P< 0.001]. On the other hand, the ventral prostate weights showed statistical non-significant 10.53% reduction. The serum level of the hormones were significantly declined. Lutenizing [LH] by 46.43% [P< 0.05], folliclestimulating [FSH] by 38.89% [P< 0.01], prolactin by 44.12% [P< 0.05] and testosterone by 39.71% [P< 0.01]. It is apparent from this study that, food restriction resulted in suppression of reproductive functions