[Heparin-induced thrombocytopenia]. / Heparininduzierte Thrombozytopenie.

Heparins are in widespread use as anticoagulants for the prophylaxis and therapy of thromboembolisms. A dangerous side-effect is heparin-induced thrombocytopenia type II (HIT type II) with the paradox of thromboembolic venous and arterial vascular occlusions. HIT type II is an immunological disease which results in activation of platelets and plasma coagulation. The main symptom is an acute onset of thrombocytopenia with a fall in thrombocytes to less than 50% of the initial value with or without newly arising thromboembolic complications between days 5 and 14 after the start of heparin therapy. Surgery patients are more often affected by subclinical antibody formation as well as by symptomatic HIT type II than clinical patients. In this review we will discuss the difficult diagnosis and the differential diagnosis with special emphasis on postoperative intensive care patients, as well as preventive measures and management on occurrence of HIT type II and associated thrombotic complications.

Alkalinization during re-oxygenation prevents functional damage by hyperglycaemic hypoxia.

Hyperglycaemia impairs recovery from transient cerebral ischaemia: the importance of tissue acidification for this phenomenon has not been clarified in detail. We investigated this issue in a less complex in vitro preparation of isolated rat dorsal spinal roots exposed for 30 min to hyperglycaemic hypoxia. Peak height of compound action potentials recovered minimally in 5 mM bicarbonate. However, recovery was greatly improved by addition of the weak base trimethylamine during re-oxygenation. Addition of the weak acid propionate had no such effect. Cytoplasmic alkalinization improved recovery in a brief time window only: application of trimethylamine after 15 min of re-oxygenation was without beneficial effect. These data emphasize the importance of cytoplasmic acidification for neurophysiological recovery from hyperglycaemic hypoxia during the initial period of re-oxygenation.

A model of cardiac nociception in chronically instrumented rats: behavioral and electrophysiological effects of pericardial administration of algogenic substances.

This report presents evidence that pericardial administration of a mixture of algogenic substances is a potentially useful model of cardiac nociception. In awake rats in which a looped silicone catheter had been placed in the pericardial sac at least 5 days previous, administration of a mixture containing equal concentrations of bradykinin (BK), acetylcholine (ACh), adenosine (ADEN), histamine (HIST), serotonin (5-HT) and prostaglandin E2 (PGE2) (total 25 nmol in 25 microliters) led to rapid acquisition of a passive avoidance behavior. In contrast, neither BK alone (5-25 nmol) nor the same mixture of ACh, ADEN, HIST, 5-HT and PGE2 without BK led to acquisition of the behavior or produced effects significantly different than produced by saline given into the pericardial sac in the same volume (25 microliters). Both BK and the mixture containing BK produced dose-dependent cardiovascular responses (pressor response and tachycardia) of similar magnitude. Neither saline nor the mixture without BK produced significant changes in mean arterial blood pressure or heart rate. In electrophysiological experiments in the same rats, thoracic spinal cord neurons responded dose-dependently to the mixture and, except for one neuron, responded also to BK in a dose-dependent manner. However, responses to BK, when compared to a similar dosage of BK contained in the mixture, were significantly less in magnitude and duration. All units received convergent somatic input from the thorax and all neurons also received convergent input from the esophagus. Balloon distension of the esophagus excited all units. Results of the behavioral characterization of algogenic substances administered into the pericardial sac of awake rats gave evidence of differences between the effects of BK and a mixture of six substances, including BK. BK in either of two dosages tested produced effects not different than saline while the mixture containing BK was aversive. In complementary electrophysiological studies, both BK and the mixture containing BK excited thoracic spinal cord neurons, suggesting that neuron responses to putative algogenic substances are not necessarily reliable measures of cardiac nociception.

Characterization of responses of T2-T4 spinal cord neurons to esophageal distension in the rat.

1. Three hundred fifty neurons in the T2-T4 spinal segments of 38 intact, pentobarbital sodium-anesthetized, pancuronium-paralyzed male rats were examined for somatic receptive fields and responses to midthoracic esophageal distension (ED). Recordings were made at a depth of 0.1-1.45 mm from the dorsal spinal cord surface and from the midline to approximately 1.0 mm lateral. 2. Fifty-six of the 350 total neurons (16%) responded to ED, produced by air inflation of a latex balloon (0.5-1.5 ml). Most of these 56 neurons (84%) were excited by ED, and all except one were excited at a short latency (< 2 s) to stimulus onset. The response to ED in about one-half of all excited neurons terminated abruptly with termination of the stimulus; the other neurons exhibited an afterdischarge of 5 to > 80 s. Repeated ED at a constant intensity (1.25 ml, 30 s every 6 min) produced stable and reproducible responses of neurons excited by ED. Twenty-one percent of neurons that responded to ED were antidromically invaded from the spinomedullary junction. 3. Graded ED (0.5-1.5 ml, 30 s every 6 min) produced linear and accelerating stimulus-response functions in the 29 neurons tested. The mean threshold for distension, determined with a least-squares regression analysis, was extrapolated to near 0.5 ml of distending volume, and no difference in response threshold was found between neuronal groups with or without after-discharge. 4. The spontaneous activity of 7 of the 56 neurons (12.5%) that responded to ED was inhibited by the stimulus. Stimulus-response functions for four neurons inhibited by ED were intensity dependent. The spontaneous activity of these neurons was inhibited to a mean of 24.5% of the prestimulus control by 1.25 ml ED. 5. Two neurons of the total sample of 56 (3.5%) responded to ED (1.50 ml) in a biphasic excitatory-inhibitory manner. The excitatory component of excitatory-inhibitory neurons encoded the intensity of ED; the inhibitory component during the second half of ED was apparent only at greater distending volumes (1.25-1.5 ml). 6. Somatic receptive fields were found for 303/350 neurons, and 98% were located on the thorax and proximal forearm (all ipsilateral). Five neurons in T2-T4 spinal segments had their cutaneous receptive fields located on caudal parts of the body (tail, hindleg, scrotum).(ABSTRACT TRUNCATED AT 400 WORDS)