Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

نویسندگان

  • E T MacKenzie
  • S Strandgaard
  • D I Graham
  • J V Jones
  • A M Harper
  • J K Farrar
چکیده

Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Intensification of brain injury and blood-brain barrier permeability by short-term hypertension in experimental model of brain ischemia/reperfusion

Introduction: Arterial hypertension is one of the causes of stroke, and as one of the vasculotoxic conditions intensifies ischemic stroke complications. The aim of the present study was to analyze the effects of short-term cerebral hypertension on ischemia/reperfusion injury and pathogenesis of ischemic stroke. Methods: The experiments were performed on three groups of rats (N=36) Sham, cont...

متن کامل

Contribution of Nitric Oxide Synthase (NOS) Activity in Blood-Brain Barrier Disruption and Edema after Acute Ischemia/ Reperfusion in Aortic Coarctation-Induced Hypertensive Rats

Background: Nitric oxide synthase (NOS) activity is increased during hypertension and cerebral ischemia. NOS inactivation reduces stroke-induced cerebral injuries, but little is known about its role in blood-brain barrier (BBB) disruption and cerebral edema formation during stroke in acute hypertension. Here, we investigated the role of NOS inhibition in progression of edema formation and BBB d...

متن کامل

Inhibition by ketanserin of serotonin induced cerebral arteriolar constriction.

We studied the effects of serotonin on pial arterioles in anesthetized cats equipped with acutely implanted cranial window for the observation of the pial microcirculation. Serotonin topically applied caused cerebral arteriolar constriction. Ketanserin, a specific 5-HT2 inhibitor, completely blocked the vascular response of serotonin. Aggregated platelet supernatant was topically applied and ca...

متن کامل

Response of cerebral arteries to sympathetic stimulation during acute hypertension.

Our goal was to determine whether sympathetic stimulation during acute hypertension constricts large cerebral arteries and attenuates increases in cerebral microvascular pressure. We measured cerebral blood flow with microspheres and pressure in small pial arteries with a servonull device in anesthetized cats. During moderate hypertension, sympathetic stimulation had little effect on resistance...

متن کامل

Combinational therapy using hypothermia and the immunophilin ligand FK506 to target altered pial arteriolar reactivity, axonal damage, and blood-brain barrier dysfunction after traumatic brain injury in rat.

This study evaluated the utility of combinational therapy, coupling delayed posttraumatic hypothermia with delayed FK506 administration, on altered cerebral vascular reactivity, axonal injury, and blood-brain barrier (BBB) disruption seen following traumatic brain injury (TBI). Animals were injured, subjected to various combinations of hypothermic/FK506 intervention, and equipped with cranial w...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Circulation research

دوره 39 1  شماره 

صفحات  -

تاریخ انتشار 1976