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PubMed2006

Bilateral segmental absence of the internal carotid artery with rete compensation associated with absence of basilar artery: case report.

BACKGROUND: Bilateral ICA absence is a rare lesion. Collateral circulation to the middle and anterior cerebral arteries in the absence of one or both ICAs may develop transcranial anastomoses from the external carotid system, a so-called CRM. Very rarely, theses arterial channels are observed in humans. CASE DESCRIPTION: In the following case study, a 38-year-old man presented himself. He had a headache and scalp laceration after having had an accident. A right external carotid angiography identified anastomoses to distal intracranial vessel through the internal maxillary artery, but the intracranial vessels were only faintly visible. A right ascending pharyngeal arteriography showed an abnormal course and anastomoses with the intracranial vessel. The right ICA was absent. The left external carotid angiography demonstrated a network of tortous arteries in the region of the cavernous and petrous portion of ICA. The plexus of vessels on the left side communicated with the proximal part of the cavernous segment of the ICA. Both vertebral angiographies demonstrated a sudden diminution in caliber at the level of vertebrobasilar junction. There was an anomalous arterial collateral circulation originating from vertebral muscular and meningeal branch. There was also an absence of the basilar artery (BA). CONCLUSION: This is the first case with CRM associated with bilateral segmental ICA and BA absence. The cause of this bilateral segmental ICA and BA absence may be maldevelopment of vessel connective tissue or extracellular matrix.

Arteriovenous Anastomosis↗
PubMedDate not supplied

Angiotensin II decreases mortality rate in gerbils with unilateral carotid ligation.

Evidence indicates that after vascular occlusion, infusion of angiotensin II restores blood supply to ischemic tissues by stimulating the development of collateral circulation through a mechanism independent of the mechanical effects of increased blood pressure. To test this effect in focal cerebral ischemia, angiotensin II was intravenously administered for four hours to gerbils immediately after unilateral carotid ligation. Three different pressor doses, 50, 250, and 500 ng/kg/min, were used, and mortality rate was evaluated at 1 and 2 days after vascular occlusion. Two additional groups similarly prepared were infused either with saline or with the pressor agent metaraminol. There was a significant inverse relationship between the infusion dose of angiotensin II and mortality: the greater the infusion dose of angiotensin II, the lower the mortality rate. Infusion of metaraminol, at the dose chosen to mimic the pressor effect of the highest angiotensin II dose, yielded a mortality rate which was statistically indistinguishable from that obtained with saline infusion. It is concluded that the mortality rate after unilateral carotid occlusion is significantly reduced by intravenous administration of angiotensin II through mechanisms unrelated to its hypertensive action. Evidence suggests that this may occur by the enhancement of the development of collateral circulation and therefore the reduction of the severity of brain ischemia.

Angiotensin II↗
PubMed1999

Systemic hemodynamic changes in mansonic schistosomiasis with portal hypertension treated by azygoportal disconnection and splenectomy.

OBJECTIVE: The aim of this study was to assess systemic hemodynamic changes in patients with Manson's schistosomiasis and portal hypertension during azygoportal disconnection and splenectomy. METHODS: Sixteen patients with portal hypertension secondary to hepatosplenic schistosomiasis with indication for surgery were studied prospectively. All underwent invasive hemodynamic monitoring with pulmonary artery catheter. The first systemic hemodynamic assessment was performed preoperatively. In the intraoperative period new hemodynamic data were collected as follows: a) after laparotomy; b) 15-30 min after splenic artery ligature; c) 15-30 min after splenectomy; and d) after ligation of the collateral circulation. RESULTS: The results indicated preoperatively that the patients presented with an increased cardiac index (4.40 +/- 0.94 L/min/m2) together with a reduction in the systemic vascular resistance index (1692.25 +/- 434.91 dyne.s/cm5.m2). The stroke index (53.74 +/- 10.40 ml/beat/m2) and both left (5.71 +/- 1.50 kg.m/m2) and right heart work indexes (1.12 +/- 0.74 kg.m/m2) were also elevated. The mean pulmonary artery pressure was increased (17.81 +/- 9.00 mm Hg) and the pulmonary vascular resistance index decreased (164.31 +/- 138.69 dyne.s/cm5.m2). From the moment that the splenic artery was ligated until the end of the procedure, the cardiac index (3.45 +/- 0.90 L/min/m2) was reduced and the systemic vascular resistance index (2059.50 +/- 590.05 dyne.s/cm5.m5) increased. The systolic index (44.25 +/- 11.01 ml/beat/m2) and the left ventricle work index (4.33 +/- 1.29 kg.m/m2) also reduced. The mean pulmonary artery pressure (19.18 +/- 9.21 mm Hg) and the right ventricle work index (0.94 +/- 0.62 mm Hg) remained elevated after the surgical procedure. CONCLUSIONS: The data allowed us to conclude that hepatosplenic schistosomiasis induces a hyperdynamic circulatory state that was corrected after splenectomy and azygoportal disconnection, remaining a mild pulmonary hypertension. Therefore, these changes are correlated with the portosystemic collateral circulation, especially as a consequence of splanchnic hyperflow.

Adolescent↗
PubMed2000

Endoscopic ultrasonographic study of the azygos vein before and after endoscopic obliteration of esophagogastric varices by injection sclerotherapy.

BACKGROUND AND STUDY AIMS: The azygos vein plays an important role as a drainage system for the superior portosystemic collateral circulation in portal hypertensive patients. Endoscopic ultrasonography (EUS) and Doppler EUS allow the performance of hemodynamic studies of the azygos vein. In this study, we observed the changes in the azygos vein which occur with variceal obliteration by endoscopic injection sclerotherapy (EIS). PATIENTS AND METHODS: We recruited patients with portal hypertension and bleeding varices who were not on portal pressure-lowering agents and who were scheduled for the EIS program. EUS was performed in these patients to study the azygos vein at the start of EIS. The azygos vein diameter, maximal velocity (Vmax), and blood flow volume index (BFVI) were measured. After variceal obliteration and within 1 week, another EUS study of the azygos vein was carried out. RESULTS: Out of 40 patients recruited into the study variceal obliteration and EUS assessment of the azygos vein, within 1 week of obliteration, was achieved in 33. We noticed a significant increase in azygos vein diameter (P<0.001) and BFVI (P=0.001) following variceal obliteration. No significant change was observed in Vmax (P>0.05). In one patient, marked caliber irregularities were observed in the azygos vein after variceal obliteration. CONCLUSIONS: Using EUS and Doppler EUS, hemodynamic studies of the azygos vein blood flow can be performed, allowing the monitoring of the effects of EIS and variceal obliteration on the superior portosystemic collateral circulation. The clinical significance of the observed changes in azygos blood flow that occur with variceal obliteration should be investigated in further studies and correlated with short-term and long-term outcome.

Adult↗
PubMed1996

Repeated coronary artery occlusions during routine balloon angioplasty do not induce myocardial preconditioning in humans.

OBJECTIVES: The purpose of the present study was to assess whether brief, repeated coronary artery occlusions during balloon angioplasty induce a myocardial ischemic protective effect. BACKGROUND: In animals, brief coronary artery occlusions preceding a more prolonged occlusion result in reduced infarct size. Whether myocardial protection against ischemia could also occur in humans during angioplasty remains controversial. METHODS: Thirteen patients with a proximal left anterior descending coronary artery stenosis with no angiographic collateral circulation underwent percutaneous transluminal coronary artery balloon angioplasty. Three 120-s balloon inflations separated by a 5-min equilibration period were performed. For each inflation, intracoronary ST segment modifications, septal wall thickening (M-mode echocardiography), left ventricular pressures and time derivatives were measured at baseline and at 30, 60 and 90 s after balloon inflation and 120 s after balloon deflation. RESULTS: Intracoronary electrocardiographic analysis showed that the time course of the maximal ST segment elevation was identical at each inflation, as were wall motion changes assessed by the decrease in septal wall thickening. For the first and last inflations, peak positive dP/dt decreased significantly by 13 +/- 9% (mean +/- SD) and 14 +/- 13%, whereas peak negative dP/dt increased by 23 +/- 15% and 22 +/- 10%, respectively (all p < 0.01 from baseline values). The relaxation time constant, tau, was altered similarly during the different inflations, from 44 +/- 6 to 74 +/- 13 ms and from 57 +/- 13 to 77 +/- 13 ms (all p < 0.001) for the first and last inflations, respectively. Left ventricular end-diastolic pressure increased to the same level after each inflation. In contrast to other hemodynamic variables, tau and left ventricular end-diastolic pressure did not return to baseline values in between the inflations, which may be due to myocardial stunning. CONCLUSIONS: In patients with proximal left anterior descending coronary artery stenosis and no evidence of collateral circulation, brief periods of ischemia, such as those used during routine coronary balloon angioplasty, do not provide any protection against myocardial ischemia.

Aged↗
PubMed2002

Assessment of coronary artery disease with second harmonic myocardial perfusion contrast echocardiography.

OBJECTIVE: To assess the relationship between myocardial regional perfusion using second harmonic myocardial contrast echocardiography (MCE) by venous injection of Levovist and coronary artery stenosis detected by coronary angiography to determine whe ther MCE can be used to detect coronary artery disease (CAD) and its sensitivity and specificity for detecting CAD. METHODS: Thirty-six patients who underwent coronary artery angiography and MCE formed the study groups. Ten myocardial segments (5 each in the apical two- and four-chamber views) from the images were scored for detecting myocardial perfusion as follows: 1, normal perfusion; 2, decreased perfusion; and 3, perfusion defect. The arteries were classified as normal or diseased. The diseased arteries were classified into three groups according to the perfusion scores. RESULTS: There were significant differences in coronary diameter stenosis among the different perfusion score groups (P < 0.001). There were 10 total occluded arteries, and the myocardial perfusion scores were different because of different collateral circulation. In the normal perfusion group (Group A), the coronary diameter stenosis was 65% +/- 12%, and the myocardial perfusion score index was 1 +/- 0.00. In the decreased perfusion group (Group B), the average coronary diameter stenosis was 82% +/- 8%, and the myocardial perfusion score was 1.93 +/- 0.16. The diameter stenosis was less than 85% in 63% of the coronary arteries (including diameter stenosis < or = 75% in 12% of the vessels). The diameter stenosis was 85%-90% in 22% of the coronary arteries and > 90% in 15% of the arteries. In the perfusion defect group (Group C), the average diameter stenosis was 90% +/- 6%, and the myocardial perfusion score index was 2.89 +/- 0.24. The diameter stenosis was > or = 85% in 94% of the coronary arteries, and the diameter stenosis was < 85% and > 75% only in 6% of the coronary arteries. The overall sensitivity and specificity of MCE in identifying angiographic coronary diameter stenosis was 67% and 100%, respectively. The false negative rate was 32.6% for the 108 coronary arteries. Further subdivided analysis showed the sensitivities in Groups A, B and C were 0, 100%, and 100%, respectively. The sensitivity increased with increased lumen diameter stenosis of coronary arteries. CONCLUSIONS: There is a close relationship between coronary artery stenosis and MCE perfusion scores. MCE with venous injection of new generation contrast can define the presence of CAD and lesion graded classifications. Some disagreements between perfusion score and coronary diameter of stenosis may indicate other factors such as different collateral circulation, which should be further investigated. As artery stenosis increases, the sensitivity of MCE is increased.

Adult↗
PubMed1995

Prodromal angina limits infarct size. A role for ischemic preconditioning.

BACKGROUND: In the experimental setting, it has been demonstrated that preconditioning myocardium before prolonged occlusion with brief ischemic episodes affords substantial protection to the cells by delaying lethal injury, thereby limiting infarct size. Whether the same occurs in humans remains unknown. METHODS AND RESULTS: This study was undertaken to determine whether new-onset prodromal angina, defined as chest pain episodes limited to the 24 hours before myocardial infarction, is the clinical correlate of the ischemic preconditioning phenomenon. Twenty-five patients with their first anterior myocardial infarction treated with thrombolysis (recombinant tissue plasminogen activator [r-TPA], 100 mg/3 hours) were retrospectively included in the study because they met the following criteria: (1) < 120 minutes from onset of symptoms to reperfusion therapy, (2) < 90 minutes from the beginning of thrombolytic therapy to reperfusion (defined as rapid ST elevation reduction > 50%), (3) a patient infarct-related coronary artery with TIMI 3 flow and complete absence of collateral circulation to the infarct related artery (assessed at 24 +/- 5 days), and (4) the presence of new-onset prodromal angina, ie, typical chest pain episodes occurring at rest within 24 hours or, alternatively, a complete absence of symptoms before onset of infarction. Therefore, on the basis of their clinical status before infarction, the patients were divided into two groups: group 1, 13 patients without prodromal angina, and group 2, 12 patients with prodromal angina. Despite no difference in time to treatment (81 +/- 19 versus 75 +/- 21 minutes in group 1 and group 2, respectively; P = NS) and time to reperfusion (58 +/- 34 versus 46 +/- 24 minutes; P = NS), the peak of CKMB release was markedly lower in group 2 (86.3 +/- 66 versus 192.3 +/- 108.3 IU/L; P < .01). In addition, although both groups were comparable in terms of area at risk (amount of myocardium beyond the infarct-related stenosis; 15.1 +/- 4.6 versus 13.7 +/- 4.6 hypokinetic segments in group 1 and group 2, respectively, P = NS), the final infarct size (11 +/- 7.5 versus 5.6 +/- 4 hypokinetic segments, P < .04) was smaller in group 2. Thus, the limitation of the infarct size was significantly greater in group 2 (69% versus 36%; P < .05), and this represents an additional 33% reduction (95% confidence intervals, 7.1% to 58.9%; P = .01) in the group of patients with prodromal angina. Also, the third index, that is, the ECG, showed a favorable trend toward a lesser number of Q waves and a higher sigma R waves, although the values did not reach statistical significance. CONCLUSIONS: Despite a similar area at risk, patients with new-onset prodromal angina showed a significantly smaller infarct size compared with patients without prodromal symptoms. Since the two groups had similar times to reperfusion and no evidence of collateral circulation to the infarct related artery, the protection afforded by angina in group 2 patients might be explained by the occurrence of ischemic preconditioning.

Aged↗
PubMed1997

The safety and efficacy of transcatheter arterial chemoembolization in the treatment of patients with hepatocellular carcinoma and main portal vein obstruction. A prospective controlled study.

BACKGROUND: Transcatheter arterial chemoembolization (TACE) has been contra-indicated for the treatment of patients with hepatocellular carcinoma (HCC) and main portal vein (MPV) obstruction because of the potential risk of hepatic insufficiency resulting from ischemia after TACE. The current controlled study was undertaken to assess the safety, efficacy, and predictive factors of favorable response to TACE in patients with HCC and MPV obstruction with good hepatic function and adequate collateral circulation around the MPV. METHODS: Of a total of 47 patients, 31 were treated with TACE, and 16 who declined the procedures were untreated controls. Thirty-six patients (77%) had diffuse-type HCC and 11 (23%) had nodular-type HCC. During the first week after TACE immediate postprocedural complications were evaluated, and the development of hepatic insufficiency as a late complication was assessed at the end of the fourth week. The cumulative survival rate was estimated by the Kaplan-Meier method, and predictors of better prognosis were obtained by univariate and multivariate analyses. RESULTS: Although no patients showed clinical evidence of hepatic insufficiency as an immediate complication, transient fever and abdominal pain were common. Progressive hepatic insufficiency developed at the fourth week; however, there was no difference between the treated and untreated groups. The survival time of treated patients was statistically no longer than that of untreated patients. In the univariate analysis, tumor type and size, the pattern of iodized oil uptake in the tumor, and the presence of iodized oil uptake in the tumor thrombi at the MPV significantly influenced the prognosis. Tumor type, whether treated or not, was the most important prognostic factor patients with nodular-type HCC had significantly longer survival time (median, 11 months) than those with diffuse-type HCC (median, 4 months). Regarding the efficacy of TACE, there was no statistical difference in survival between treated and untreated diffuse-type HCC patients. In comparison, with nodular-type HCC it seemed that survival time was longer for TACE-treated patients (median, 30 months) than for untreated patients (median, 7 months). CONCLUSIONS: TACE may be a safe modality for the treatment of patients with HCC and MPV obstruction, provided that the patients have good hepatic function and collateral circulation around the MPV. However, TACE was not efficacious in the treatment of diffuse-type HCC. The authors recommend TACE for treating nodular-type HCC because of the potential benefit of prolonged survival.

Adult↗
PubMed1985

Significance of the Q wave in acute myocardial infarction.

Acute myocardial infarction may be associated with the development of Q waves on the electrocardiogram (ECG), or with changes limited to the ST segment or T wave. The ECG changes do not accurately differentiate transmural from nontransmural infarction. However, the presence or absence of a Q wave does correlate with some aspects of the clinical course of patients after myocardial infarction, and is therefore of prognostic value. Q-wave infarctions are more likely to be complicated by congestive heart failure during hospitalization. The in-hospital mortality is also higher after a Q-wave infarction than after a non-Q infarction. Both of these findings are probably due to the association of a Q wave with a larger mass of infarcted myocardium. The long-term mortality, however, is the same for Q-wave and non-Q-wave infarctions. This is probably due to an increased late mortality after non-Q infarctions, related in part to a higher rate of reinfarction. The differences between Q-wave and non-Q-wave infarctions are not due to obvious differences in extent and location of coronary artery obstructions. However, there may be differences in the collateral circulation, with more extensive collaterals associated with non-Q infarcts. Appreciation of the prognostic significance of the ECG changes in acute myocardial infarction may help direct the evaluation and management of the patient after myocardial infarction.

Cardiac Catheterization↗
PubMedDate not supplied

Management of inadvertent injury to the carotid artery during head and neck surgery.

Rare, inadvertent injury to the carotid artery during head and neck surgery may result in disastrous neurologic sequelae or even death. Several cases are presented and used as the stimulus for an analytical discussion of the pathogenesis and management of cerebrovascular complications following head and neck surgery. The major pathogenetic mechanisms are identified as (1) microembolism from an ulcerated plaque; (2) intravascular thrombus with occlusion; (3) unintentional ligation, laceration, or transection; (4) ligation of a dominant external carotid; and (5) transient reduction in cerebrovascular perfusion pressure. Methods for identifying and evaluating the patient at risk for developing cerebrovascular complications are discussed and recommendations are made. The central question in the management of inadvertent arterial injury concerns whether to ligate the vessel or to restore blood flow. The controversies surrounding this issue are discussed in perspective through an analysis of current physiological concepts and of the collective clinical experiences of head and neck, vascular, and neurological surgeons handling extracranial cerebrovascular occlusive disease, penetrating injuries to the carotid artery, and tumor-related carotid catastrophes. Several factors are considered critical in determining appropriate management of any individual case; these include (1) whether recognition of the injury occurs intraoperatively or postoperatively; (2) the presence and severity of neurological deficits; (3) time from the injury to its recognition; (4) a quantitative assessment of collateral circulation; (5) a history of wound contamination or radiation therapy; (6) overall prognosis. These and other considerations are organized into a working framework through which the otolaryngologist and head and neck surgeon can better understand and manage the problem of inadvertent injury to the carotid artery.

Adult↗
PubMed1993

Angiogenic effects of low molecular weight heparin in patients with stable coronary artery disease: a pilot study.

OBJECTIVES: The study was designed to assess the feasibility of conducting a trial to investigate whether exercise and low molecular weight heparin therapy with dalteparin sodium (Fragmin) would improve collateral function to the ischemic myocardium in patients with coronary artery disease. BACKGROUND: The severity of myocardial ischemia in patients with coronary artery disease is at least partly dependent on the status of the collateral circulation. Therefore, improvement in collateral function would potentially provide a unique way of alleviating myocardial ischemia. Because the combination of ischemia and heparin has previously been demonstrated to enhance collateral growth, we studied the anti-ischemic effects of combined treatment with dalteparin sodium and exercise-induced ischemia in patients with coronary artery disease. METHODS: Twenty-three patients with stable coronary artery disease were randomized to receive either subcutaneous dalteparin sodium or placebo for a 4-week period. Patients received either placebo or 10,000 IU of dalteparin sodium by subcutaneous injection once daily for weeks 1 and 2 and 5,000 IU daily for weeks 3 and 4. During the 1st 2 weeks, patients were exercised to ischemia three times a day. At baseline and 4 weeks after treatment, treadmill exercise testing, exercise radionuclide ventriculography and 48-h ambulatory ST segment monitoring were performed. RESULTS: Eight (80%) of the 10 dalteparin sodium-treated patients compared with 4 (31%) of 13 placebo-treated patients (p < 0.02) had an increased rate-pressure product at the onset of 1 mm of ST segment depression. The duration of exercise to ischemia increased in all patients treated with low molecular weight heparin and in 62% of placebo-treated patients (p < 0.03). The number and duration of episodes of ST segment depression during ambulatory monitoring decreased by 30% and 35%, respectively (p < 0.05), in the dalteparin sodium group but were unchanged in the placebo group. The decrease in left ventricular ejection fraction with exercise was lower in 80% of dalteparin sodium-treated patients compared with 54% of placebo-treated patients (p = 0.06). When all five factors reflecting collateral function were considered together in a multivariate analysis of variance, there was a significant improvement in low molecular weight heparin-treated patients compared with placebo-treated patients (p = 0.014). CONCLUSIONS: This study provides preliminary evidence suggesting that exercise and low molecular weight heparin therapy with dalteparin sodium lessen myocardial ischemia and that the improvement is likely to be mediated by enhanced collateral function.

Aged↗
PubMed1990

Shunt for bypass graft of the cavernous carotid artery: an anatomical and technical study.

During direct surgery of neoplastic and vascular lesions of the cavernous sinus, the intracavernous carotid artery may be injured beyond repair, or its total isolation may be necessary for surgical management of these lesions. The newly developed procedure of a saphenous vein graft bypass of the cavernous carotid artery allows re-establishment of carotid circulation. Patients with poor collateral circulation are at high risk for ischemic complications induced by the prolonged temporary occlusion required to perform the bypass graft. Optimal management of these patients is to perform the venous bypass graft for permanent vascularization while maintaining carotid cerebral circulation through an intraoperative shunt. We studied this procedure in cadavers, and three shunt types were evaluated: the external intrapetrous-supraclinoid shunt (Type A), the internal intrapetrous-supraclinoid shunt (Type B), and the neck internal carotid-supraclinoid shunt (Type C). Anatomical landmarks, techniques, distances, caliber, and materials used are presented. The rationale and candidates for such a procedure are discussed. The specifications of an optimal balloon shunt are presented, and the three procedures are compared.

Anastomosis, Surgical↗
PubMed2006

Pressure-derived collateral flow index: a strong predictor of late left ventricular remodeling after thrombolysis for acute myocardial infarction.

OBJECTIVE: Despite proved efficacy of pressure-derived collateral flow index in determining microvascular dysfunction in patients with acute myocardial infarction, its role in prediction of left ventricular remodeling at long term has yet to be demonstrated. In this study, we investigated the relationship between quantitatively assessed microvascular dysfunction by using intracoronary pressure wire and late left ventricular remodeling. PATIENTS AND METHODS: The study population consisted of 28 patients with first acute myocardial infarction. They were treated with fibrinolytic therapy. The inclusion criteria were thrombolysis in myocardial infarction grade II-III flow in infarct-related artery and all destined for stent implantation. Cardiac catheterization and stent implantation were performed in mean of 3.3 days after acute myocardial infarction. During the stent implantation procedure, the pressure-derived collateral flow index was measured by using intracoronary pressure wire. Control angiograms were performed at 6+/-2 months. Echocardiographic left ventricular volume indexes were measured at discharge, at 6 months and at 1 year. Changes in left ventricular volumes from baseline to 1 year were followed. RESULTS: Left ventricular end-diastolic volume index at 1 year correlated significantly with the pressure-derived collateral flow index (r=0.69, P<0.01). A significant correlation was also observed between the change in left ventricular end-diastolic volume index from baseline to 1 year and the pressure-derived collateral flow index (r=0.65, P<0.01). The most important predictor of 1-year left ventricular remodeling was the pressure-derived collateral flow index (P<0.0001), and collateral circulation (P=0.03). CONCLUSION: The pressure-derived collateral flow index is a powerful independent predictor of 1-year left ventricular dilatation. Given its simplicity of measurement, and correlation with microvascular obstruction and left ventricular outcome at long term, the pressure-derived collateral flow index may provide useful and valuable estimates of clinical outcomes after acute myocardial infarction.

Aged↗
PubMed1992

Pharmacology of portal-systemic collaterals in portal hypertensive rats: role of endothelium.

The portal-systemic collateral circulation of portal hypertensive rats was studied. The collaterals were perfused through the mesenteric vein with Krebs solution, which was allowed to escape through the jugular veins. The portal-collateral resistance can be quantitated from slopes of the pressure-flow relationships. In collaterals perfused at constant flow, both norepinephrine (NE) and 5-hydroxytryptamine (5-HT) increased the perfusion pressure. Phentolamine caused surmountable antagonism of the constrictor effects of NE, suggesting an involvement of alpha-adrenoceptors. The effects of 5-HT were competitively blocked by the 5-HT2 receptor-selective antagonist ICI 169,369. Isoproterenol dilated NE-preconstricted collaterals. The effect of isoproterenol was blocked by propranolol, demonstrating that the effect was mediated by beta-adrenoceptors. Acetylcholine (ACh) dilated NE-preconstricted collaterals. The dilatation effect of ACh was absent in collaterals in which the endothelium was removed. The competitive inhibitor of the nitric oxide synthase, N omega-nitro-L-arginine (L-NNA), increased collateral resistance and prevented the ACh-induced dilatation of the collaterals. The constrictor response to L-NNA and the blockade of the ACh-induced relaxation by both L-NNA and removal of endothelium are consistent with an involvement of nitric oxide. This experimental model can thus be used to explore the pathophysiological and the pharmacological properties of the collateral venous bed in portal hypertensive states.

Animals↗
PubMed1981

Evidence for increased protein synthesis in myocardial microvessels after chronic sympathectomy in the dog.

Using histochemical methods, evidence of increased protein synthesis was observed in microvessels (diameter less than 100 micrometers) from dog hearts which had been sympathectomized 2 weeks earlier when compared to controls. Such evidence consisted of increased staining intensity for the enzyme glucose-6-phosphate dehydrogenase and for the nucleic acids RNA and DNA. Increases in reaction intensities were noted in approximately 30% of the microvessels examined from the sympathectomized hearts, and may imply a vascular proliferation in these hearts. However, since no increase in capillary density was observed in sympathectomized hearts, a vascular proliferation, if it occurred, may have been involved in development of the coronary collateral circulation. These data support previous results indicating that collateral resistances are reduced following chronic cardiac sympathectomy while resistance of the coronary vascular bed itself is not altered.

Animals↗