[Pretreatment with heparin in experimental trauma and haemorrhagic shock]. / Prophylaktische Heparinisierung nach experimentellem Trauma und hämorrhagischem Schock.

A severe shock is produced in 18 mongrel dogs by standardized bone trauma and haemorrhagic shock. Impairment of microcirculation is demonstrated by acidosis, reduced oxygen uptake and disseminated intravascular coagulation (DIC). Further, a specific increase in pulmonary vascular resistance--independent of the reduction in blood flow--is evoked, concomitantly with the occurrence of microthrombi, oedema and haemorrhage in lung tissue. Pretreatment with heparin inhibits disseminated intravascular coagulation and reduces impairment of microcirculation and the consecutive damage of intestinal organs. However increase of pulmonary vascular resistance is unchanged and pulmonary haemorrhage is pronounced. Therefore heparin pretreatment enhances pulmonary histologic impairment after trauma and haemorrhagic shock.

Efficiency of cardioplegia in the presence of coronary occlusion.

Myocardial tissue pH and temperatures (MT) were continuously measured in dogs on total cardio-pulmonary bypass (CPB) after acute distal coronary artery occlusion. Measurements were performed in a collateralized area with myocardial blood flow (MBF) ranging from 20 to 80 ml/100 g-min (microspheres). Immediately after coronary artery occlusion the aorta was clamped and the heart perfused with a cardioplegic solution (Bretschneider HP, 41 ml/kg, 4 degrees C). Prolonged regional fibrillation was observed and MT fell to 20 degrees C in 10 min in the low perfusion area (LPA) and in 2 min in the control area (CA). Whereas MTs were practically identical 15 min after termination of cardioplegic perfusion the magnitude of H+ accumulation continued to be greater in the LPA. During blood reperfusion with the coronary snare released MBF was significantly lower in the LPA as opposed to the CA indicating a microcirculatory derangement. Accordingly the bipolar ECG revealed signs of regional ischemia even after 30 min of reperfusion. We conclude that myocardial protection may be inadequate in areas located distal to coronary occlusion. This is true not only in cases of acute severe ischemia but also when collateral resistance is sufficiently high to impede the flow of cold viscous cardioplegic solutions. Results derived from intermittent MT measurements may be erroneous because intramyocardial heat equilibration may mask the inhomogeneous cardioplegic perfusion.

Regional myocardial blood flow after hypothermic arrest and cardioplegia.

Malperfusion due to increased coronary vascular resistance is presumably one of the factors responsible for incomplete functional recovery of the heart after aortic cross-clamping. Myocaridal blood flow (MBF, radioactive microspheres) was measured before and after 60 min of hypothermic ischemia in 16 dogs on cardiopulmonary bypass. After ischemia the hearts were reperfused for 30 min. MBF was measured in the empty beating heart and in the isovolumetrically contracting ventricle loaded with enddiastolic volumes (EDV) of 10, 20 and 30 ml (intraventricular latex balloon).

[Regional myocardial blood flow and ventricle function following hypothermic ischemia and cardioplegia]. / Regionale Myokarddurchblutung und Ventrikelfunktion nach hypothermer Ischämie und Kardioplegie.

Regional myocardial blood flow (MBF) and left ventricular (LV) function were measured in 18 dogs after 60 min hypothermic (14-16 degrees C) arrest with (group I) and without cardioplegia (group II). Regardless whether postischemic LV function was severely (group II) or only moderately (group I) impaired, the amount of MBF and its transmural distribution was not significantly altered after 30 min reperfusion. In contrast to topical hypothermia, additional cardioplegia maintained metabolic regulation of coronary flow.

[Coagulation inhibition caused by selective thrombin blockade with hirudin]. / Gerinnungshemmung durch selektive Thrombinblockade mit Hirudin.

Hirudin causes a rapid inhibition of blood coagulation as shown by in vitro and in vivo experiments in the dog. The substance appears to be a rather specific antithrombin. Its inhibitory action is linearly dose related and therefore easy to control and reproduce. Side effects can be expected to be abolished after further purification of the substance.

[Preventive treatment with methylprednisolone and heparin in experimental trauma and hemorrhagic shock]. / Prophylaktische Therapie mit Methylprednisolon und Heparin bei experimentellem Trauma und hämorrhagischem Schock.

Twenty-six anesthesized mongrel dogs were subjected to a standardized traumatic hemorrhagic shock. Compared with the control group prophylactic treatment with high doses of methylprednisolone reduced functional and histologic alterations of the lung. Methylprednisolone in combination with heparin pretreatment prevents microthrombi but produces more alveolar bleeding.

[Pulmonary microembolism: pulmonary hemodynamics following trauma and hemorrhage (author's transl]. / Pulmonale Mikroembolie: Pulmonale Hämodynamik nach Trauma und Blutentzug

Standardized bone trauma by means of open osteotomy is performed on both hind legs of 16 out of 24 anaesthetised mongrels. During the following 6 hours the most important parameters of blood coagulation and the serum lipids are estimated at regular intervals. Subsequently in a number of the animals 50% of the total blood volume is withdrawn continuously over a period of one hour. All animals without the preceding trauma survive the hemorrhage. The animals in the trauma group die on the average 42 minutes after the beginning of the hemorrhage. The trauma causes an acute decrease in total platelet count (GTZ) to 40% of the pretraumatic value. During an initial phase of hypercoagulability there is a formation of reversible microaggregations containing platelets and fibrin, caused by an increased turnover of coagulation factors. Secondary fibrinolysis develops in the traumatised animals. A further increase in coagulation is caused by the following hemorrhage. In combination with decreased and inhibited fibrinolysis, a disseminated intravascular coagulation state is found and results in irreversible pulmonary microthrombosis. Massive pulmonary fat deposits cannot be found histologically in spite of an increase in serum triglycerid levels to 35% above the pretraumatic values. In dogs great amounts of fat are filtered by the glomeruli and are demonstrable in the tubular epithelium. Histological examinations show a marked disseminated pulmonary microthrombosis of platelets, fibrin and fat in those animals with trauma and hemorrhage. Only the accompanying hypovolemia produces the characteristic histologic changes of the so-called Pulmonary Microembolism Syndrome.

Changes of coagulation and fat-metabolism following pulmonary microembolism after trauma and hemorrhage.

In 16 of 24 anesthetized mongrel dogs a standardized bone trauma was performed to both hind legs by open osteootmy. During the following 6 hours the most important hemodynamic parameters, total platelet count (GTZ) and its separate fractions (NKF, KF) were continously monitored. Five hours after the trauma 50% of the total blood volume (taken to be 80 ml/kg body weight) was withdrawn from two of the four groups of animals. The trauma caused no direct effect on the pulmonary hemodynamics. In the following hours there was a slight decrease of cardiac output (HZV) in the traumatised animals. Besides a moderate increase in mean pulmonary pressure (MPP), pulmonary vascular resistance (PVR) increased by 72% of the pretraumatic values. The application of intravascular catheters diminished the total platelet count markedly in the injured, as in the uninjured animals. The increase in PVR was caused less by a mechanical obstruction of the pulmonary capillary bed than by vasoactive substances released by the platelets. The following hemorrhage led to a more marked hemodynamic reaction in the injured animals. All these animals died before the end of the calculated hemorrhage. All animals without trauma survived. Irreversible aggregation of platelets developed in the pulmonary capillary bed caused by the marked pulmonary hypocirculation. Histological examination showed a marked disseminated pulmonary microthrombosis in all animals with trauma and hemorrhage. The initial phase of experimental pulmonary microembolism caused by trauma was characterized by pulmonary hypocirculation and an activated coagulation with simultaneously diminished total platelet count.