ABSTRACT
Subarachnoid hemorrhage (SAH) is associated with significant morbidity and mortality. We implemented an in-scanner rat model of mild SAH in which blood or vehicle was injected into the cistern magna, and applied multimodal MRI to study the brain prior to, immediately after (5min to 4h), and upto 7days after SAH. Vehicle injection did not change arterial lumen diameter, apparent diffusion coefficient (ADC), T2, venous signal, vascular reactivity to hypercapnia, or foot-fault scores, but mildly reduce cerebral blood flow (CBF) up to 4h, and open-field activity up to 7days post injection. By contrast, blood injection caused: (i) vasospasm 30min after SAH but not thereafter, (ii) venous abnormalities at 3h and 2days, delayed relative to vasospasm, (iii) reduced basal CBF and to hypercapnia 1-4h but not thereafter, (iv) reduced ADC immediately after SAH but no ADC and T2 changes on days 2 and 7, and (v) reduced open-field activities in both SAH and vehicle animals, but no significant differences in open-field activities and foot-fault tests between groups. Mild SAH exhibited transient and mild hemodynamic disturbances and diffusion changes, but did not show apparent ischemic brain injury nor functional deficits.
Subject(s)
Brain Mapping , Brain , Magnetic Resonance Imaging , Subarachnoid Hemorrhage/pathology , Animals , Brain/blood supply , Brain/diagnostic imaging , Brain/pathology , Disease Models, Animal , Hemodynamics , Image Processing, Computer-Assisted , Locomotion , Magnetic Resonance Angiography , Male , Radiography , Rats , Rats, Sprague-Dawley , Subarachnoid Hemorrhage/physiopathology , Time Factors , VasoconstrictionABSTRACT
The currently applied techniques recommended for the repair of pectus excavatum anomalies are discussed, set against a historical review of early clinical studies and surgical interventions. The issues of the future direction pectus excavatum surgery may take are analyzed in detail, with the reviewer expressing reservations in connection with the recent trend to closed repair and concern over the potential for serious complications associated with the application of this technique.
Subject(s)
Funnel Chest/history , Orthopedic Procedures/history , Plastic Surgery Procedures/history , Thoracic Surgical Procedures/history , Austria , Biocompatible Materials/history , Funnel Chest/surgery , History, 17th Century , History, 19th Century , History, 20th Century , History, 21st Century , History, Medieval , Humans , Orthopedic Fixation Devices/history , Orthopedic Procedures/methods , Prostheses and Implants/history , Plastic Surgery Procedures/methods , Plastic Surgery Procedures/trends , Spain , Sternum/surgery , Switzerland , Thoracic Surgical Procedures/methods , Thoracic Surgical Procedures/trends , Thoracic Wall/surgery , Treatment Outcome , United StatesABSTRACT
In the decades preceding the Fontan operation, there was an intensive experimental and clinical quest to bypass the right heart. Whereas right heart bypass was successfully achieved in animal experiments, clinically only partial bypass (superior cava-right pulmonary artery anastomosis) was applied successfully. This intensive experimental and clinical activity provided the background for the Fontan operation.
Subject(s)
Heart Bypass, Right/history , Animals , Fontan Procedure/history , History, 19th Century , History, 20th Century , HumansABSTRACT
It is hypothesised that oxidative stress is a key mechanism of ethanol neurobehavioural teratogenicity, resulting in altered endogenous antioxidant status and increased membrane lipid peroxidation in the hippocampus of chronic prenatal ethanol exposure (CPEE) offspring. To test this hypothesis, timed pregnant guinea-pigs (term, approximately gestational day (GD) 68) received chronic daily oral administration of (i) 4 g ethanol kg(-1) maternal bodyweight, (ii) isocaloric sucrose with pair feeding, or (iii) water. At GD 65 (term fetus) and postnatal day (PD) 0 (neonate), individual offspring were killed, the brain was excised and the hippocampi were dissected. Glutathione (GSH) concentration was measured in the cytosolic and mitochondrial fractions of hippocampal homogenate. The occurrence of lipid peroxidation was determined by measuring the concentration of 8-iso-prostaglandin F2+/- (8-iso-PGF2+/-). There was CPEE-induced decreased brain weight and hippocampal weight at GD 65 and PD 0, decreased mitochondrial GSH concentration in the hippocampus at PD 0, with no change in mitochondrial GSH concentration at GD 65 or cytosolic GSH concentration at GD 65 or PD 0, and no change in mitochondrial or whole-homogenate 8-iso-PGF2+/- concentration in the hippocampus at GD 65 or PD 0. The data demonstrate that CPEE produces selective mitochondrial dysfunction in the hippocampus of the neonatal guinea-pig, involving GSH depletion.
