Biomedical subjects

N N Zwetnow

Publications and source records attributed to N N Zwetnow.

At least 19 recordsLinked to original sources

PubMed1997

MR imaging of experimental subdural bleeding. Correlates of brain deformation and tissue water content, and changes in vital physiological parameters.

PURPOSE: To evaluate morphological and physiological changes during acute lethal subdural bleeding in 2 models of anaesthetized dogs. MATERIAL AND METHODS: In model I, blood from the aorta was led into a collapsed subdural rubber balloon while in model II, the blood was directed into the subdural compartment over the left cerebral frontoparietal lobe. Eight vital physiological parameters were continuously registered. MR imaging visualized the compression and displacement of cerebral tissue, and assessed the dynamic changes in cerebral tissue water. RESULTS: In model I, tissue herniation and compression of cerebral ventricles led to death at a haematoma volume corresponding to 8% of the intracranial volume. In model II, the extravasated blood progressed infratentorially and into the spinal sac with a volume that was 3 times larger than that of the lethal haematoma. Tissue water increased almost linearly during bleeding in both models. CONCLUSION: The high level of mortality after acute subdural haematoma is caused by a reduction in intracranial volume tolerance with a critical decrease in cerebral perfusion pressure, resulting in a fatal cerebral ischaemia.

Animals↗

PubMed1993

Studies on supratentorial subdural bleeding using a porcine model.

A porcine model for an acute lethal arterial subdural bleeding in man is presented. Blood from the abdominal aorta was led via an electronic drop recorder into a collapsed intracranial subdural rubber balloon. Systemic arterial pressure (SAP), two intracranial pressures and 6 other vital parameters were monitored continuously in spontaneously breathing (n = 4) and mechanically ventilated (n = 4) pigs. In both animal groups bleeding caused an immediate rise in intracranial pressures (ICP) with transtentorial pressure gradients developing. As a result the cerebral perfusion pressures (CPP) decreased progressively, leading to an isoelectric EEG. In spontaneously breathing animals, the pressure changes resulted in apnoea within 2-4 minutes, irregularities in heart rhythm and in a marked rise in SAP (the Cushing reaction). A final collapse of all pressures occurred after 222 +/- 68 sec at a mean bleeding volume of 10.3 +/- 1.9 ml. In contrast, in mechanically ventilated animals, the course of bleeding was less dramatic. No change in cardiac rhythm or rise in SAP appeared despite a larger mean bleeding volume (12.0 +/- 1.6 ml). Instead, SAP slowly fell, reaching a level of approximately 40 mm Hg within 1 hour, while CPP concomitantly decreased from 120 mm Hg to 15 mm Hg. The findings in this and in a parallel study are explained in terms of the intracranial volume tolerance concept (Zwetnow et al. 1986). The beneficial effect of assisted ventilation on the course of subdural bleeding is multifactorial, involving both metabolic and mechanical mechanisms.

Animals↗

PubMed1993

Regional blood flow in brain and peripheral tissues during acute experimental arterial subdural bleeding.

The effects of a large intracranial arterial subdural bleeding on regional blood flow in the brain (rCBF) and in other body organs were studied, using a porcine model. The bleeding was produced by leading blood through a catheter from the abdominal aorta via an electronic drop recorder into the subdural compartment (SDC) over the left cerebral hemisphere. Pressures in the right lateral cerebral ventricle and in the cisterna magna were recorded along with 15 other vital parameters. Measurements of rCBF were carried out using radioactive microspheres 1) before the start of bleeding, 2) during the early bleeding phase, and 3) during the late bleeding phase. When the bleeding was initiated, the intracranial pressures rose within one minute to a level approximately 40 mmHg below the systemic arterial pressure, whilst the latter usually decreased 30-40 mmHg. In the subsequent early bleeding phase the cerebral perfusion pressure and the bleeding pressure fluctuated at a level of approximately 40 mmHg for several minutes. In the late bleeding phase, the perfusion pressure decreased maximally, even when a Cushing reaction was activated. During the early bleeding phase the changes in rCBF varied between the cerebral regions. However, the mean flow remained largely constant in the presence of a decreasing cerebrovascular resistance, indicating that autoregulation of CBF was intact. Concomitantly, cardiac output and heart rate decreased, whilst regional blood flow in extracerebral organs tended to increase, possibly due to an intracranial effect on the autonomic nervous system. In the late bleeding phase, rCBF was critically reduced in all regions, in spite of a marked rise in systemic arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1993

Changes in intracranial morphology, regional cerebral water content and vital physiological variables during epidural bleeding. An experimental MR study in dogs.

Epidural bleeding was produced in 8 anaesthetised and heparinised dogs by an artificial system. Changes in vital physiological variables were related to intracranial shifts and tissue water content assessed with MR imaging. Six animals survived while 2 succumbed. In the surviving animals intracranial shifts and compressions remained unchanged from an early stage. The cerebral perfusion pressure was reduced from between 80 and 110 mm Hg to between 40 and 60 mm Hg. Some increase in supratentorial white matter tissue water was observed. In the lethal experiments cerebral perfusion pressure fell to less than 40 mm Hg. Moreover, secondary delayed anatomical changes were seen including hydrocephalus. Increase in cerebral tissue water was more intense and widespread than in the survivors. These findings indicate that the outcome of epidural bleeding is related to cerebral perfusion pressure with secondary deterioration resulting from additional volume loading from increased tissue water and hydrocephalus.

Animals↗

PubMed1993

Progressive brain compression. Changes in vital physiological variables, correlated with brain tissue water content and brain tissue displacement. Experimental MR imaging in dogs.

Continuous recording of vital physiological variables and sequential MR imaging were performed simultaneously during continuous expansion of an epidural rubber balloon over the left hemisphere in anaesthetised dogs. Balloon expansion led to a progressive and slightly nonlinear rise in intracranial CSF pressures and a fall in local perfusion pressures. Changes in systemic arterial pressure, pulse rate, and respiration rate usually appeared at a balloon volume of 4% to 5% of the intracranial volume (reaction volume), together with a marked transtentorial pressure gradient and MR imaging changes consistent with tentorial herniation. Respiratory arrest occurred at a balloon volume of approximately 10% of the intracranial volume (apnoea volume), which was associated with occlusion of the cisterna magna, consistent with some degree of foramen magnum herniation. Increase in tissue water was observed beginning at approximately the reaction volume, presumably due to ischaemic oedema, due to the fall in perfusion pressures.

Animals↗

PubMed1992

Changes in CSF pressures during experimental acute arterial subdural bleeding in pig.

The effects of acute arterial subdural bleeding on cerebrospinal fluid (CSF) pressure and 12 other vital parameters were studied in spontaneously breathing pigs (group 1, n = 9) and in mechanically ventilated pigs (group 2, n = 18) to analyze quantitatively the bleeding course and the lethal mechanism. Spontaneously breathing animals all succumbed after a mean bleeding volume of 45.6 +/- 8.9 ml, corresponding to about 50 per cent of the intracranial volume, and a mean bleeding duration of 11.0 +/- 2.6 min. Rapid rise in CSF pressures, marked transtentorial pressure gradients, and progressive reductions of cerebral perfusion pressure leading to a permanently iso-electric EEG, apnoea and to a terminal rise in arterial pressure (Cushing response), was the rule in these animals. The mechanically ventilated animals had smaller bleeding volumes (34.3 +/- 8.1 ml), but longer bleeding durations (13.8 +/- 5.8 min). In this group 7 animals survived. They had no pressure gradients, and only moderate changes in arterial pressure and EEG. The 11 animals that succumbed had marked transtentorial pressure gradients, but smaller increments in arterial pressure than the spontaneously breathing animals. At autopsy, subdurally located blood was found throughout the intracranial and spinal subdural compartments and along the spinal nerve roots in both groups. The results of this study suggest that survival after acute subdural haematoma is influenced by the presence of transtentorial pressure gradients and by the spinal sac acting as a space for expansion. The beneficial effect of artificial ventilation is discussed.

Animals↗

PubMed1990

A quantitative study of some factors affecting the outcome of experimental epidural bleeding in swine.

During an experimentally induced aggressive epidural bleed the effect on outcome of haematoma volume, cerebral perfusion pressures, intracranial pressure gradients and ventilation were examined in a swine model. Two groups of experiments were performed using either spontaneous ventilation (group 1, n = 6) or mechanical ventilation for 1 hour (group 2, n = 7). The preparations were otherwise identical. An animal was considered to have succumbed when the EEG became irreversibly isoelectric within a total follow-up time of 80 minutes. Mechanical ventilation had a marked effect on survival. All spontaneously ventilated animals succumbed, 4 of them in less than 60 minutes, the remaining 2 between 60 and 80 minutes after the start of bleeding. All mechanically ventilated animals survived for the 60 minutes while the ventilator was connected. Following disconnection 2 animals started to breathe spontaneously and survived the final 20 minutes of the 80 minutes of the follow-up time. The remaining 5 succumbed following apnoea. The size of haematoma did not differ significantly between the groups. Two additional factors, hypoventilation and a secondary rise in supratentorial pressure, contributed to a lethal outcome. Hypoventilation was an inevitable precursor of the isoelectric EEG. There was a close correlation between the development of hypoventilation and intracranial herniation. A secondary rise in supratentorial pressure, unrelated to ventilation, was seen after cessation of bleeding in 8/13 cases. It was associated with a falling supratentorial perfusion pressure and EEG attenuation, suggesting a secondary intracranial expansion, possibly due to oedema, hydrocephalus or both. It is concluded that mechanical ventilation in the acute stage of epidural bleeding may be of clinical value.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Cerebral blood flow during experimental epidural bleeding in swine.

Regional cerebral blood flow (rCBF) was studied during an aggressive epidural bleed, using a ventilated swine model. rCBF, regional organ blood flow and cardiac output were measured using the radioactive microsphere technique. Blood flows were measured prior to the start of bleeding (Stage 1), when intracranial pressures had reached a plateau and supratentorial perfusion pressure was reduced by about 50% (Stage 2), and at isoelectric EEG (Stage 3). Supratentorial rCBF did not change significantly between stages 1 and 2 while rCVR decreased, implying autoregulatory activity. Cerebral ischaemia developed between stages 2 and 3 when rCBF values fell to levels between 20 and 50% of control values. Infratentorial rCBF changes were similar but less marked, so that adequate brain stem perfusion was maintained below the upper mesencephalon. The left temporal and left parietal cortex and upper mesencephalon suffered a greater reduction in rCBF than other regions, due to proximity to the haematoma and tentorial herniation. The supratentorial perfusion pressure at stage 2 was 60 mm Hg associated with a haematoma volume of 6% of the intracranial volume (ICV). The infratentorial perfusion pressure never fell below 60 mm Hg. The Cushing response was absent when the EEG became isoelectric. This is tentatively ascribed to the absence of hypoxia, because mechanical ventilation was used. Instead systemic arterial hypotension accompanied bleeding in this ventilated model. This hypotension was due to falling cardiac output and peripheral vasodilation.

Animals↗

PubMed1990

Rebound of ICP after brain compression. An MRI study in dogs.

The rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion was studied in an epidural balloon compression model. Intracranial morphology and brain tissue water content were assessed with magnetic resonance imaging (MRI). Fast and slow components of the transverse relaxation time (T2) were used as indicators of brain oedema development. During balloon compression a progressive prolongation of both the fast and the slow T2 components took place. Following deflation of the balloon both components increased rapidly, particularly the slow-T2. The MR scans displayed progressive occlusion of the aqueduct, and obliteration of the ambient and pontine cisterns. The changes in morphology and in water content after decompression had largely the same time course as the development of the rebound of ICP. In contrast, no changes in morphology and tissue water content occurred after hydrostatic brain compression achieved by subarachnoid fluid infusion. The findings suggest that the intracranial pressure rebound is caused by cerebral oedema accumulated during and particularly in the recirculation phase after an ischaemic injury of adequate intensity and adequate duration.

Animals↗

PubMed1990

Cerebral blood flow in experimental intracranial mass lesions. Part I: The compression phase.

We have shown that a rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion is a threshold phenomenon dependent upon the cerebral perfusion pressure (CPP) during compression and the duration of the compression. In the present study regional cerebral blood flow (rCBF) was measured during balloon compression of a degree critical for the development of a postdecompression rebound. The effects were compared with those of hydrostatically raised pressure which under similar conditions rarely produces a rebound of ICP. Disproportionately marked reductions in flow occurred in the hemisphere ipsilateral to the balloon, especially in white matter and in cortex adjacent to the balloon with flow values of, respectively, 1.1 +/- 0.9 and 6.4 +/- 3.4 ml 100 g-1 min-1. The differences in flow between balloon and hydrostatic compression were found to be due to an increased cerebrovascular resistance (CVR) caused by a direct compressive effect by the balloon overriding the generalized vasodilation which occurs in response to the raised ICP. Thus the increase in CVR attributable to compression by the balloon added to the reduction in CPP caused by the diffuse increase in ICP. As a consequence flow in large regions of the brain was reduced below the thresholds for structural infarction and for ischaemic damage to the blood-brain barrier.

Animals↗

PubMed1990

Cerebral blood flow in experimental intracranial mass lesions. Part II: The postdecompression phase.

Cerebral haemodynamics were evaluated after a period of cerebral compression produced by subarachnoid fluid infusion or inflation of an epidural balloon. Release of the compression resulted in a marked cerebral hyperperfusion which was generalized in the case of hydrostatically raised pressure but restricted to supratentorial structures after balloon compression. A rebound of intracranial pressure (ICP) occurred only after balloon compression, indicating that loss of vasomotor tone per se was not the primary reason for the rebound of ICP. In the balloon compression experiments the hyperaemia passed into a stage of hypoperfusion attributable in part to a reduction in cerebral perfusion pressure due to the rebound of ICP and in part to an increase in flow resistance probably related to external compression of the vascular bed by the accumulation of brain oedema. The observed flow changes, i.e. delayed hypoperfusion preceded by hyperaemia, were similar to those after temporary ischaemia, indicating that the rebound response is a non-specific postischaemic phenomenon.

Animals↗

PubMed1988

Analysis of the dynamics of experimental epidural bleeding in swine.

The effects on epidural bleeding of two major factors were studied in a swine model. These were detachment of the dura from the skull and an epidural arteriovenous shunt. Firstly the effect of differing degrees of detachment of dura was studied in the absence of a shunt. Secondly the effect of the shunt was examined with a constant degree of dural detachment. Increasing the degree of the detachment of the dural from the skull increased the rate and volume of bleeding. In addition the greater the degree of dural detachment from the skull the easier it was for further dura stripping to take place. The shunt reduced the epidural pressure and increased the bleeding pressure. Sometimes it reduced the force which, acting on the dura would strip more dura free, but never enough to preclude further dura stripping. Larger shunts were associated with a longer bleeding duration. It is concluded that the effects of dura detachment and the epidural shunt acting in concert can explain the delayed expansion of an epidural haematoma and are consistent with the known variability of clinical epidural haematomas.

Animals↗

PubMed1988

Regional cerebral blood flow during acute left ventricular failure in the dog: effect of converting enzyme inhibition.

Regional cerebral blood flow (rCBF) was studied in anesthetized dogs subjected to acute left ventricular failure and its treatment with enalaprilat (MK-422). When failure was induced a reduction in rCBF paralleling the reduction in systemic blood pressure was observed. After treatment rCBF did not change in spite of further blood pressure reduction. The results are explained by changes in vascular resistance of larger cerebral arteries. Vasoconstriction in these vessels during failure was counteracted by enalaprilat through reduction in circulating angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1986

Effects of continuously expanding intracranial lesions on vital physiological parameters. An experimental animal study.

The work described in this report confirms and extends the results described in a preliminary communication (Löfgren, J. and Zwetnow, N.N., Acta Neurol. Scand. (1970, 625) which examined the effects in cats of an expanding mass, in the form of an intracranial supratentorial balloon, on vital physiological parameters. In the present study, particular emphasis was placed on the possible significance of the rate of expansion of the mass in the range usually encountered in the clinical situation of intracranial haemorrhages. Results from the experiments on 37 cats and 8 dogs showed that changes in vital parameters appeared when the balloon had reached a volume of about 5% of the intracranial volume (the "reaction volume") while respiratory arrest occurred at an intracranial volume of about 10% (the "apnoea volume"). Both threshold volumes were independent of the rate of expansion within the range used. Alterations in EEG, heart rate, respiratory rate and systemic arterial pressure usually occurred simultaneously with the development of a transtentorial pressure gradient. When respiratory arrest occurred, the cerebral perfusion pressure was markedly reduced, usually to a value of about 30 mm Hg, suggesting that brain tissue ischaemia is an important component in the lethal mechanism underlying intracranial expanding lesions. It is proposed that the volume load tolerance of the organism towards an expanding intracranial lesion, as expressed by the reaction volume and the apnoea volume, may represent a biologically useful parameter potentially suitable for quantitative evaluation of adverse agents and therapeutic procedures.

Animals↗

PubMed1986

Magnetic resonance imaging of brain tissue displacement and brain tissue water contents during progressive brain compression. An experimental study in dogs.

Continuous recording of vital physiologic parameters and magnetic resonance imaging (MRI) was performed during continuous expansion of extradural rubber balloons in spontaneously ventilated anesthetized dogs. Initial physiologic changes appeared when the pontine cistern was compressed while respiratory arrest was regularly paralleled by marked tentorial and tonsillar herniation. Local increase in brain tissue water progressed during brain compression and was most marked in white matter of the brain. This was related to the regional decrease in cerebral perfusion pressure. The correlation between the morphologic and physiologic course of events during brain compression has a predictive value.

Animals↗

PubMed1986

Magnetic resonance imaging of water intoxication. An experimental study in dogs.

Sequential magnetic resonance imaging (MRI) was performed to correlate signs of herniation and increase in local brain tissue water content with continuous changes in vital physiologic parameters during progressive water intoxication in anaesthetized dogs. The intracranial pressure increase ultimately resulted in respiratory and cardiac arrest. MRI concomitantly showed an increase in local brain water content starting and dominating in the cerebral cortex but progressing to all parts of the central nervous system. The late appearance of transtentorial pressure gradients and of brain herniation suggests that development of cerebral edema occurs in at least two stages, an intracellular osmotic edema appearing first, being followed by an ischemic edema related to a progressive decrease in local perfusion pressure.

Animals↗

PubMed1986

Magnetic resonance imaging of cerebral compression and local brain tissue water content during continuous extradural bleeding. An experimental study in dogs.

Continuous recording of vital physiologic parameters and magnetic resonance imaging were performed during progressive extradural bleeding in spontaneously ventilated anesthetized dogs. The volume of the bleeding could exceed the intracranial volume by 500 per cent due to the formation of an extradural arteriovenous shunt. The rate of hematoma growth was dependent on the area of stripped dura. Midline shift, herniation and lateral ventricle compression occurred early, corresponding to changes in vital parameters. Local brain water increased non-linearly with white matter preceding gray matter. Water increase started first in the ipsilateral hemisphere followed by the contralateral hemisphere, brain stem and cerebellum. The correlation between local tissue water increase and local perfusion pressure supports the notion of an ischemic brain edema being formed during an extradural bleeding.

Animals↗

PubMed1986

Evaluation of intracranial pressure rebound after evacuation of intracranial expanding lesions. An experimental study in dogs.

Sequential magnetic resonance imaging was used to follow brain displacement, signs of herniation and increase in local brain tissue water content during expansion and after evacuation of an extradural balloon in anesthetized, artificially ventilated dogs. A fatal intracranial pressure (ICP) rebound occurred if the cerebral perfusion pressure (CPP) was critically reduced to 20 mm Hg for more than half an hour. Despite reduction of brain displacement after balloon evacuation brain water content continued to increase. Compression of CSF outflow pathways and signs of herniation remained. CPP continuously fell to zero. ICP rebound is a grave situation significantly influenced by a large increase in brain tissue water.

Animals↗