The most important characteristic of calcium channels is a selective regulation of a slow incoming current of calcium into the tissue cells with tendency of a slow growth of the action potential. Such tissues include smooth muscles of the blood vessels, cardiocities and hearth noduses (AVand SAnode). Different calcium antagonists have different influences on the mentioned tissues, because they also have different chemical components. Verapamil, Nifedipin and Diltiazem have the most common usage. Verapamil is a product of papaverine, nifedipin is a product of dehydroperidine while diltiazem is a product of benzodiazepine. Their common characteristic is blocking the calcium channels which cause blood vessels vasodilatation, negative inotropic and negative chronotropic influence. By blocking calcium to enter through channels spores of miofibrile smooth muscles, calcium antagonists are reducing the amount of available calcium for contraction, which causes vasodilatation. One of the best-known and the commonest calcium antagonist is verapamil. In electrophysiological terms, it inhibits action potential of the heart noduses (especially AV node), where the most important thing for depolarisation, is a slow entrance of calcium. By extending the refractory period of SA node, it reduces the frequency of impulse generation (heart frequency), while by extending the refractory period of AVnode, it slows down the work of chambers in cases of flater and atrium fibrillation. Taking into consideration the fact that verapamil shows cardiodepresive effects, the aim of our work is to study closely its effects on electrocardiogram and hemodynamic parameters. The experiment was conducted on six adult, healthy dogs which were, after 10 minutes 0,9% NaCl infusion, treated with i.v. bolus verapamil injections on every 5 minutes until the appearance of intoxication signs, which causes bradycardia, heart rhythm disorder and the fall of arterial blood pressure. The average verapamil dose was 4 mg per kilogram. After i.v. verapamil administration, heart frequency and middle arterial pressure have a significant fall, while central venous pressure has a significant rise. Larger verapamil doses nd rd can significantly extend T-P and P-R interval with the appearance of AV-block (2 and 3 grade), while the Q-T interval doesn't show any significant change.

The Early Warning Score is a simple physiological scoring system that can be calculated at the patient's bedside, using parameters which are mesured in the majority of unwell patients. Patients suffering in-hospital cardiac arrest often have abnormal clinical observations documented prior to the arrest. Study objestives:This study assesses wheather these patients have less favourable outcome following in-hospital cardiac arrest. Matherials and the methods:For the present study, the patients' hospital charts were reviewed to identify possible abnormal observations within 8 h prior to the arrest. Results: From the total of 100 patients who sufferd in-hospital cardiac arrest, 64 patients had documentation of vital signs and 9 patients had no documentation of vital signs. Of the patients with documented vital signs 27 (29,7%) had normal vital signs and 64 (70,3%) had abnormal observations. Among these 64 patients the distribution was as follows: 17 patients (13,1%) had respiatory rate below 8 or over 20 per min, 40 (30,8%) had puls rate below 40 or over 140 beats per min, 20 patients (15,4%) had systolic arterial blood pressure below 90 or over 200 mmHg, 5 (3,7%) had temperature (˚C) below 36,1 or over 37,9 ˚C, 20 (15,4%) had oxygen saturation below 90%, 14 (10,8%) had decrease in consciousness and 14 (10,8%) had urine output below 50 ml/2hours). Compared with patients whose EWS were 0-2 (ОR 1,2; 95% CI: 0,935-1,507) patients with EWS 3 or more were 6,5 times more likely to die in first 24 hours (OR: 7,8; 95% CI: 1,205-50,205). Conclusions:Patients with documented clinically abnormal observations prior to in-hospital cardiac arrest have a worse outcome than those without. The main implication of these is that these patients need to be identified in time thereby possibly avoiding arrest. This can also be used when assessing the prognosis of in-hospital patients after achieved ROSC.

Autors reports 20 ten old boy received penetrating vulns thorasic with naif at midle linea.subksifoid area. Patient with angina pectoris, hypovolemic shock end cardiac arrest received at department intensive care Clinic hospital centre Prishtine in Gracanica. In cardiogenic arrest under reanimation is introduction in general endotracheal anestesy and intervention surgery. Maden midle sternotomy and verification laesio pericardii under right cordis longth of 20 mm,hematopericard and vulnus at parietis diaphragmalis right ventricular in area septoapicalis.Past evacuation sangui from pericard heart mobilisation and made compresion phingin.Placement closure laesion with cardiorraphia prolen 0000 sec.Cooley.Lesion right pleurae mediastinalis and placement drain in right torasic cavum and drain mediastine in restrosternal area i aspiration undervother sec. Bilay. Fixation sternum with fillum metalicum sec. Kurschner. Reanimation intensive care all time and past realisation complete haemostasis along linae sutturae heart folow up substitution adecquat failure volumen total sangui plasm and cristolid. Realisation total stability hemodinamic and patient move at department intensive care. Control EKG, echocardiography and cardiac ensims 5 and 10 dely psotoperative show fingins corectly. Not signs ischemic laesaoin and disfunction conducti and arrhythmi. Haert pariets is all corectly viability and cinesy.

Glucagon is polypeptide hormone derived from pancreas which in addition to its metabolic actions has also certain cardiovascular stimulatory effects. We've explored the effects of glucagon on hemodynamic variables (mean arterial pressure, heart rate and central venous pressure) and on catecholamine level and the electrolite level in the kanine sera. It was estimated that glucagon expressed the positive chronotropic effect and significantly lowers the central venous pressure while inconsiderably inceases mean arterial blood pressure. It also leads to transient (short-lasting) hipokaliemia and nonsignificant hipocalcemia. As the result of the action of the glucagone, the serum adrenaline concentrations were significantly increased while the serum noradrenaline concentratios were significantly decreased

It is known that the intoxication with heavy metals and pesticides is most often unmedical poisoning. In contrast to other heavy metals, for example: mercury, lead, cadmium and zinc, toxic copper activity and the mechanism of its effect are not known enough and they are not yet explained. Because of that, the aim of this work was ( with acute dog intoxication with copper sulfate ) to contribute to better clearing of biochemical mechanism as a result of copper toxical effect and to make analysis of its tissue distribution. Researching was done on adult dogs, both sexes, different races and body mass of 14- 20 kg, who were given a 10% water solution of copper sulfate in the dosage of 33mg/b.m. divided into 5 equal doses. The analysis of biochemical blood structure took the following things: total proteins, albumins, globulins, total lipids, chole2+ sterol, glucoze, transaminase (AST,ALT), catalase, peroxidase, vitamin C, proteine SH, the contretation of Cu in the serum 2+ and the content of Cu in the tissues. The results are presented in the charts and graphic presentation. All these changes can be the important directions in an biological monitoring as a biochemical indication of copper pollution in the surroundings.

Scientific research of effects of glucagon on the cardiovascular system have shown that glucagon has some
cardiostimulatory potential. The very interesting fact is that glucagon shows its cardiostimulatory effects by activating its
own, higly specific glucagonic receptors. That is way we wanted to research not only the effects of glucagon on the C.V.S.
but also its effects during the depression of the C.V.S. with high dosses of beta blocators (presolol) expecting a good
hemodinamic response. The experiment has been performed on two groups of 6 dogs. The first group of animal was treated
with i.v. bolus injections of glucagon and other group with presolol (15 mg/kg b.w.) i.v., and after that with i.v. bolus
injection of glucagon. Hemodinamic variables (mean arterial pressure, central venal pressure and hearth frequency) were
registred at the 1-st, 2-nd, 3-rd, 10-th, 20-th, 30-th and 40-th minute. The hearth frequency was registred by continous
monitoring, mean arterial pressure was registred with cateter in the arterial femoralis, while the central venal pressure was
registred over central venal cateter in v. femoralis. After the i.v. bolus injection glukagon shows higly positive effects,
followed by short-term increase of the mean arterial pressure, while the c.v.p. considerably falls. During the administration
of presolol the hearth frequency and mean arterial pressure fall considerably and progressively, while the c.v.p. rises
considerably. Glucagon, in conditions of c.v.s. depresion by high doses of presolol (15 mg /kg b.w.) considerably increases
hearth frequency and mean arterial pressure, while the c.v.p. falls considerably.