Regarding "Altered endothelial and smooth muscle cell reactivity caused by University of Wisconsin preservation solution in human saphenous vein".
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Adenosine↗
Biomedical subjects
J D Edwards
Publications and source records attributed to J D Edwards.
Importance of the sampling site for measurement of mixed venous oxygen saturation in shock.
OBJECTIVES: To determine if oxyhemoglobin saturation in blood samples taken from the superior vena cava or right atrium can be substituted for oxyhemoglobin saturation in blood taken from the proximal pulmonary artery (SVO2) in patients in shock. DESIGN: Prospective clinical investigation. SETTING: Mixed surgical/medical intensive care unit in a university hospital. PATIENTS: Thirty consecutive patients in severe circulatory shock who required insertion of a pulmonary artery flotation catheter (PAFC) immediately on intensive care unit admission. All patients fulfilled the criteria described below which were established in advance. MEASUREMENTS AND MAIN RESULTS: Oxyhemoglobin saturation in the superior vena cava, right atrium, and pulmonary artery (SVO2) was measured by cooximetry in consecutive blood samples from each site during initial insertion of the PAFC. The mean standard deviation of values from these sites was similar: 74 +/- 12.5%, 70.+/- 13%, and 71.3 +/- 12.7%, respectively. However, when superior vena cava and right atrial oxyhemoglobin saturations and SvO2 were compared, the ranges and 95% confidence limits were found to be clinically unacceptable. The ranges were -19.3 to 23.1% and -19.7 to 16.7%, respectively, and the 95% confidence limits were -18.4 to 24.2% and -18.6 to +17.3%, respectively. CONCLUSIONS: These wide range differences and confidence limits would lead to large errors if superior vena cava or right atrial oxyhemoglobin saturations were substituted for true mixed venous blood in oxygen transport or pulmonary venous admixture calculations, or if clinical decision making was based on individual results. In patients in shock in whom clinical decisions may be based on the value of mixed venous oxyhemoglobin, oxyhemoglobin saturation is only reliably measured in samples taken from the pulmonary artery.
Adult↗
Functional and morphological evaluation of canine veins following preservation in different storage media.
Injuries of endothelial and smooth muscle cells of autologous vein due to preservation in standard storage media may be responsible for graft failure. The effects of vein preservation with University of Wisconsin solution (UWs) on endothelial and smooth muscle cell function and morphology were compared to the effects of preservation with autologous whole blood (AWB) and normal saline (NS), which are frequently used in cardiovascular surgery. Canine external jugular and common femoral vein segments were preserved in the different solutions at 4 degrees C for 45 min and 24 hr. Rings (4-5 mm in length) from control and preserved veins were evaluated by isometric tension studies at 37 degrees C and by scanning and transmission electron microscopy. Differences between groups were evaluated by Student's t test or Mann-Whitney U test and by analysis of the variance, and considered to be significant at P < 0.05. Sensitivities to norepinephrine (NE) showed that a 45-min vein storage in AWB (5.7 +/- 0.2 mumol/L) but not in NS (5.8 +/- 0.2 mumol/L) or UWs (6.5 +/- 0.2 mumol/L) had a deleterious effect on function of smooth muscle (P < 0.05) when compared to control veins (6.6 +/- 0.2 mumol/L). Maximum contractile responses and sensitivities to NE were significantly altered (P < 0.05) after 24-hr vein storage in AWB (0.09 +/- 0.02 g/mm2 and 5.4 +/- 0.07 mumol/L) and NS (0.12 +/- 0.03 g/mm2 and 5.6 +/- 0.08 mumol/L) but not in UWs (0.36 +/- 0.06 g/mm2 and 6.4 +/- 0.07 mumol/L). With both storage times, acetylcholine-induced endothelium-dependent maximum relaxations and sensitivities were significantly reduced (P < 0.05) in veins stored in AWB and NS, but not in UWs, compared with controls. Similarly, transmission electron microscopy revealed marked neutrophil migration beneath the intimal surface of vessels and extensive separation and desquamation of endothelial cells with exposure of subendothelial structures in veins stored in AWB and NS. The results suggest that UWs is a suitable storage medium when compared to AWB and NS.
Animals↗
Short-term preservation of autogenous vein grafts: effectiveness of University of Wisconsin solution.
BACKGROUND: Suboptimal preservation of autologous veins in storage solutions causes endothelial cell damage that can contribute to graft failure. The purpose of this study was to compare the effects of short-term storage of veins in autologous whole blood (AWB), 0.9% normal saline solution (NS), and University of Wisconsin solution (UWs) on vein structure and function after grafting. METHODS: Autogenous jugular and femoral veins were atraumatically harvested from mongrel dogs. One vein segment was immediately implanted to serve as a control, and the other segments were stored for 45 minutes in AWB, NS, or UWs. The veins were implanted as reversed interposition graft in the carotid or femoral arteries. After 6 weeks light and scanning electron microscopy and isometric tension studies were performed on explanted vein grafts. RESULTS: Morphologic studies revealed an intact endothelium that stained positively for factor VIII. Intimal thickness was similar between controls (48 +/- 12 microns) and veins stored in UWs (53 +/- 8 microns) (p = not significant), but it was significantly increased in veins stored in AWB (151 +/- 29 microns) and NS (149 +/- 18 microns) (p < 0.05). Sensitivity and maximum contraction to norepinephrine were not altered in veins preserved in UWs (6.0 +/- 0.1 mumol/L and 0.19 +/- 0.02 gm/mm2) but were significantly reduced (p < 0.05) in those stored in AWB (7.2 +/- 0.1 mumol/L and 0.08 +/- 0.02 gm/mm2) and NS (7.0 +/- 0.3 mumol/L and 0.09 +/- 0.02 gm/mm2) compared with controls (5.9 +/- 0.2 mumol/L and 0.20 +/- 0.02 gm/mm2). The sensitivity and maximum relaxation to acetylcholine and sodium nitroprusside of veins preserved in AWB, NS, and UWs were similar to controls (p = not significant). CONCLUSIONS: Vein storage in UWs preserves smooth muscle cell function compared with veins stored in NS or AWB. Therefore UWs is a more suitable medium for short-term preservation of veins in cardiovascular operation.
Adenosine↗
Cell adhesion molecules and insulin-like growth factor-1 in vascular disease.
PURPOSE: Recent advances in the understanding of the biologic mechanisms of vascular diseases suggest that multifactorial stimulation of the endothelial cell and its subsequent adhesion to leukocytes is a prerequisite to the formation of atherosclerotic and restenotic lesions. As leukocyte-endothelial cell interaction is coordinated by a variety of cell adhesion molecules (CAMs), we hypothesized that the expression of certain CAMs is up-regulated in the vasculature of patients who have peripheral vascular disease. In addition, we proposed that insulin-like growth factor-1 (IGF-1) increases monocyte-endothelial adhesion by means of upregulation of these CAMs. METHODS: Using immunohistochemical techniques, the expression of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and P-selectin was examined in human vascular disease specimens. Normal aortas obtained from the organ retrieval system were studied as control specimens. Adhesion studies between human umbilical vein endothelial cells (HUVECs) incubated with IGF-1 and purified human blood monocytes labeled with 51chromium were completed. Western blotting and flow cytometry were performed to show CAM expression on IGF-1-treated HUVECs. RESULTS: Of the CAMs, ICAM-1, P-selectin, and E-selectin were distinctly increased in diseased specimens when compared with control specimens (p < 0.05). Adhesion studies showed an increase in monocyte-endothelial cell adhesion of as much as 40% to 45% (p < 0.01) over baseline, with peak adherence occurring 4 hours after treatment with IGF-1. IGF-1 increased adherence in a dose- and time-dependent manner. The threshold concentration of IGF-1 that induced increased adhesion was 20 ng/ml, with a maximum effect occurring at 150 ng/ml. This increased adhesion was attenuated by pretreatment with IGF-I receptor antibody, as well as with genistein and herbimycin-A, which are potent and selective tyrosine kinase inhibitors. Increased adhesion correlated with an increase in the expression of CAMs on the surface of the HUVECs. An additive effect on adhesion was observed between IGF-1 and tumor necrosis factor-alpha (TNF-alpha) and endothelin-1 (ET-1). Finally, immunohistochemical analysis of human vascular disease specimens revealed an increased expression of IGF-1 receptors as compared with control specimens (p < 0.05). CONCLUSIONS: These results suggest that IGF-1 may be important in the pathogenesis of peripheral vascular disease by increasing endothelial cell-monocyte adhesion by means of an increase in the expression of ICAM-1 and VCAM-1.
Aorta↗
Continuous thermodilution cardiac output: a significant step forward in hemodynamic monitoring.
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Bias↗
The dynamics of composite licensing boards from the chiropractic perspective.
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Chiropractic↗
Endothelin-1 induces tyrosine phosphorylation in human blood monocytes.
Mediators including the neuropeptide endothelin-1 (ET-1), which are released in response to injury, modulate the expression of cell adhesion molecules on leukocytes and endothelial cells. The mechanisms underlying this process are not clear. In this study we investigated the effect of endothelin-1 on the expression of tyrosine phosphorylated proteins in human blood monocytes. Endothelin-1 caused an increase in tyrosine phosphorylated proteins in monocytes in a time-dependent and dose-dependent manner, the Mr 60, 80 and 110 kDa proteins being the most prominent. This effect was blocked by pre-incubating the monocytes with the selective tyrosine kinase inhibitors genistein or herbimycin A. Endothelin-1 induced upregulation of tyrosine phosphorylated proteins appears to be mediated by the ETA receptor. Unlike our previously reported studies in endothelial cells, immunoprecipitation with anti-src or anti-JAK antibodies followed by immunoblotting with PY20 in human blood monocytes revealed that these proteins of Mr 60, 80 and 110 kDa were not related to src or JAK kinases. These findings suggest that ET- exerts its effect on monocytes by a pathway involving tyrosine kinases other than src or JAK kinases.
Adult↗
Fresh vein allograft survival in dogs after cyclosporine treatment.
Synthetic grafts are widely used for peripheral arterial reconstructions when autologous veins are not available, but their results have not been satisfactory. Venous allograft may be used as an alternative to synthetic prostheses. The aim of the study was to explore the immunosuppressive efficacy of Cyclosporine A (CyA) as a means of preventing venous allograft failures and rejection. We utilized 56 mongrel dogs. Immunological incompatibility was checked with the skin graft method. Donor inferior vena cava was transplanted into the infrarenal abdominal aorta of recipient animals. One group (group 1, 10 dogs) served as a control and three groups received CyA treatment regimens. Group 2 (10 dogs) received postoperative oral CyA treatment for 30 days. Group 3 (12 dogs) received a vein graft pretreated with a CyA solution without postoperative immunosuppressive therapy. Group 4 (9 dogs) received a vein graft pretreated with a CyA solution and postoperative CyA treatment for 30 days. Allografts were examined at 30 days for patency, aneurysmal dilatation, gross structural changes, inflammatory response, and lymphocytic infiltration. Sex chromatine assessment determined the origin (donor or recipient) of the endothelial cells. The allografts from groups 1 and 3 showed significant aneurysmal dilatation and perivenous inflammation when compared to dogs treated with oral CyA therapy (P < 0.0002). Moreover allografts treated with CyA therapy had a better-developed venous neointima (P < 0.009) with less fibrin (P < 0.02) and thinner medial (P < 0.0009) with less fibrin (P < 0.02), and thinner medial (P < 0.0009) and adventitial layers (P < 0.02). No significant differences were observed in neointimal thickness among the four groups. Lymphocytic infiltration was greater in the group of animals who did not receive oral CyA therapy (P < 0.0004). Barr bodies status showed significant differences between oral CyA treated groups and nontreated groups (P < 0.0003). Oral CyA therapy reduced aneurysmal dilatation and immunological response, promoted the development of a neoendothelium, and preserved the structure of the venous layers. Graft pretreatment with CyA flushing did not have a significant immunosuppressive effect.
Animals↗
Ischemia-induced peripheral arterial vasospasm role of alpha 1- and alpha 2-adrenoceptors.
Ischemia produces functional and structural alterations in peripheral blood vessels. Our study was designed to investigate alpha-adrenoceptor modifications induced by prolonged ischemia and their role in enhancing the contractile response during reperfusion in canine femoral arteries. Unilateral vessel ischemia was created by double crossclamping a femoral artery and was maintained for 3 hr. Reperfusion was allowed for 1 hr. The contralateral femoral artery was utilized as a control. The vessels were harvested for contractile and binding studies. Isometric tension studies revealed that the magnitude of the maximum contractile response to norepinephrine (NE), potassium chloride (KCl), and methoxamine was 671 +/- 82 mg/mm2 versus 245 +/- 43 mg/mm2 (P < 0.01), 485 +/- 46 mg/mm2 versus 229 +/- 62 mg/mm2 (P < 0.05), and 486 +/- 88 mg/mm2 versus 126 +/- 38 mg/mm2 (P < 0.01), respectively for ischemic and nonischemic femoral arteries. EC50 values showed that ischemic vessels were more sensitive to NE, KCl, and methoxamine (P < 0.05). Sodium nitroprusside induced concentration-dependent and complete relaxation in all arterial rings (100% relaxation) but the ischemic femoral artery showed less sensitivity (P < 0.05). Binding studies showed that the number of binding sites (Bmax) for [3H]Prazosin and [3H]Rauwolscine were significantly increased in ischemic versus nonischemic vessels (1261 +/- 95 fmole/mg versus 704 +/- 113 fmole/mg, P < 0.03, and 490 +/- 86 fmole/mg versus 175 +/- 15 fmole/mg, P < 0.04, respectively). Furthermore, a significant decrease in affinity (Kd) for [3H]Prazosin and [3H]Rauwolscine was observed in ischemic versus nonischemic tissues (9.4 +/- 1.7 nM versus 4 +/- 0.2 nM, P < 0.02, and 6.4 +/- 1.5 nM versus 1.8 +/- 0.6 nM, P < 0.01, respectively). The increase in canine femoral artery vasoreactivity, following prolonged ischemia, seems to be also due to an increased density and functional activity of alpha-adrenoceptors expressed by the ischemic arterial smooth muscle cells.
Animals↗
Effects of ischaemia and reperfusion on vasoactive neuropeptide levels in the canine infrarenal aortic revascularization model.
Infrarenal aortic cross-clamping is associated with remote vascular events, including myocardial infarction and renal insufficiency. The purpose of this study was to determine whether hindlimb ischaemia and reperfusion associated with infrarenal aortic cross-clamping results in the production of vasoactive regulatory neuropeptides. A canine model of infrarenal aortic cross-clamping was used for the study. Serial blood samples were drawn, prior to, at the time of, and serially following placement of the clamp and subsequent release of the clamp and reperfusion. Ischaemia resulted in increased mean(s.e.m.) plasma levels of neuropeptide Y (NPY) (initial 10.0(1.8) pmol/l versus ischaemia 24.7(2.3) pmol/l, P < 0.001) and vasoactive intestinal polypeptide (VIP) (initial 2.53(0.5) pmol/l versus ischaemia, 7.3(1.3) pmol/l, P < 0.05). Reperfusion produced three-fold elevation of VIP (initial 2.5(0.5) pmol/l versus reperfusion 9.6(1.5) pmol/l, P < 0.001), two-fold elevation in the plasma levels of endothelin-1 (initial 1.3(0.1) pmol/l versus reperfusion maximum 2.5(0.3) pmol/l, P < 0.01) and NPY (initial 10.0(0.8) pmol/l versus reperfusion maximum 23.9(2.3) pmol/l, P < 0.001). Ischaemia and reperfusion did not alter calcitonin gene-related peptide (CGRP) (a potent vasodilator) levels. Endothelin-1 (ET-1) plasma levels were also increased following haemorrhagic shock (initial 1.3(0.1) pmol/l versus exsanguination 3.4(0.4) pmol/l, P < 0.001), but not during ischaemia (initial 1.3(0.1) pmol/l versus ischaemia maximum 1.7(0.2) pmol/l, P = 0.7). It was concluded that vasoactive regulatory peptides are released following ischaemia, reperfusion and shock in the canine infrarenal aortic revascularization model and, therefore could contribute to remote vascular events observed with infrarenal aortic cross-clamping.
Animals↗
Modulation of monocyte adherence to endothelial cells by endothelin-1 involvement of Src (p60src) and JAK1-like kinases.
PURPOSE: The purpose of this study was to determine the transmembrane signaling pathway by which endothelin-1 (ET-1) enhances monocyte adherence to human umbilical vein endothelial cells (HUVECs) and to investigate the role of tyrosine kinases in this mechanism. METHODS: Adherence of purified human blood monocytes to HUVEC monolayers was assessed with radiolabeled monocytes. Tyrosine kinase activation was examined by immunoprecipitation and Western blotting. RESULTS: ET-1 potentiated monocyte adherence to HUVECs in a biphasic manner with peaks at 10(-10) mol/L and 10(-7) mol/L. A potent antagonist to ET B receptors, when used alone, had no effect. However, the antagonist, when combined with ET-1, significantly enhanced monocyte adherence to HUVECs. Incubation of ET-1 (10(-12) mol/L to 10(-7) mol/L) with HUVECs activated tyrosine kinases in a biphasic manner as identified by immunoblotting with PY20 antibody to tyrosine phosphorylated proteins. Phosphorylated proteins with Mr 60, 110, and 130 kDa were observed after ET-1 stimulation of HUVECs. Of interest, ET A or ET B receptor antagonists failed to antagonize the effect of ET-1. Rather, these receptor antagonists significantly augmented ET-1 induced tyrosine phosphorylation in HUVECs. Immunoprecipitation with antibodies to p60SRC and JAK1 kinases followed by immunoblotting with PY20 antibody suggested that ET-1 receptor response coupling in HUVECs involves the activation of p60SRC and JAK1-like kinases. CONCLUSIONS: These data suggest an association between activation of p60SRC and JAK1-like kinases and monocyte adherence in response to ET-1. ET-1-induced monocyte adherence is upregulated by ET B receptor antagonist, suggesting a negative feedback on cell adhesion through this receptor.
Blotting, Western↗
An audit of the cochlear implant service in Manchester.
The adult cochlear implant programme in Manchester was established in 1988 and the evaluation of the cochlear implant service involved the first 58 implants users (mean age = 51.65 years, range 19-75 years). Questionnaires were sent to implant users and their partners to evaluate the service with regard to provision of information, clinical care during in-patient assessments, waiting times, operation for cochlear implant and post-operative rehabilitation. The results show that the majority of patients (78 per cent) felt that the implant gave them as much or more benefit than expected. Areas identified for improvements include provision of more written information about cochlear implants; reduction in waiting times for first appointments; more information about the surgical risks and more instruction about home auditory training exercises for family and friends. As a consequence of the audit results the clinical practice and service provision for cochlear implantation in Manchester has been modified.
Adult↗
Arterial embolism from anatomical variation at the thoracic outlet.
Thoracic outlet syndrome (TOS) represents a constellation of symptoms arising from the compression of the neurovascular bundle as it exits the thorax. We report a unique case of multiple rare anatomical anomalies resulting in TOS manifested by distal arterial embolism. These anomalies include the combination of: (1) a unilateral right cervical rib, Gruber's type II (Gruber 1869), (2) nonunion of the first thoracic rib, (3) abnormal fibrous insertions of the anterior scalene muscle onto the epineurium of the brachial plexus and adventitia of the subclavian artery, (4) anterior position of the brachial plexus in relation to the third portion of the subclavian artery, and (5) the bifurcation of a single root of the phrenic nerve at the level of the anterior scalene muscle. This series of findings suggest an underlying developmental abnormality with a delayed onset of symptomatology consisting of the thoracic outlet syndrome.
Abnormalities, Multiple↗
University of Wisconsin solution effects on intimal proliferation in canine autogenous vein grafts.
This study was carried out to investigate if the University of Wisconsin solution (UWs) is suitable for long-term preservation of autogenous vein grafts (AVG) prior to transplantation, compared to autologous whole blood (AWB) and normal saline (NS). Autogenous jugular and femoral veins were harvested from adult mongrel dogs, using a "no-touch" technique. One segment of vein was immediately implanted to serve as a control, while other segments were stored for 24 hr at 4 degrees C in AWB, NS, or UWs. The control and the preserved veins were implanted as reversed interposition grafts in the common carotid or femoral artery positions. After 6 weeks, scanning electron microscopy revealed an intact endothelial cell monolayer in all vein grafts that was stained positively for factor VIII. The degree of intimal thickening, as assessed by light microscopy in the middle position of the grafts, was similar in controls (52.0 +/- 15.8 microns) and in veins stored in UWs (58.5 +/- 16.1 microns), but it was significantly increased (P < 0.05) in veins preserved in NS (198.9 +/- 19.5 microns) and in AWB (312.0 +/- 171.6 microns). Isometric tension studies revealed that maximum contraction and sensitivities (assessed by EC50) to norepinephrine were significantly reduced (P < 0.05) in AVG stored in AWB (0.05 +/- 0.02 g/mm2 and 5.5 +/- 2.8 microM), but not in UWs (0.16 +/- 0.03 g/mm2 0.92 +/- 0.34 microM) and NS (0.09 +/- 0.03 g/mm2 and 3.0 +/- 1.1 microM), compared with controls (0.17 +/- 0.03 g/mm2 and 0.99 +/- 0.38 microM). Acetylcholine (Ach)-induced maximum relaxations were similar in all of the veins.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Effect of endothelin-1 on arterial response to Bay K 8644. A comparison of ischemic and nonischemic arteries.
Endothelin-1 (ET-1) has been proposed as one of the possible mediators of the vasoconstriction seen following ischemia and reperfusion. We investigated the effect of ischemia and reperfusion on the contractile response of canine renal and iliac arteries to the dihydropyridine-type calcium channel agonist (+/-)Bay K 8644, following subthreshold doses of ET-1. No significant difference in the maximum tension was observed between the ischemic and nonischemic arteries in response to Bay K 8644 in the absence of ET-1. The addition of subthreshold dose of ET-1 (10(-10) M) resulted in a significant increase in sensitivity to Bay K 8644 in both the ischemic-reperfused and non-ischemic-reperfused arteries, with a 38 fold increase in iliac arteries and about 8 fold increase in the renal arteries. However, the ET-1 potentiated response was enhanced in the ischemic-reperfused in comparison to the non-ischemic-reperfused vessels in the iliac artery. These data suggest that the potentiating mechanism of ET-1 is not only intact, but enhanced in ischemic-reperfused vessels. Since the enhanced release of ET-1 in vivo is preceded by ischemia and reperfusion, the vasospastic phenomenon observed following these events could well be mediated by ET-1.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
G-proteins in rat blood vessels--I. Identification.
1. The purpose of this investigation was to identify various types of conventional, low and high molecular weight G-proteins in purified membranes of rat aorta and mesenteric artery. 2. In both blood vessels, immunoblotting of G-proteins using AS/7 antibody specific for Gi-1/2, EC/2 antibody specific for Gi-3 and RM/1 antibody specific for Gs-type conventional G-proteins demonstrated the presence of M(r) 28-43 kDa, M(r) 41 and 48 kDa, and M(r) 36-46 kDa polypeptides, respectively. Immunoblotting using a common antibody (GA/1) for the Gs and Gi alpha-subunits also revealed the existence of multiple polypeptides (M(r) 24-52 kDa) in both aorta and mesenteric artery, some of which were identified by the specific antibodies. The intensity and number of bands detected by most of the antibodies were greater in mesenteric artery than in aorta. 3. Cholera toxin (CT) catalyzed ADP-ribosylation of two Gs alpha (M(r) 43, 46 kDa) in both types of blood vessels with similar intensities of bands. Pertussis toxin (PT), on the other hand, catalyzed ADP-ribosylation of one Gi alpha (M(r) 41 kDa) polypeptide, and the intensity of this band was greater in aorta than in mesenteric artery. The polypeptides ADP-ribosylated by the toxins corresponded with their identification by antibodies. 4. Nitrocellulose blot overlay with [35S]GTP gamma S identified at least seven low molecular weight G-proteins (M(r) 21-30 kDa) in both aorta and mesenteric artery, with greater intensity of bands in mesenteric artery.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Diphosphate Ribose↗
G-proteins in rat blood vessels--II. Assessment of functional involvement.
1. In this study, we compared G-protein-mediated contractile responses of rat aorta and mesenteric artery rings induced by the alpha-adrenoceptor agonist, norepinephrine (NE) and by the direct G-protein activator, sodium fluoride, using various probes. 2. Activator of the stimulatory G-protein (Gs), cholera toxin (CT), attenuated the sensitivity and maximum contractile response of both aorta and mesenteric artery to NE and sodium fluoride. The effect of the toxin on the NE-sensitivity was greater in mesenteric artery. 3. Pretreatment of tissues with the inhibitor of Gi-protein, pertussis toxin (PT), reduced the sensitivity as well as maximum contraction of both the aorta and mesenteric artery to sodium fluoride, and of the mesenteric artery to NE. PT attenuated only the sensitivity but not the maximum contraction of the aorta to NE. The inhibitory effect of PT on sensitivity to NE or sodium fluoride was greater in the aorta. 4. NE and sodium fluoride-induced contractions were reduced by the sulfhydryl G-protein inhibitor, N-ethylmaleimide (NEM) in both blood vessels. NEM produced greater inhibitory effect on the sensitivity of the aorta to both contractile agents. 5. These data demonstrate that CT, PT and NEM-sensitive G-proteins are involved in NE- and sodium fluoride-induced contractile responses of the rat aorta and mesenteric artery. The differential effects of the G-protein probes indicate that certain variations in G-protein-mediated contractile responses exist among the two blood vessels, suggesting that G-protein involvement in functional responses may vary with the type of blood vessel investigated.
Animals↗