Effect of Platelet Activation on Coronary Collateral Blood Flow

Abstract

Background-The platelet products thromboxane A 2 and serotonin have been shown to cause constriction of welldeveloped coronary collateral vessels. This study was performed to determine whether intravascular platelet activation produced with platelet activating factor (PAF) can cause a decrease in coronary collateral blood flow. Methods and Results-Collateral vessel growth was induced by embolization of a hollow stainless steel plug into the left anterior descending coronary artery (LAD) of adult dogs. The animals were returned to the laboratory 3 to 6 weeks later for surgical instrumentation and measurement of collateral blood flow. Collateral flow was assessed by measuring retrograde blood flow from the cannulated collateral-dependent artery. PAF (10 nmol) was injected into the left main coronary artery to allow products of platelet activation to reach collateral vessels arising from the left coronary system. PAF caused a vasoconstrictor response, which became maximal 3 minutes after injection and resulted in a 40.3Ϯ7.4% decrease in retrograde blood flow (32.1Ϯ2.1 to 19.6Ϯ3.2 mL/min; PϽ0.05). By 15 minutes after the PAF injection, both retrograde blood flow and transcollateral resistance had returned to normal. After pretreatment with the thromboxane A 2 receptor antagonist SQ30,741, the vasoconstrictor response to PAF was abolished and, in contrast to the decrease in retrograde blood flow from PAF alone, a weak vasodilator effect was unmasked. Conclusions-PAF caused a decrease in coronary collateral blood flow. This vasoconstrictor response required the participation of thromboxane A 2 .

A curve model for association of serum homocysteine with carotid artery hemodynamics

“…In addition, Mohan et al [22] suggested that exposure to Hcy could induce platelet activation and hypercoagulability. Since platelet activating factor can reduce reducing coronary blood flow [23], these results indicate that Hcy may affect hemodynamics.…”

Increased platelet-activating factor-induced periventricular brain microvascular constriction associated with immaturity

“…PAF is an important phospholipid with diverse physiological and pathological roles in vivo, including effects on circulation (5,22,30). Due to its potent actions on blood vessels, PAF might be a putative mediator in ischemic brain injury (25,26).…”

“…PAF exerts its effects by interacting with a specific PAF receptor (30). Depending on the species and tissues, PAF causes constriction or dilation according to different coupling mechanisms (5,22,26). For instance, PAF is a potent constrictor of cerebral arterioles in newborn pigs (5) and produces vasodilatation in mesenteric circulation in dogs (30).…”

“…The production and release of PAF in the brain have been reported under various pathological conditions, including oxidant stress-induced ischemic injury in newborn (4,25). PAF is a modulator of vasomotor tone and induces pulmonary, coronary, and cerebral vasoconstriction (5,10,22). The mechanism of the vascular action of PAF is controversial, but many investigators have shown that some of its effects might be mediated through the formation of cyclooxygenase products of arachidonic acid metabolism in response to activation of PAF receptors (11,22).…”

“…PAF is a modulator of vasomotor tone and induces pulmonary, coronary, and cerebral vasoconstriction (5,10,22). The mechanism of the vascular action of PAF is controversial, but many investigators have shown that some of its effects might be mediated through the formation of cyclooxygenase products of arachidonic acid metabolism in response to activation of PAF receptors (11,22). However, the direct effects of PAF on brain intraparenchymal vasculature, implicated in the genesis of periventricular ischemic encephalopathies, remain unknown.…”