Collateral Perfusion Pressure Research Articles

Abstract WP45: Outcomes of Patients With Cerebral Large Vessel Occlusions Undergoing Mechanical Endovascular Revascularization Based on the Quantification of Pial Collateral Perfusion

Introduction: Patient outcomes after Mechanical Endovascular Revascularization (MER) are dependent on both patient-specific and procedure-specific factors. The pial collateral perfusion to the ischemic penumbra during a cerebral large vessel occlusion (LVO) is one of the most important factors in overall patient outcome. Using our technique of Quantifying of Pial Collateral Perfusion (QPCP) previously described, patient outcomes after MER for cerebral LVO were assessed. Methods: Fifty consecutive patients with proximal middle cerebral artery M1 occlusions for whom QPCP were recorded were included in the study. In addition to patient demographics, the primary outcomes investigated were National Institutes of Health Stroke Scale (NIHSS) scores post-procedure reduction compared to pre-procedure score, and modified Rankin Scale (mRS) score at 30-day and 3-month follow-up. In addition, overall stroke volume, time spent in hospital, and the incidence of hemorrhagic conversion were also assessed. Regression models were used to estimate the association between pial collateral perfusion pressure and the above outcomes. Results: Patients demonstrated for every 5-unit increase in pial collateral perfusion pressure (measured in mmHg) an association with a 0.54-unit decrease in the post-procedure NIHSS score with a P-value of 0.07 (β= -0.54; 95% CI -1.12,0.03). A 5-unit increase in pial collateral perfusion pressure was also associated with 11% lower odds of having a 30-day mRS of 4-5 vs. 0-1 or 2-3 with a P-value of 0.18 (OR=0.89; 95% CI 0.75,1.06). A higher pial collateral perfusion pressure was also associated with a 0.07-unit decrease in the log of the stroke volume (P-value - 0.32). There was no association with higher pial collateral perfusion pressure and incidence of hemorrhagic conversion on post-procedure imaging. Conclusions: The QPCP is an objective measure for predicting patient outcomes after MER for cerebral LVO. Higher pial collateral perfusion pressures are associated with greater improvements in post-reperfusion NIHSS scores and 30-day mRS scores.

Current strategies of spinal cord protection during thoracoabdominal aortic surgery.

Despite improved survival rates after thoracoabdominal aortic aneurysm repairs, paraplegia remains a devastating complication with high incidence, ranging from 3 to 10%. Ischemic insults to the spinal cord are unavoidable during thoracoabdominal aortic aneurysm repairs. There is no single measure that can prevent paraplegia alone. A multimodality approach is required to minimize the ischemic insults during thoracoabdominal aortic aneurysm repairs and postoperative second hit to the spinal cord. Distal aortic perfusion is important to maintain the collateral network perfusion pressure, while cerebrospinal drainage allows to directly maintain the spinal cord perfusion. Reattachment of segmental arteries T8-T12 is encouraged to lower the incidence of both immediate and delayed paraplegia. Systemic arterial pressure should be maintained above 130mmHg and cerebrospinal drainage should be continued until the second postoperative day, despite intact neurological status. In this article, we describe our current operative techniques and perioperative management in patients undergoing repairs of thoracoabdominal aortic aneurysm. A review of recent updates on spinal protection strategies is also reported.

Diabetes Diminishes the Portal-Systemic Collateral Vascular Response to Vasopressin via Vasopressin Receptor and Gα Proteins Regulations in Cirrhotic Rats

Liver cirrhosis may lead to portal-systemic collateral formation and bleeding. The hemostatic effect is influenced by the response of collateral vessels to vasoconstrictors. Diabetes and glucose also influence vasoresponsiveness, but their net effect on collaterals remains unexplored. This study investigated the impact of diabetes or glucose application on portal-systemic collateral vasoresponsiveness to arginine vasopressin (AVP) in cirrhosis. Spraque-Dawley rats with bile duct ligation (BDL)-induced cirrhosis received vehicle (citrate buffer) or streptozotocin (diabetic, BDL/STZ). The in situ collateral perfusion was done after hemodynamic measurements: Both were perfused with Krebs solution, D-glucose, or D-glucose and NaF, with additional OPC-31260 for the BDL/STZ group. Splenorenal shunt vasopressin receptors and Gα proteins mRNA expressions were evaluated. The survival rate of cirrhotic rats was decreased by STZ injection. The collateral perfusion pressure changes to AVP were lower in STZ-injected groups, which were reversed by OPC-31260 (a V2R antagonist) and overcome by NaF (a G protein activator). The splenorenal shunt V2R mRNA expression was increased while Gα proteins mRNA expressions were decreased in BDL/STZ rats compared to BDL rats. The Gαq and Gα11 mRNA expressions also correlated with the maximal perfusion pressure changes to AVP. Diabetes diminished the portal-systemic collateral vascular response to AVP in rats with BDL-induced cirrhosis, probably via V2 receptor up-regulation and Gα proteins down-regulation.

Effects of simvastatin on the portal-systemic collateral vascular response to endothelin-1 and shunting degree in portal hypertensive rats

Objective. Endothelin-1 (ET-1) exerts vasoconstrictive effect on portal-systemic collateral vascular bed of portal hypertensive rats. Statins are lipid-lowering agents with nitric oxide (NO)-related vasodilatory effects. Considering NO-associated vascular hyporesponsiveness to vasoconstrictors and shunting formation in portal hypertension, this study investigated the effects of simvastatin on 1) the portal-systemic collateral vascular responsiveness to ET-1 and 2) the portal-systemic shunting degree. Materials/methods.Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Simvastatin (20 mg/kg/day) or distilled water (control) was randomly administered by oral gavage since 2 days prior to until 7 days after PVL. Systemic and portal hemodynamics were measured on the 8th day. In another series, collateral perfusion with Krebs solution at different flow rates was performed to get flow–pressure curves which serve as an index of shunting degree. To survey the direct vascular effect, PVL rats randomly underwent preincubation with 1) Krebs solution, that is, the control group; or Krebs solution plus 2) simvastatin; 3) simvastatin + Nω-nitro-l-arginine (NNA, a NO synthase inhibitor); 4) simvastatin + indomethacin (a cyclooxygenase inhibitor), followed by ET-1 to evaluate the collateral vascular responsiveness. Results. Chronic simvastatin treatment significantly reduced portal pressure. The flow–pressure curves were similar between two groups. Simvastatin preincubation reduced collateral perfusion pressure changes to ET-1 (p < 0.05), which were partially reversed by NNA (p < 0.05), but not by indomethacin. Conclusions.Chronic simvastatin treatment significantly improved portal hypertension. The effect was at least partially exerted by decreased portal-systemic collateral vascular resistance through NO-mediated vascular hyporesponsiveness. The severity of portal-systemic collaterals was not influenced by simvastatin.

Correlation of Intraoperative Collateral Perfusion Pressure During Carotid Endarterectomy and Status of the Contralateral Carotid Artery and Collateral Cerebral Blood Flow

The optimal method for predicting when carotid shunting is not necessary during carotid endarterectomy (CEA) is controversial. This study will analyze the correlation of collateral perfusion pressure and the status of contralateral carotid/cerebral collaterals and determine whether preoperative duplex ultrasound/cerebral angiography can predict when CEA can be done without shunting. Ninety-eight patients were randomized into routine shunting and 102 into selective shunting when the collateral perfusion pressure (systolic carotid stump pressure) was <40 mm Hg during CEA. All patients had preoperative carotid duplex ultrasound and 87 had angiography, the results of which were evaluated for the presence of collateral flow from the contralateral carotid artery or posterior circulation through the anterior and/or posterior communicating arteries. The perioperative stroke rate was 1.5% for the entire group. There was no correlation between preoperative symptoms and the status of the contralateral carotid artery (normal, stenosed, or occluded). The mean collateral perfusion pressure was inversely related to the severity of the contralateral carotid stenosis: 60, 57, 55, 56, and 38 mm Hg for normal, <50% stenosed, 50-69% stenosed, 70-99% stenosed, and occluded arteries, respectively (p = 0.005). There was a direct relation between the number of patients with a collateral perfusion pressure of <40 mm Hg (shunted group) and the severity of the contralateral carotid stenosis: 6 of 62 (10%) for normal carotid, 7 of 43 (16%) for <50% stenosis (OR = 1.82), 12 of 69 (17%) for 50-69% stenosis (OR = 1.97), 3 of 10 (30%) for 70-99% stenosis (OR = 4, CI = 0.81-19.68), and 9 of 13 (70%) for occlusion (OR = 21, CI = 4.98-89.32) (p < 0.0001). None of the patients (0/56) with normal to <70% contralateral carotid stenosis with cross-filling had a collateral perfusion pressure of <40 mm Hg (no shunting was necessary). However, 9 of 17 (47%) patients with <70% contralateral carotid stenosis and no cross-filling had a collateral perfusion pressure of <40 mm Hg (p < 0.0001), whereas 6 of 7 (86%) patients with ≥70% contralateral carotid stenosis and cross-filling versus 2 of 7 (29%) with ≥70% contralateral carotid stenosis and no cross-filling had a collateral perfusion stump pressure of >40 mm Hg (p = 0.1026). Overall, 62 of 63 (98.4%) patients with cross-filling versus 10 of 24 (42%) without cross-filling had a collateral perfusion pressure of ≥40 mm Hg (p < 0.0001). There was an inverse correlation between collateral perfusion pressure and severity of contralateral carotid stenosis, and patients with severe contralateral carotid stenosis/occlusion were more likely to be shunted. The presence of cross-filling with normal to<70% contralateral carotid stenosis was associated with a collateral perfusion stump pressure of ≥40 mm Hg in 100% of patients for whom shunting was not carried out in our series.

Pravastatin administration does not induce detrimental effects on hemodynamics and collaterals of portal hypertensive rats

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor can enhance endothelial nitric oxide synthase expression and induce vasodilatation. The vasodilatory effect may be detrimental to portal-systemic collaterals due to aggravating the shunting degrees. The present study investigated the effects of pravastatin, a HMG-CoA reductase inhibitor, on the collateral vascular responsiveness to endothelin-1 (ET-1) and portal-systemic shunting in portal hypertensive rats. The partial portal vein-ligated (PVL) rats received either pravastatin (25 mg/kg per day) or distilled water since 2 days prior to until 7 days after ligation. On the 8(th) day following hemodynamic measurements, the collateral vascular responsiveness to ET-1 was evaluated by an in situ collateral perfusion model. The shunting degrees of collaterals were evaluated by constructing vascular flow-pressure curves and color microsphere study, respectively. PVL rats underwent pre-incubation with: (i) Krebs solution (control); or Krebs solution plus (ii) 2 x 10(-5) M pravastatin; (iii) pravastatin + N(omega)-nitro-L-arginine (10(-4) M); and (iv) pravastatin + indomethacin (10(-5) M), followed by ET-1 (10(-10)-10(-7) M) administration to evaluate the collateral vascular responsiveness. In chronic study, pravastatin did not modify systemic and portal hemodynamics and collateral vascular responsiveness to ET-1. The resistances of flow-pressure curves and the microsphere study demonstrated similar shunting degrees between both groups. Furthermore, pravastatin pre-incubation didn't reduce collateral perfusion pressure to ET-1. Chronic pravastatin administration does not induce detrimental effects on hemodynamics and collaterals in PVL rats, nor does it influence the shunting degree. In addition, it does not modify the vasoconstrictive effect of ET-1 on the collaterals of PVL rats.

Chronic Thalidomide Administration Enhances Vascular Responsiveness to Vasopressin in Portal-systemic Collaterals of Bile Duct-ligated Rats

Arginine vasopressin (AVP) controls gastroesophageal variceal bleeding, partly due to its vasoconstrictive effect on portal-systemic collaterals. It has been shown that chronic thalidomide treatment decreases portal pressure, attenuates hyperdynamic circulation and inhibits vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-alpha in partially portal vein-ligated rats. This study investigated the effects of chronic thalidomide treatment on portal-systemic collateral vascular responsiveness to AVP in common bile duct-ligated (CBDL) cirrhotic rats. In the first series, CBDL-induced cirrhotic rats received thalidomide (50 mg/kg/day orally) or distilled water (control) from the 35th to 42nd day after ligation. On the 43rd day after ligation, the body weight, mean arterial pressure, portal pressure, and heart rate were measured. An in situ collateral vascular perfusion model was used to obtain the cumulative concentration-response curves of collateral vessels to AVP (10(-10) to 3 x 10(-7) M). Plasma levels of VEGF and TNF-alpha were measured, and expressions of VEGF and TNF-alpha mRNA in the left adrenal veins were also determined. In the second series, the cumulative concentration-response curves of collateral vessels to AVP in CBDL rats with or without thalidomide (10(-5) M) preincubation in the perfusate were obtained. The thalidomide and control groups were not significantly different in terms of heart rate, mean arterial pressure and portal pressure (p > 0.05). The collateral vascular perfusion pressure change to AVP was significantly enhanced at 10(-8) M after thalidomide treatment (p = 0.041). Compared with the control group, thalidomide-treated rats had significantly lower plasma VEGF levels (p < 0.001), accompanied by an insignificant reduction in plasma TNF-alpha levels (p > 0.05). The expressions of VEGF and TNF-alpha mRNA in the left adrenal veins of thalidomide-treated CBDL rats were not significantly changed compared with those of the control group. In addition, thalidomide did not significantly elicit changes in vascular responsiveness to AVP in collateral vessels of CBDL rats when it was added into the perfusate. In cirrhotic rats, chronic thalidomide treatment improves the portal-systemic collateral vascular responsiveness to AVP, which was partly related to VEGF inhibition.

Chronic Indomethacin Treatment Enhances the Portal-systemic Collateral Vascular Response to Vasopressin in Bile-duct Ligated Rats

Liver cirrhosis is often accompanied by portal-systemic collateral formation with hemorrhage and encephalopathy. Prostacyclin participates in hyperdynamic circulation and vascular hyporeactiveness to vasoconstrictors in cirrhosis. It has been shown that arginine vasopressin (AVP) induces direct collateral vasoconstriction in portal hypertensive rats, which is potentiated by indomethacin preincubation. However, the influence of chronic indomethacin administration in cirrhosis remains unexplored. This study was performed on male Sprague-Dawley rats with liver cirrhosis induced by common bile duct ligation. They received subcutaneous indomethacin (5 mg/kg/day) or distilled water (control) injection from the 36th to 42nd day after operation. On the 43rd day, systemic and portal hemodynamics were evaluated and the following experiments were performed with an in situ collateral perfusion model: in the first series, concentration-response curves to AVP (10(-10) to 10(-7) M) were obtained; in the second series, flow-pressure curves were plotted (Krebs solution, 6-18 mL/min), where the slope represents an index of collateral vascular resistance (the higher the resistance, the smaller the amount of shunting vessels, that is, the lower the degree of shunting). The mean arterial pressure and portal pressure were similar between indomethacin and control groups (p > 0.05). Indomethacin elevated the collateral perfusion pressure to AVP (3 x 10(-9), 10(-8) M, p < 0.05) but did not influence the slope of the flow-pressure curve (p > 0.05). In bile duct-ligated cirrhotic rats, indomethacin improves the portal-systemic collateral vascular responsiveness to AVP without alleviating the severity of shunting.

The role of heart rate and the benefits of heart rate reduction in acute myocardial ischaemia

In myocardial ischaemia, detailed analyses of experimental data show that regional myocardial blood flow and contractile function are reduced proportionately—this being contrary to the common notion that the underlying pathological mechanism is a supply/ demand imbalance. Such perfusion–contraction matching is maintained at an increased heart rate. In the normal myocardium, metabolic regulation prevails and tachycardia results in an increased coronary blood flow. In post-stenotic myocardium that has an exhausted dilator reserve, a reduction in diastolic duration prevails, and coronary blood flow is decreased with tachycardia. In the presence of collaterals, both metabolic vasodilation of the normal microcirculation and reduced diastolic duration act in concert to decrease collateral perfusion pressure and collateral flow into the post-stenotic coronary microcirculation. Tachycardia results from sympathetic activation and activation of beta-adrenoceptors. Accordingly, beta-adrenergic blockers have been used to treat patients with stress-induced myocardial ischaemia. The benefits of heart rate reduction by beta-blockade are in part counterbalanced by unmasked alpha-adrenergic coronary vasoconstriction. Selective heart rate-reducing agents can decrease heart rate without unmasking alpha-adrenergic coronary vasoconstriction. They improve the blood flow distribution into the ischaemic myocardium and, as a consequence, improve regional myocardial function. Ivabradine is the only clinically available selective heart rate-reducing agent, and it exerts anti-ischaemic actions in patients with chronic stable angina.

Chronic cyclooxygenase blockade enhances the vasopressin responsiveness in collaterals of portal hypertensive rats

Objective. Collateral vascular responsiveness to vasoconstrictors may be crucial in the management of acute variceal bleeding. In an in situ perfusion model, arginine vasopressin (AVP) has been shown to cause a direct vasoconstrictive effect on portal-systemic collaterals and this effect is enhanced by preincubation of indomethacin (INDO). The purpose of this study was to investigate the effects of chronic INDO administration on the portal-systemic collateral responsiveness to AVP and the degree of portal-systemic shunting in portal hypertensive rats. Material and methods. Rats with partial portal vein ligation randomly received daily subcutaneous injections with INDO (5 mg/kg) or distilled water (control group) 2 days prior to until 7 days after ligation. Systemic and portal hemodynamics was evaluated on the 8th day. Using an in situ collateral perfusion model, AVP (10−10–10−7 M) at a constant flow rate (20 ml/min) was applied. In another series, Krebs solution with different flow rates (5–30 ml/min) was used to obtain flow-pressure curves: the slopes represent collateral vascular resistances – the higher resistances indicate fewer collaterals. Results. Mean arterial pressure and portal pressure were not significantly different between the INDO-treated group and the control group (p>0.05). In the first series of experiments, INDO treatment increased the collateral perfusion pressure to AVP at 10−8 M, 3×10−8 M, and 10−7 M (p<0.05). In the second series, INDO did not change collateral vascular resistance, which suggests that the degree of shunting was not altered. Conclusions. Chronic INDO treatment improves the collateral vascular responsiveness to AVP without ameliorating portal-systemic shunting in portal hypertensive rats.

Reciprocal relationship between left ventricular filling pressure and the recruitable human coronary collateral circulation

The aim of our study in patients with coronary artery disease (CAD) and present, or absent, myocardial ischaemia during coronary occlusion was to test whether (i) left ventricular (LV) filling pressure is influenced by the collateral circulation and, on the other hand, that (ii) its resistance to flow is directly associated with LV filling pressure. In 50 patients with CAD, the following parameters were obtained before and during a 60 s balloon occlusion: LV, aortic (Pao) and coronary pressure (Poccl), flow velocity (Voccl), central venous pressure (CVP), and coronary flow velocity after coronary angioplasty (V(Ø-occl)). The following variables were determined and analysed at 10 s intervals during occlusion, and at 60 s of occlusion: LV end-diastolic pressure (LVEDP), velocity-derived (CFIv) and pressure-derived collateral flow index (CFIp), coronary collateral (Rcoll), and peripheral resistance index to flow (Rperiph). Patients with ECG signs of ischaemia during coronary occlusion (insufficient collaterals, n = 33) had higher values of LVEDP over the entire course of occlusion than those without ECG signs of ischaemia during occlusion (sufficient collaterals, n = 17). Despite no ischaemia in the latter, there was an increase in LVEDP from 20 to 60 s of occlusion. In patients with insufficient collaterals, CFIv decreased and CFIp increased during occlusion. Beyond an occlusive LVEDP > 27 mmHg, Rcoll and Rperiph increased as a function of LVEDP. Recruitable collaterals are reciprocally tied to LV filling pressure during occlusion. If poorly developed, they affect it via myocardial ischaemia; if well grown, LV filling pressure still increases gradually during occlusion despite the absence of ischaemia indicating transmission of collateral perfusion pressure to the LV. With low, but not high, collateral flow, resistance to collateral as well as coronary peripheral flow is related to LV filling pressure in the high range.

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Influence of poststenotic collateral pressure on blood flow velocities within high-grade carotid artery stenosis: Differences between morphologic and functional measurements

Purpose: The driving force for blood flow through a high-grade stenosis in the internal carotid artery can be expressed as the pressure gradient over the stenosis itself, which, however, might be reduced by the back pressure exerted by distal collateral vessels. Theoretically the maximum blood flow velocity as a measure of the functional grade of obstruction may therefore be lower than what is expected from morphologic gradations of the stenosis. This study was designed to test prospectively the influence of intracranial collateral vessels on blood flow velocities within high-grade internal carotid artery stenoses. Patients and Methods: Forty-five consecutive patients (age 66 ± 11) with high-grade internal carotid artery stenoses were investigated before and during carotid endarterectomy. The preoperative investigations included duplex ultrasound scanning of the neck vessels, transcranial Doppler scanning for assessment of collateral flow to the middle cerebral artery and angiography. Carotid endarterectomy was performed with patients under deep general anesthesia without a shunt. Systolic and diastolic internal carotid artery blood pressures were measured before and during intraoperative cross-clamping (ie, stump pressure) of the carotid arteries. Results: Within high-grade internal carotid artery stenoses, maximum systolic and end-diastolic blood flow velocities showed a significant inverse correlation to the corresponding systolic and diastolic stump blood internal carotid artery blood pressures. All patients with spontaneous collateral flow to the ipsilateral anterior part of the circle of Willis were divided into a group with relatively high and another one with low end-diastolic blood flow velocities. The stump pressure was significantly lower in patients with high end-diastolic blood flow velocities in spite of the fact that the mean angiographic grade of stenosis did not differ significantly between the groups. Conclusions: Flow velocities within a high-grade internal carotid artery stenosis are inversely dependent on the stump pressure, that is the poststenotic collateral perfusion pressure. This should be taken into consideration in case of discrepancies between angiography and ultrasound outcome. (J Vasc Surg 2001;34:263-8.)

High diastolic flow velocities in severe internal carotid artery stenosis: A sign of increased surgical risk?

We reviewed the history and preoperative investigations of patients with early postoperative neurologic events after carotid thromboendarterectomy in an attempt to identify risk factors for neurologic complications. Patients with neurologic events/complications (S group, n = 14 patients) were compared with an age- and disease-matched control group (C group, n = 42 patients) selected from the whole carotid thromboendarterectomy material between 1987 and 1996. In this retrospective study, we re-evaluated the maximum systolic and end diastolic flow velocities within the internal carotid artery (ICA) using video recordings of preoperative Duplex ultrasound scan investigations. The flow velocity variables were compared with preoperative carotid angiography and intraoperative ICA stump pressure measurement. S-group did not differ from C-group concerning either cardiovascular risk factors or diseases, ipsilateral and contralateral angiographic grade of ICA stenosis, or history of cerebral infarctions. Nevertheless, in contrast to control subjects, patients with early postoperative major stroke had higher end diastolic flow velocities and lower ICA stump pressures. Patients with postoperative minor stroke, transient ischemic attack, or amaurosis fugax did not differ significantly from the control subjects. Among patients with ICA stenosis of 75% or more, end diastolic flow velocities were correlated to the diastolic stump pressures. Diastolic flow velocities within severe internal carotid artery stenosis are dependent on the level of the collateral perfusion pressure distally to the stenosis (ie, high values indicate a low internal carotid artery stump pressure), which seems to be a risk factor for early postoperative strokes.

High diastolic flow velocities in severe internal carotid artery stenosis: A sign of increased surgical risk?

Purpose: We reviewed the history and preoperative investigations of patients with early postoperative neurologic events after carotid thromboendarterectomy in an attempt to identify risk factors for neurologic complications.Metbods. Patients with neurologic events/complications (S group, n = 14 patients) were compared with an age- and disease-matched control group (C group, n = 42 patients) selected from the whole carotid thromboendarterectomy material between 1987 and 1996. In this retrospective study, we re-evaluated the maximum systolic and end diastolic flow velocities within the internal carotid artery (ICA) using video recordings of preoperative Duplex ultrasound scan investigations. The flow velocity variables were compared with preoperative carotid angiography and intraoperative ICA stump pressure measurement.Results: S-group did not differ from C-group concerning either cardiovascular risk factors or diseases, ipsilateral and contralateral angiographic grade of ICA stenosis, or history of cerebral infarctions. Nevertheless, in contrast to control subjects, patients with early postoperative major stroke had higher end diastolic flow velocities and lower ICA stump pressures. Patients with postoperative minor stroke, transient ischemic attack, or amaurosis fugax did not differ significantly from the control subjects. Among patients with ICA stenosis of 75% or more, end diastolic flow velocities were correlated to the diastolic stump pressures.Conclusion: Diastolic flow velocities within severe internal carotid artery stenosis are dependent on the level of the collateral perfusion pressure distally to the stenosis (ie, high values indicate a low internal carotid artery stump pressure), which seems to be a risk factor for early postoperative strokes.

Linear response of collateral cerebral perfusion pressure during carotid clamping

Phenylephrine is frequently used to increase systemic arterial pressure during carotid endarterectomy. However, little is known of its effect on collateral cerebral perfusion pressure, particularly in patients with high collateral cerebral vascular resistance who are at increased risk of cerebral ischemia during carotid clamping. We tested the hypothesis that this subset of patients can have collateral perfusion pressure, and hence collateral cerebral blood flow, increased in a predictable way by elevating systemic arterial pressure. We measured mean systemic arterial pressure ( P a), jugular venous pressure ( P v), and mean carotid back pressure ( P c), and calculated collateral cerebral perfusion pressure ( P = P c - P v) and the ratio of collateral to ipsilateral hemisphere cerebral vascular resistance ( R c R h ) in 18 patients with low P. Initial measurements were P a = 84 ± 8.8 (mm Hg, mean ± SD), P v = 7.8 ± 3.9, P c = 26 ± 5.1, P = 18 ± 4.5 and R c R h = 3.4 ± 1.15 . During phenylephrine infusion, P a = 108 ± 11, P c = 32 ± 6.5, and P = 24 ± 7.2, increases of 29, 23, and 33%, respectively ( P < 0.05). Unchanged were P v = 8.2 ± 4.1 (5%) and R c R h = 3.5 ± 1.30 (3%) ( P > 0.8). The latter two findings indicate that cerebral perfusion pressure and mean systemic arterial pressure are linearly related according to the fluid mechanics equation governing these parameters: P a = P( R c R h + 1) + P v . These results support the use of phenylephrine to increase collateral blood flow during carotid endarterectomy in patients with low cerebral perfusion pressure.

The Relationship of Early Hypertension Following Carotid Endarterectomy to Intraoperative Cerebral Ischemia

The relationship between early hypertension following carotid endarterectomy, and intraoperative cerebral ischemia was investigated. Two measures of the adequacy of collateral cerebral circulation during carotid clamping were used: collateral cerebral perfusion pressure (delta P), and the ratio of collateral to ipsilateral cerebral vascular resistance (R/R). Change in blood pressure was measured by the ratio of mean early post to preendarterectomy pressure (P/P). Nitroprusside or nitroglycerin (NN) was used after endarterectomy to maintain systolic blood pressure less than 160 mmHg. The mean values for NN (n = 26) and no NN (n = 81) groups were: delta P = 30.0 and 40.2 mmHg (p less than 0.001); R/R = 1.93 and 1.24 (p less than 0.005); and P/P = 1.03 and 0.857 (p less than 0.001 p by unpaired t test). Linear regression analysis of the two measures of cerebral perfusion with the ratio of post-to preoperative blood pressure gave correlation coefficients between 0.629 and 0.841 with a probability that the slope of the regression line greater than 0 of less than 0.01. Low delta P and high R/R correlate with early postcarotid endarterectomy hypertension. These results support the hypothesis that one determinant of early post endarterectomy hypertension is inadequate collateral cerebral circulation during carotid clamping.

Changes of collateral perfusion pressure and segmental coronary resistances during reactive hyperemia in anesthetized dogs.

Changes of collateral perfusion pressure (CPP) and segmental coronary resistances during reactive hyperemia were studied in nine chloralose-urethan-morphine anesthetized open-chest dogs. Coronary perfusion pressure was controlled by a cannula in the left main coronary artery and inflow measured by an electromagnetic flowmeter. The first or second diagonal branch of the left anterior descending coronary artery was cannulated and perfused from a carotid artery; inflow was abolished by embolization with latex microspheres (diameter: 25 +/- 5 mu) and peripheral coronary pressure was assumed to represent CPP. Segmental coronary resistances were defined as follows: Proximal coronary resistance (R1) was calculated from the difference between coronary perfusion pressure and CPP divided by coronary inflow. Distal coronary resistance (R2) was calculated from CPP divided by coronary inflow. Reactive hyperemia was produced by interruption of coronary inflow for 15 s and analysed at 30 s and 60 s of reperfusion when cardiac function had recovered. At baseline, R1 was 0.52 +/- 0.04 mm Hg X min X 100 g/ml (RU) and R2 0.63 +/- 0.07 RU. At 30 s, R1 was reduced by 19 +/- 3% (P less than 0.01) this was less (P less than 0.05) than R2 which was reduced by 32 +/- 3% (P less than 0.01). At 60 s R1 and R2 were reduced by 11 +/- 2% and 13 +/- 2%, respectively; this was not significantly different. Accordingly, CPP (baseline: 59 +/- 4 mm Hg) at 30 s was reduced by 7 +/- 2% (P less than 0.03), at 60 s the reduction was not significant. The data suggest that reactive hyperemia, as a model of metabolic coronary dilatation, may reduce CPP equivalent to a coronary steal phenomenon.

Influence of the ischemic coronary bed on collateral blood flow.

The purpose of this study was to determine the influence of the resistance of the terminal vascular bed of an occluded coronary artery on collateral blood flow and collateral resistance. In 6 anesthetized dogs, left anterior descending coronary artery (LAD) was ligated, cannulated, and the terminal vascular bed was occluded by latex microspheres (diameter: 25 mu). Retrograde flow was measured using a new technique, which allowed control of outflow pressure of retrograde flow (PRF) at the LAD cannula. When retrograde flow was interrupted, pressure in the occluded vessel represented collateral perfusion pressure (CPP) within the border zone of the ischemic vessel. Collateral resistance was determined dividing the pressure difference across the collateral bed (CPP-PRF) by retrograde flow. Variation of PRF was used as a model for changes in resistance of the ischemic bed. Retrograde flow fell when PRF was increased from 11.0 +/- 3.0 ml X min-1 X 100 g-1 (PRF = 0) to 8.3 +/- 2.4 (p less than 0.01)(PRF = 24.6 +/- 6 mm Hg). For the same PRF range, collateral resistance fell from 9.68 +/- 2.96 to 8.30 +/- 2.50 mm Hg X ml-1 X min X 100 g (p less than 0.01). These results indicate that the vascular resistance of the terminal ischemic bed may considerably influence collateral blood flow and resistance.

HALOTHANE IMPROVES THE BALANCE OF OXYGEN SUPPLY TO DEMAND IN ACUTE EXPERIMENTAL MYOCARDIAL ISCHAEMIA

Acute myocardial infarction was induced by ligation of the anterior descending branch of the left main coronary artery in greyhound dogs anaesthetized with pentobarbitone. Blood flow in the area of ischaemia was measured by xenon clearance and compared with flow in the circumflex artery measured with electromagnetic flow meters. Halothane 1% produced an approximate 40% reduction in flow to both ischaemic and normal areas in association with a 20% reduction in collateral perfusion pressure and a 40% reduction in mean arterial pressure. Comparison of the percentage change in the ratio of oxygen availability/consumption in response to halothane revealed a significant difference between the ischaemic and the normal areas. The former increased to 113 +/- 9.3% (mean +/- SEM) whilst the latter decreased to 91 +/- 5.02%. This suggests that, in the non-failing heart, halothane improves oxygenation in areas of acute myocardial ischaemia.