Biofilm development capacity of Salmonella strains isolated in poultry risk factors and their resistance against disinfectants.

Prevention of Salmonella contamination of poultry products requires detailed knowledge of the most important risk factors associated with its presence in the production system. The aim of this study was to identify the risk factors for Salmonella contamination in 44 broiler and 51 layer farms and determine the biofilm development capacity of the strains isolated. Then, glutaraldehyde (50% vol/vol), formaldehyde (37% vol/vol), and hydroxide peroxide (35% vol/vol) were applied to evaluate their capacity to remove Salmonella, biofilm and nonbiofilm strains, isolated from each risk factor in an artificial contamination test in field conditions. Samples of feces, dust, surfaces, meconium, delivery-box liners, water tank, water dispensers, litter, vectors (rodents, flies, and beetles), and surfaces of the slaughter trucks were taken throughout the rearing period. All samples were analyzed in accordance with ISO 6579:2002 (Annex D). To evaluate biofilm development, a screening method based on the fluorescence of Salmonella colonies on calcofluor agar plates was used. In the artificial contamination test, the chemical solutions were prepared at a concentration of 1.0% and applied at exact times (1, 15, or 60 min). Our results showed that the most important risk factors for Salmonella contamination were dust, surfaces, and feces. Moreover, day-old broiler chicks reached the farm highly contaminated, and wild carriers played an important role in the recirculation of Salmonella in laying hen houses. The serotype most commonly isolated from each risk factor was Salmonella enteritidis, and irrespective of the origin of different serotypes, around 50% were able to produce biofilm. Finally, the use of glutaraldehyde, formaldehyde, and peroxygen at a concentration of 1.0% in field conditions are inadequate for Salmonella elimination irrespective of the serotype, the biofilm development capacity, and the disinfectant contact time.

Amlodipine reduces predicted risk of coronary heart disease in high-risk patients with hypertension in Spain (The CORONARIA Study).

We evaluated the efficacy and safety of amlodipine besylate alone or in combination with other antihypertensive agents in high-risk hypertensive patients in Spanish primary care. In this 1-year, open-label, prospective cohort study, 7468 patients were treated with amlodipine 5 - 10 mg as a monotherapy or as an add-on therapy to attain blood pressure control (target of < 140/90 mmHg or, in patients with conditions such as diabetes or chronic kidney disease, < 130/85 mmHg). At 12 months, the primary outcome (change from baseline in predicted 10-year coronary heart disease risk) was -8.6%, down from 24.7% at baseline (relative risk reduction, 31.6%). Change in blood pressure from baseline (162.5/95.3 mmHg) was -26.7/-14.6 mmHg, and 38.6% of patients achieved their blood pressure target. In summary, significant reductions in predicted coronary heart disease risk and blood pressure were observed with amlodipine both as a monotherapy and as an add-on therapy. Amlodipine was well tolerated and compliance with treatment was good.

[Troponine T as possible myocardial injury marker. Its application in myocardial stunning and silent ischemia]. / La troponina T como posible marcador del daño miocárdico menor. Su aplicación en el miocardio aturdido y en la isquemia silente.

INTRODUCTION AND OBJECTIVES: The need for more specific, more sensitive and earlier biochemical markers of acute myocardial infarction, has led to the development of alternative methods to CK-MB). The aim of this work is to assess the usefulness of TnT measurement, in comparison with other markers for detecting transitory ischemic processes without necrosis in some experimental models. METHODS: The plasma levels of Troponine T, CK, CK-MB and adenosine were assessed as markers of ischemic myocardial injury. Two protocols were used: in Series I and II very brief (2 min ischemia with 3-min reperfusion) repeated (20 episodes) ischemias were induced, while Series III involved a single 15-min ischemia with a 60-min reperfusion. In Series I the coronary occlusor was placed close to the anterior descending coronary artery (AD); in Series II and III it was placed distally in the AD. Blood samples were taken from the peripheral vein (PVB) and corresponding coronary segment vein; in a basal situation, during ischemia, upon reperfusion, after 24 hours, and after 5 and 10 days. The plasma levels of adenosine, troponine T, CK and CK-MB as well as general and regional function parameters were measured. RESULTS: In Series I we observed hypokinesis that lasted 10 days, reaching its maximum on days 4-5. In Series II and III regional function was restored by 24 hours. CK and CK-MB showed similar behaviour; they rose significantly when the chest was opened (p < 0.05) reaching the highest value at 24 hours in all the series. Adenosine rose significantly only during reperfusion (p < 0.05). Troponine T increased after ischemia but not before, remained high for 5 days in all series (PVB). CONCLUSIONS: Troponine T rises in absence of necrosis, preferably when the ischemia is longer.

[Effects of nitroglycerin and nifedipine on stunned myocardium due to brief repeated ischemias]. / Efectos de la nitroglicerina y nifedipino sobre el miocardio aturdido por isquemias breves repetidas.

OBJECTIVE: To analyze whether nitroglycerin and nifedipine can reduce myocardial stunning due to very brief, repeated coronary ischemias. MATERIAL AND METHODS: In 33 anaesthetized and open chest dogs, the lengthening and shortening fractions were analyzed with ultrasonic crystals in the ischemic and control myocardial areas. Twenty repeated coronary occlusions of 2 minutes each, with a recovery time of 3 minutes between each occlusion, were induced. At the beginning of the experiment, nitroglycerin (0.3 mg i.v. and 80 micrograms/kg/min perfusion) was administered in series A (n = 8), nifedipine (5 mu/kg i.v. and 1 microgram/kg/min perfusion) in series B (n = 9). The results were compared with control results (n = 16) without drugs. RESULTS: Changes in the shortening fraction of the ischemic area during coronary occlusions were similar in all three series; after the last occlusion the shortening fraction in the control series was -14.9% with respect to basal values, -14.6% in series A and -16.6% in series B. Sixty minutes after the last ischemia, the shortening fraction impairment in respect to the basal values was larger in the control series (-18.9%) and in series A (-16.9%). In series B there was recovery (-13.5%) (p < 0.05 vs control series). CONCLUSIONS: Our study indicates that nitroglycerin does not seem to have cardioprotective effects against brief, repeated ischemia. However, nifedipine decreases postischemic dysfunction due to this model of ischemia, probably by avoiding the intracellular Ca overload produced during cardiac ischemia.

Functional and ultrastructural alterations of canine myocardium subjected to very brief coronary occlusions.

The effects of very brief and recurrent coronary occlusions on myocardial regional shortening and its ultrastructure have been analysed. Ultrasonic crystals were implanted in the left ventricular subendocardium of 23 anaesthetized dogs with the thorax open, to measure the shortening fractions of an ischaemic and a control segment. Twenty 2 min total occlusions were provoked in the left anterior descending coronary artery, with 3 min recovery intervals (reperfusion) between occlusions. The shortening fraction decreased progressively with each occlusion, reaching a value 18.9% lower than the basal after the last ischaemic episode (P < 0.05); 32.3% after 4 h of reperfusion (P < 0.01), and 28.6% after 24 h (P < 0.01). Qualitative and quantitative ultrastructural analysis showed an increase in the mitochondrial volume of the ischaemic tissue (158% vs control, P < 0.001) with significant damage to the cell components (7.7-fold increases vs control mitochondria). These results show that when the myocardium is subjected to very brief and repeated coronary occlusions, there is progressive deterioration of systolic function with structural alterations, mainly at the mitochondrial level. These modifications are still observable 24 h after the end of ischaemic stimulation and could be the cause of transitory and/or chronic systolic dysfunctions in the absence of previous heart attack.

Effects of captopril on regional segment motion during acute coronary occlusion.

The effects of captopril on myocardial segment function in different degrees of transient coronary occlusion were studied using ultrasonic dimension gauges in 15 open-chest dogs. The occlusion procedures (OP) were performed on the left anterior descending coronary artery (LAD) in eight dogs and on the left circumflex coronary artery (Cx) in seven dogs. To measure the changes in segment shortening in the subendocardium we used eight dogs (ischemic and control zones: four dogs LAD and four dogs Cx). To measure the changes in wall thickening we used seven dogs (ischemic and control zones: three dogs LAD and four dogs Cx). Total coronary OP lasting 1 min and partial OP (70-80%) lasting 1 min and 2 min 30 s, before and after captopril (0.25 mg/kg i.v.) were performed. Left ventricular pressure, dP/dt, coronary flow, and ECG were monitored. Total coronary OP (1 min) changed segment shortening (18% LAD; 14% Cx) and wall thickening (19% LAD; 18% Cx) to values of dyskinesis (-3% and -4% for shortening; -6% and -5% for thickening). Captopril improved regional function maintaining positive values for shortening (4% LAD; 3% Cx) and thickening (0.3% LAD; 4% Cx). Similar responses were obtained during partial OP and captopril. Results suggest that captopril produced a significant improvement in the regional function parameters affected by ischemia both in total and partial obstructions.

Sick sinus syndrome: strategies for reducing mortality.

The evolution of sick sinus syndrome is slow, and its clinical and electrocardiographic manifestations are intermittent. A-V and I-V conduction disturbances often arise, but incidence of defects with clinical consequences is too low. Death rate, when large groups are considered, is slightly higher than that of the general population of the same age and with similar pathologies. Mortality depends on concomitant pathologies, on the development of congestive heart failure, on the arterial thromboembolism and on the type of sinus disease. The use of ventricular pacemakers (VVI) did not reduce mortality. Atrial pacing (AAI) gives the auricles electrical stability preventing fibrillation and systemic embolism. The hemodynamic role of the auricles is also preserved. As a consequence, death rate is reduced when AAI is used. In cases with a-v conduction disturbances or with paroxysmal atrial fibrillation, dual chamber pacing (DDD) is preferable because it permits ventricular pacing to be continued even if a-v block or paroxysmal or chronic atrial fibrillation appears. When using ventricular pacing and in cases in which pacing is not considered, warfarin or aspirin can prevent strokes and systemic embolism. In bradycardia-tachycardia syndrome requiring treatment of arrhythmias dual chamber pacemaker must be implanted.

[The cardioprotective action of nifedipine during short-term transient ischemia]. / Estudio de la acción cardioprotectora de la nifedipina durante las isquemias transitorias de duración breve.

To determine the therapeutic activity on regional myocardial function of nifedipine intravenous administration (0.16 mg/kg) during short term myocardial induced ischemia, we used 6 mongrel dogs anesthetized and intubated those who we have implanted 3 pairs of ultrasonic crystals in the subendocardial layer. Utilizing an open chest canine model we performed total 1 minute and partial 2 minutes 30 seconds alternative obstructions, controlled with electromagnetic flowmeters in the anterior descending (AD) and circumflex (Cx) coronary arteries before and after drug administration. During the 70-80% obstructions we have shown a significant improvement in segment shortening, reduced by ischemia, in the ischemic and peri-ischemic zone. The ischemic markers, per cent increment of end diastolic length (% IEDL) and per cent increment of end systolic length (% IESL), have shown significant improvement during partial obstructions in the ischemic and peri-ischemic zone. After total obstructions the improvement on regional myocardial function is less marked and limited to ischemic zone.

[Regional differences in the contractile function of the subendocardium and subepicardium of the left ventricle in the dog]. / Diferencias regionales en la función contráctil del subendocardio y el subepicardio del ventrículo izquierdo en el perro.

With the objective to study the regional differences in myocardial function of different left ventricular (LV) segments, twelve pairs of ultrasound crystals were implanted in six open-chest dogs. Six pairs in the subendocardium and six in the subepicardium in three zones of the left ventricle (4 in the apex, 4 in the left anterior descending region and 4 in the circumflex region). In each zone of subendocardium one pair was placed parallel to the epicardial fibers (long axis) and the other following the circumferential plane of the left ventricle (short axis); the same orientation was followed in the subepicardium. Left ventricular pressure, coronary flow (electromagnetic flow-meters), peripheral ECG leads, dp/dt, and segmental shortening were measured. The extent of shortening and the fraction of shortening were considered. The extent of shortening is always higher in the long axis than in the short axis crystals. Similarly, the shortening in the subendocardium is higher than in the subepicardium. The greater extent of shortening and fraction of shortening appeared in the apex, above all in the subendocardium. There are differences in the time-course of fibrillar shortening between subepicardium and subendocardium; the subendocardial contraction was simultaneous with a lengthening of the subepicardial segments. In conclusion, there are differences in myocardial contraction depending on the myocardial region and the layer. Also the shortening of the subendocardium is not synchronous with the subepicardium.