https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:39452 Wed 29 Mar 2023 14:38:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43990 Wed 29 Mar 2023 14:36:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40646 Wed 29 Mar 2023 14:12:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52020 Wed 27 Sep 2023 09:54:11 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29687 p = 0.03). Infarct and edema volumes were not significantly different between groups. These data demonstrate ICP may also increase 24 h post-stroke in aged rats, and that short-duration hypothermia treatment has a profound and sustained preventative effect. These findings may have important implications for the use of hypothermia in clinical trials of aged stroke patients.]]> Wed 19 Jan 2022 15:19:48 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24428 140 years. More widespread use of advanced clinical imaging in the past decade has led to increasing recognition of the key importance of collaterals in ischemic stroke outcome. However, recent studies from several groups indicate that failure of initially good collateral supply is a key feature of patients with delayed infarct expansion. This clinically challenging problem typically occurs in the first 1 to 2 days after hospital admission in patients with initially mild stroke symptoms. Rethrombosis of reperfused vessels was previously thought to be the likely cause of delayed infarct expansion in most patients. However, this theory is not supported by more recent evidence from imaging studies. Despite the important recent observations, there is limited understanding of the dynamic control of the collateral circulation, in particular, the cause of collateral blood flow failure. In this article, we will discuss recent observations from our experimental stroke model, indicating a dramatic increase in intracranial pressure (ICP) occurring around 24 hours after onset of even small stroke. We have also shown a significant linear reduction of collateral blood flow in response to progressive ICP elevation. We believe that a similar transient ICP elevation occurring during the first 1 to 2 days post stroke is a likely mechanism to explain delayed infarct expansion in patients with minor stroke. Perhaps surprisingly, we can find no published data on ICP at 24 hours in patients with minor stroke. The preclinical findings suggest that gathering such data should be a priority.]]> Wed 19 Jan 2022 15:18:00 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47149 P<0.05). Rapamycin dilated leptomeningeal anastomoses by 80±9%, which was abolished by nitric oxide synthase inhibition. In spontaneously hypertensive rats, rapamycin increased collateral perfusion by 32±25%, reperfusion cerebral blood flow by 44±16%, without reducing acute infarct volume 2 hours postreperfusion. Reperfusion cerebral blood flow was a stronger predictor of brain damage than collateral perfusion in both Wistar and spontaneously hypertensive rats. Conclusions: Rapamycin increased collateral perfusion and reperfusion cerebral blood flow in both Wistar and comorbid spontaneously hypertensive rats that appeared to be mediated by enhancing eNOS activation. These findings suggest that rapamycin may be an effective acute therapy for increasing collateral flow and as an adjunct therapy to thrombolysis or thrombectomy to improve reperfusion blood flow.]]> Wed 14 Dec 2022 15:27:41 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16985 Wed 11 Apr 2018 15:07:10 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22101 Wed 11 Apr 2018 10:59:34 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16993 450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.]]> Wed 11 Apr 2018 09:23:28 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52178 Wed 04 Oct 2023 11:05:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54067 Tue 30 Jan 2024 13:56:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42682 Thu 01 Sep 2022 08:45:21 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53129 Fri 17 Nov 2023 12:17:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53077 Fri 17 Nov 2023 12:03:34 AEDT ]]>