Biomedical subjects

F Tabibnia

Publications and source records attributed to F Tabibnia.

4 recordsLinked to original sources

PubMed2002

Traumatic subarachnoidal hemorrhage in the developing rat.

The aim of the present study was to utilize an experimental traumatic subarachnoidal hemorrhage model in the developing rat. Diffuse brain injury was produced in intubated and ventilated 21 to 25 days old Sprague-Dawley rats (N = 10) using a modification (1 m/100 g) of the Marmarou-model. Before induction of the injury heparin was administered i.v. and antagonised after injury by protamine. Mean arterial blood pressure and intracranial pressure was measured continuously. Histopathological investigations were performed. The results were compared to readings in adult animals (N = 12) subjected to a 1.5 m/500 g injury. In the developing rat ICP increased immediately following injury from 11.4 +/- 2.1 mm Hg to 55.9 +/- 20.3 mm Hg. It remained elevated till the end of the experiment 1 h after injury. MABP increased from 79.8 +/- 8.7 mm Hg to 100.2 +/- 21.7 mm Hg immediately following injury, returning to 61.3 +/- 28.7 mm Hg at the end of the experiment resulting in a marked decrease of CPP. The mortality rate was 60%. All brains showed a severe subarachnoidal hemorrhage in the basal cisterns. The increase of ICP following injury is attributable to the bleeding similar as in adult animals. The high mortality is due to the marked decrease of CPP. Rat pups are more vulnerable to t-SAH compared to adult rats.

Aging↗

PubMed2000

ICP and MABP following traumatic subarachnoid hemorrhage in the rat.

Traumatic subarachnoidal hemorrhage (t-SAH) is a common finding in head-injured patients occurring with a frequency of 39% according to data of the Traumatic Coma Data Bank. The present study is the first description of a t-SAH-model with particular emphasis on patterns of intracranial pressure (ICP) changes and mean arterial blood pressure (MABP) response. Diffuse brain injury was produced in intubated and ventilated adult Sprague-Dawley rats (N = 24) using a brass weight (500 gm) free falling from a predetermined height (1.5 m) on a steel disc glued to the skull of the rat. Before induction of the injury, heparin was administered intra-arterially (i.a.) and antagonised after injury by protamine. MABP-recordings and ICP-recordings were performed continuously. Histopathology was undertaken. Following injury MABP decreased from 138 +/- 14 mmHg to 89 +/- 22 mmHg. During 5 to 15 min ICP increased up to 89.4 +/- 50.4 mmHg, decreasing slowly within 60 min in surviving animals. The mortality rate was 41.6%. All brains showed a severe subarachnoid hemorrhage in the basal cisterns and cell-loss within the brainstem. Experimental t-SAH is possible. Following t-SAH there is a subacute increase of ICP due to the actual bleeding. The model may provide deeper understanding in the basic physiological patterns of t-SAH.

Animals↗

PubMed2000

Influences of secondary injury following traumatic brain injury in developing versus adult rats.

Hypoxia and hypotension are both common findings following traumatic brain injury occurring with a frequency of up to 46% according to data of the Traumatic Coma Data Bank. In the present study the influence of secondary injury on intracranial pressure and the cardiovascular response is investigated in developing rats. Differences from adult rats are determined. Diffuse brain injury was produced in intubated and ventilated 17-20 days old Sprague-Dawley rats (N = 16) using a modification of the Marmarou-model. Hypoxia was induced by reducing O2-concentration to 8% lasting for 15/30 min. Mean arterial blood pressure recordings and intracranial pressure recordings were performed continuously. Animals were divided into two groups, sustaining hypoxia alone (N = 9) and trauma/hypoxia (N = 7). The results were compared to readings in adult animals subjected to hypoxia (N = 5) and trauma/hypoxia (N = 5) (450 gm/150 cm). Immediately following the onset of hypoxia in the developing rat, MABP decreased from 76.5 +/- 13 mm Hg to 35.8 +/- 7 mm Hg. In the adult rat the decrease was more marked (from 93.3 +/- 8 mm Hg to 33.5 +/- 5.7 mm Hg) (p < 0.05). Mortality rate in developing rats with trauma/hypoxia was 43% with no significant change of ICP (from 13 +/- 5.2 to 22.3 +/- 11). All adult animals recovered following trauma/hypoxia with no relevant ICP-increase within one hour post-trauma. Hypoxia induces hypotension in adult and developing rats. However, developing rats appear to be more vulnerable to hypoxia associated with trauma.

Age Factors↗

PubMed1998

Traumatic brain injury in the developing rat pup: studies of ICP, PVI and neurological response.

Diffuse brain swelling is a common complication in young victims of a seven head injury but, there is a lack of data on relevant models of injury. We produced diffuse brain injury in 21 day old Lewis rat pups (N = 33) by modifying a recently established weight-drop-model. The trauma threshold, neurological response, histological changes, intracranial pressure (ICP), and arterial blood pressure (ABP) were determined. In addition, the pressure-volume-index (PVI) was measured 15 min before, 2 min, and 1 h after brain injury. In the 1 m/100 g group 4 of 5 rats died, whereas in the 0.5 m/100 g only 4 of 28 died. The PVI increased at 2 min after traumatic brain injury (TBI) but ICP was unchanged, except for a minor increase immediately after injury. Histological studies revealed diffuse neuronal death, predominantly involving the cortex and hippocampus. The results of the present study indicate that determination of ICP in the developing rat pup during and after diffuse brain injury is possible. A 0.5 m/100 g weight-drop-trauma results in a morphologically severe injury but with low mortality. The increase in PVI can be attributed to a decrease of cerebral perfusion pressure (CPP) after injury. However, the absence of a further increase of ICP after injury in the developing rat indicates that this may not be a primary consequence of injury in paediatric patients.

Age Factors↗