Effects of prostacyclin, indomethacin, and heparin on cerebral blood flow and platelet adhesion after multifocal ischemia of canine brain.

نویسندگان

  • P M Kochanek
  • A J Dutka
  • K K Kumaroo
  • J M Hallenbeck
چکیده

Seven anesthetized dogs treated with prostaglandin I2, indomethacin, and heparin were compared with 12 controls to test the hypothesis that the salutary effect of treatment on recovery of neuronal function and cerebral blood flow (CBF) after ischemia is coupled to the inhibition of platelet accumulation. In this model of right hemisphere multifocal ischemia, cortical somatosensory evoked response (CSER) amplitude, 14C autoradiographic blood flow, and 111In-labeled platelet accumulation were measured. The ratio of injured to noninjured hemispheric 111In activity (cpm/g) provided an index of platelet accumulation. Treatment improved CBF of the injured hemisphere compared with control after 4 hours of reperfusion (74 +/- 17 versus 53 +/- 13 ml/100 g/min, p less than 0.05), and it enhanced recovery of CSER amplitude (percent of baseline) after 1 hour of reperfusion compared with control (27.1 +/- 4.7% [treatment] versus 15.5 +/- 2.8% [control], p less than 0.05). However, the effect on CSER was not sustained after 4 hours of recovery. Despite these effects on CSER and CBF, treatment failed to inhibit 111In-labeled platelet accumulation in the injured hemisphere (1.7 +/- 0.3% [treatment] versus 1.5 +/- 0.1% [control], p greater than 0.05). Platelets may adhere to damaged endothelium despite aggressive platelet antiaggregant therapy.

برای دانلود 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

Indomethacin, prostacyclin, and heparin improve postischemic cerebral blood flow without affecting early postischemic granulocyte accumulation.

Six anesthetized dogs treated with indomethacin, prostacyclin (PGI2), and heparin were compared with 7 anesthetized controls (ischemia without treatment) to determine whether cyclooxygenase inhibition would lead to enhanced granulocyte accumulation because of preferential formation of lipoxygenase products. Cortical somatosensory evoked response, [14C]iodoantipyrine autoradiographic blood flow,...

متن کامل

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

Effect of Pentoxifylline on Ischemia- induced Brain Damage and Spatial Memory Impairment in Rat

Objective(s) The brief interruption of cerebral blood flow causes permanent brain damage and behavioral dysfunction. The hippocampus is highly vulnerable to ischemic insults, particularly the CA1 pyramidal cell layer. There is no effective pharmacological strategy for improving brain tissue damage induced by cerebral ischemia. Previous studies reported that pentoxifylline (PTX) has a neuroprot...

متن کامل

Acute nicotine treatment accelerates photochemically induced platelet aggregation in cerebral arterioles of mice: an in vivo study

When tobacco is smoked, chewed or snuffed, nicotine is absorbed by the lungs or mucous membrane and quickly moved into the bloodstream, where it is circulated throughout the brain. In fact nicotine is highly dangerous to be consumed in any form. The present study was conducted to know the adverse effects of nicotine on the platelet aggregation in cerebral microvessels of mice. Male mice of aver...

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

ذخیره در منابع من


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

برای دانلود 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

عنوان ژورنال:
  • Stroke

دوره 19 6  شماره 

صفحات  -

تاریخ انتشار 1988