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Biomedical subjects

D Freilich

Publications and source records attributed to D Freilich.

7 recordsLinked to original sources

Coagulation patterns following haemoglobin-based oxygen carrier resuscitation in severe uncontrolled haemorrhagic shock in swine.

Massive blood loss due to penetrating trauma and internal organ damage can cause severe haemorrhagic shock (HS), leading to a severely compromised haemostatic balance. This study evaluated the effect of bovine polymerized haemoglobin (Hb) (Hb-based oxygen carrier, HBOC) resuscitation on haemostasis in a swine model of uncontrolled HS. Following liver injury/HS, swine received HBOC (n= 8), Hextend (HEX) (n= 8) or no resuscitation (NON) (n= 8). Fluids were infused to increase mean arterial pressure above 60 mmHg and to reduce heart rate to baseline. At 4 h, the animals were eligible for blood transfusions. Prothrombin time (PT), activated partial thromboplastin time, fibrinogen, thromboelastography (TEG) and platelet function analyser closure time (PFA-CT) were compared by using mixed statistical model. At 4 h, blood loss (% estimated blood volume) was comparable for HBOC (65.5 +/- 18.5%) and HEX (80.8 +/- 14.4%) and less for NON (58.7 +/- 10.1%; P < 0.05). Resuscitation-induced dilutional coagulopathy was observed with HBOC and HEX, as indicated by reduced haematocrit, platelets and fibrinogen (P < 0.05). At 4 h, PT was higher in HEX than in HBOC groups (P < 0.01). In the early hospital phase, a trend to increased TEG reaction time and PFA-CT indicates that dilutional effects persist in HBOC and HEX groups. PFA-CT returned to baseline later with HBOC than with HEX (48 vs. 24 h) following blood transfusion. At 4 h, all surviving HEX animals (n= 3) required transfusion, in contrast to no HBOC (n= 7) or NON (n= 1) animals. In this severe uncontrolled HS model, successful resuscitation with HBOC produced haemodilutional coagulopathy less than or similar to that produced by resuscitation with HEX.

Abdominal Injuries↗

Decreased lactic acidosis and anemia after transfusion of o-raffinose cross-linked and polymerized hemoglobin in severe murine malaria.

Severe anemia is a major cause of death in falciparum malaria. Blood transfusion increases survival in humans and in animal models of this disease. Because of logistic constraints and viral contamination of the blood supply, transfusions are frequently not practical in endemic regions. Modified hemoglobin is an effective O2 carrier in hemorrhagic shock. It is free of infectious contamination, may not require refrigeration, and because of its nitric oxide scavenging and small size, may have pharmacologic benefits in malaria. The effects of transfusions of modified hemoglobin in rats with high-grade parasitemia were evaluated. Modified hemoglobin decreased lactic acidosis and corrected anemia as well as transfusions with red blood cells; these findings may correlate with improved survival and suggest a possible proerythropoietic effect. Further study of this novel therapy is warranted.

Acidosis, Lactic↗

Is it migraine?

BACKGROUND: Migraine is a common disorder affecting 8-10% of the population. It results in significant morbidity and has social and economic consequences. Vascular and neurogenic mechanisms are involved in the genesis of migraine. Serotonin plays an important part. Attacks are brought on by internal (not identified) and external (identified) trigger factors in people predisposed to the condition, often on an hereditary basis. OBJECTIVE: The diagnosis of migraine depends on the recognition of the features specific to the condition. This article aims to define these features. DISCUSSION: There are diagnostic criteria which define the two main types of migraine--migraine with aura and migraine without aura. The variants of migraine need to be recognised and migraine needs to be distinguished from cluster headache. It is also important to recognise and exclude sinister causes of headache. Treatment is not discussed.

Adult↗

Time course of alpha-1-acid glycoprotein and its relation to myocardial enzymes after acute myocardial infarction.

The acute phase reactant, alpha-1-acid glycoprotein, binds to a number of basic antiarrhythmic drugs, including lidocaine, quinidine, propranolol, imipramine and disopyramide. Binding to alpha-1-acid glycoprotein accounts for a decrease in free drug fraction and may alter the expected concentration: response relation of drugs particularly when there are unpredictably large or rapid changes in alpha-1-acid glycoprotein. To determine the time course and magnitude of alpha-1-acid glycoprotein for 1 month after acute myocardial infarction (AMI), blood samples were collected from 27 patients, 14 with AMI and 13 with a chest pain syndrome but no AMI. Patients with AMI had a significant increase in alpha-1-acid glycoprotein after 72 hours (mean 153 +/- 35 mg/dl) (p less than 0.05), and the maximum was observed on day 7 (mean 165 +/- 53 mg/dl) (p less than 0.05), returning to baseline by 28 days. There was no significant change in alpha-1-acid glycoprotein in patients with chest pain but no AMI. Regression analysis showed a significant relation between creatine kinase (p less than 0.005) and lactic dehydrogenase (p less than 0.001) vs alpha-1-acid glycoprotein indicating alpha-1-acid glycoprotein concentration is high in patients with large AMI. Changes in binding resulting from alpha-1-acid glycoprotein during AMI could account for misinterpretation of total drug concentration and response to antiarrhythmic drugs acutely, during convalescence and at discharge.

Adult↗

Cauda equina lesion due to thorotrast.

Thorotrast (Thorium dioxide) has been used in the past as a radiological contrast medium. Its use resulted in serious side-effects, often after a delay of many years. There was an increased incidence of tumours and blood dyscrasias. Meningeal fibrosis, hydrocephalus and progressive lesions of the cauda equina have followed its injection into the sub-arachnoid spaces. A patient with such a cauda equina lesion is reported.

Cauda Equina↗

Diagnosis and management of tuberculous paraplegia with special reference to tuberculous radiculomyelitis.

Paraplegia occurred in eight of 17 patients with central nervous system tuberculosis. In six of these paraplegia was the presenting feature. Paraplegia may complicate tuberculous meningitis, or vertebral tuberculosis, but it may also occur, as in three of our cases, as a primary localised spinal tuberculous radiculomyelitis. These cases are presented in relation to the concept that paraplegia complicating these forms of tuberculosis is caused by radiculomyelitis.

Adolescent↗

16alpha-bromoepiandrosterone, a dehydroepiandrosterone (DHEA) analogue, inhibits Plasmodium falciparum and Plasmodium berghei growth.

Dehydroepiandrosterone (DHEA) and its analogue, 16alpha-bromoepiandrosterone (alpha-epi-Br), may have activity against viral and parasitic infections, including human immunodeficiency virus (HIV) and Cryptosporidium parvum. Therefore, we evaluated its antimalarial effects on Plasmodium falciparum and Plasmodium berghei. In vitro, chloroquine (CQ)-sensitive and resistant strains of P. falciparum parasitized red blood cells were incubated with escalating doses of alpha-epi-Br or CQ. In vivo, 62 rats were infected with P. berghei and treated with CQ or alpha-epi-Br. At the highest doses tested against a CQ-sensitive strain, parasitemias decreased from 25.4% in the saline control group to 4.3% and 4.8% in the alpha-epi-Br and CQ groups, respectively (P < 0.05). Against two CQ-resistant strains, parasitemias decreased from 22.3-28.8% and 24.8-30% in the CQ and saline groups, respectively, to 2.5-2.7% in the alpha-epi-Br groups (P = 0.003). In vivo, on Day 4, parasitemias decreased from 23% in the saline group to 9-12% and 12% in the in alpha-epi-Br and CQ groups, respectively (P < 0.05). These data demonstrate that alpha-epi-Br shows activity against CQ-sensitive and resistant strains of P. falciparum in vitro. At the doses tested against P. berghei in vivo in rats, alpha-epi-Br is comparable to CQ.

Androsterone↗