Acute normovolaemic haemodilution decreases postoperative allogeneic blood transfusion after total knee replacement

We hypothesized that the success of postoperative blood conservation after acute normovolaemic haemodilution (NVHD) is influenced by the extent of intraoperative bleeding and surgical trauma, and the timing of autologous blood transfusion. As total knee replacement is associated with minimal intraoperative but extensive postoperative blood loss, this procedure is ideally suited to acute NVHD. Therefore, to test our hypothesis, 30 patients undergoing elective total knee replacement were enrolled in a prospective, randomized, controlled study. In groups NVHD-2 and NVHD-6, before induction of anaesthesia patients were bled to a target packed cell volume (PCV) of 28-30%, and in the post-anaesthesia care unit autologous blood was transfused over a 2-h period terminating after operation at 2 and 6 h, respectively. In the control group, NVHD was not performed. After operation, platelets, fibrinogen, prothrombin and partial thromboplastin time, and liver function, urea and electrolytes were measured and compared with preoperative baseline values. Significantly (P < 0.024) more allogeneic blood was transfused in the control group (21 u.) compared with either group NVHD-2 (7 u.) or group NVHD-6 (5 u.). In the control group, despite the allogeneic blood transfusion, postoperative PCV decreased until day 4 after operation. Coagulation profile, liver function and urea and electrolytes concentrations were unaffected by the method of treatment. We conclude that for total knee replacement, acute NVHD is an effective blood conservation strategy. However, there was no difference in allogeneic blood administration between the two NVHD groups. Coagulation and liver function, and urea and electrolyte concentrations were unaffected by treatment.      

Neurobehavioral effects of antihypertensive medications.

Although millions of hypertensive individuals receive chronic treatment with antihypertensive medication, the effect on the central nervous system by these drugs is poorly understood. Such treatment, while generally well tolerated, frequently produces symptoms of drowsiness, weakness, altered memory and impaired concentration. In addition to subjective evidence derived from patient reports, a large number of investigations have now been published which attempt to objectively assess the influence of antihypertensive medication on behavioral or cognitive performance. This paper summarizes and critically evaluates experimental studies of the effect of antihypertensive medication on subjects' performance of neuropsychological tasks and reviews the pharmacologic mechanisms by which these drugs may affect behavior. The literature is incomplete in its assessment of all domains of neuropsychological performance and all drug classes, and methodologic deficiencies are common. Nonetheless, the consensus of all studies and the findings of well-designed studies in particular do not identify any notable areas of performance impairment in patients receiving antihypertensive medication. Moreover, results suggest that, in certain instances, drug treatment may even enhance performance. In light of the limitations of the literature, however, an adequate understanding of the effects of antihypertensive therapy on behavioral functioning awaits completion of large, well-designed investigations including all major drug classes and thorough neurobehavioral assessments.     

Modulatory synaptic actions of an identified histaminergic neuron on the serotonergic metacerebral cell of Aplysia

Possible sources of excitatory synaptic input to the serotonergic metacerebral cell (MCC) were determined by stimulating various neurons in the cerebral ganglion. Firing of the previously identified histaminergic neuron C2 was found to produce synaptic input to the MCC. The synaptic input consists of fast excitatory-inhibitory synaptic potentials on a background of a slow EPSP. The slow EPSP appears to be monosynaptic and chemically mediated since it persists in a solution of high divalent cations; broadening of the presynaptic spike enhances the EPSP; the size of the EPSP is a function of the Mg2+ and Ca2+ concentrations of the bathing solution; and the EPSP can be mimicked by application of histamine to the MCC. The slow EPSP, in addition to firing the MCC, can increase the excitability of the cell, even under conditions in which C2 is fired at a rate too slow to produce a measurable EPSP when the MCC is at rest potential. This property appears to be due to the fact that the slow EPSP results from an apparent decrease of membrane conductance so that the size of the EPSP increases markedly as the cell is depolarized, and the EPSP appears to be highly voltage-dependent so that it is small or absent close to the rest potential of the MCC. When the MCC is voltage-clamped, application of histamine to the bath results in an inward current that disappears when the MCC is hyperpolarized. The potential at which the histamine-induced current reverses or disappears is dependent on the concentration of external potassium, suggesting that, at least in part, the slow EPSP is due to a decrease of potassium conductance. The data on C2 are consistent with its being an element of the neuronal system that mediates a state of food arousal in Aplysia.     

Clonal chromosomal abnormalities in cutaneous T-cell lymphoma

Chromosome analysis from stimulated and unstimulated lymphocytes of blood, skin, and lymph nodes demonstrated a clonal chromosomal abnormality in eight of 46 patients with cutaneous T-cell lymphoma (CTCL). Nonclonal abnormalities were found in nine other patients. Unstimulated lymph node cultures identified the highest proportion of clonal changes. Clonal changes were found most often in patients with advanced disease, and in patients who tested positive with a monoclonal antibody previously shown to detect the T-cells involved in CTCL. Analysis of the eight abnormal clones and seven others found before or since this consecutive series showed that identifiable changes involving the known sites of T-cell receptor genes on chromosomes #7 and #14 were not usually present. An association between CTCL and chromosome rearrangements of chromosome #10 is suggested both from our cases and those found in the literature. This observation is of interest because this chromosome contains the gene for the interleukin-2 receptor.     

Nitrous oxide withdrawal reduces intracranial pressure in the presence of pneumocephalus

Nitrous oxide anesthesia has been implicated as contributing to the development of delayed tension pneumocephalus following surgery performed in the sitting position. The authors tested the hypothesis that withdrawal of nitrous oxide anesthesia administered during formation of an intracranial gas cavity would lead to a decrease in intracranial pressure (ICP) as N2O diffuses from the cavity back into the blood. Ten halothane-anesthetized rabbits were prepared for measurement of supracortical ICP and arterial blood pressure (BP) and for intracranial volume alterations via a cisterna magna infusion catheter. Hyperventilation (Paco2 = 28-30 mmHg) and mannitol were used to shrink the brain to accommodate intracranial infusion of either air or lactated Ringer's (LR) solution, which was used to elevate ICP to between 10-15 mmHg from a baseline ICP of 2.1 +/- 2.5 mmHg over a period of 8 to 10 min. Following stabilization at an elevated ICP, inhalation of nitrous oxide (75%) was either initiated or withdrawn (if already present during the induced ICP increase) and the subsequent changes in mean ICP and BP were recorded. Following ICP elevation with LR to 10 +/- 1 mmHg, initiation of 75% N2O administration resulted in no change in ICP and modest increases (P less than 0.05) in BP and cerebral perfusion pressure (CPP = BP - ICP) after 4 min. However, when ICP was raised (to 12 +/- 3.5 mmHg) with intracranial air infusion, subsequent initiation of 75% N2O inhalation caused an abrupt ICP increase to 22.3 +/- 9 mmHg (from control P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Eyelid penetration of a hard contact lens, simulating a neoplasm

A hard contact lens penetrated the right upper lid at the level of the aponeurosis of the levator palpebral superior's muscle. Later tumor-like symptoms developed of a hard movable mass with blepharoptosis.