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PubMed1993

Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow.

OBJECTIVES: The purpose of this study was to test the utility of measuring respiratory variation in pulmonary venous flow by transesophageal echocardiography. BACKGROUND: Respiratory variation of atrioventricular and central venous flow velocities by Doppler echocardiography has been used to differentiate constrictive pericarditis from restrictive cardiomyopathy. METHODS: We performed pulsed wave Doppler transesophageal echocardiography of the left or right pulmonary veins in 31 patients with diastolic dysfunction. Fourteen patients had constrictive pericarditis, and 17 had restrictive cardiomyopathy. We measured the pulmonary venous peak systolic and diastolic flow velocities and the systolic/diastolic flow ratio with transesophageal echocardiography during expiration and inspiration. The percent change in Doppler flow velocity from expiration to inspiration (%E) was calculated. RESULTS: Pulmonary venous peak systolic flow in both inspiration and expiration was greater in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak systolic flow tended to be higher in constrictive pericarditis (19% vs. 10%, p = 0.09). In contrast, pulmonary venous peak diastolic flow during inspiration was lower in constrictive pericarditis than in restrictive cardiomyopathy. The %E for peak diastolic flow was larger in constrictive pericarditis (29% vs. 16%, p = 0.008). The pulmonary venous systolic/diastolic flow ratio was greater in constrictive pericarditis in both inspiration and expiration. The combination of pulmonary venous systolic/diastolic flow ratio > or = 0.65 in inspiration and a %E for peak diastolic flow > or = 40% correctly classified 86% of patients with constrictive pericarditis. CONCLUSIONS: The relatively larger pulmonary venous systolic/diastolic flow ratio and greater respiratory variation in pulmonary venous systolic, and especially diastolic, flow velocities by transesophageal echocardiography can be useful signs in distinguishing constrictive pericarditis from restrictive cardiomyopathy.

Blood Flow Velocity↗
PubMed2001

Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy.

This study assesses how the newer modalities of tissue Doppler echocardiography and color M-mode flow propagation compare with respiratory variation of Doppler flow in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. We studied 30 patients referred for further evaluation of diastolic function who had a diagnosis of constrictive pericarditis or restrictive cardiomyopathy established by diagnostic tests, including clinical assessment, magnetic resonance imaging, cardiac catheterization, endomyocardial biopsy, and surgical findings. Nineteen patients had constrictive pericarditis and 11 had restrictive cardiomyopathy. We performed 2-dimensional transesophageal echocardiography combined with pulsed-wave Doppler of the pulmonary veins and mitral inflow with respiratory monitoring, tissue Doppler echocardiography of the lateral mitral annulus, and color M-mode flow propagation of left ventricular filling. Respiratory variation of the mitral inflow peak early (peak E) velocity of > or =10% predicted constrictive pericarditis with 84% sensitivity and 91% specificity and variation in the pulmonary venous peak diastolic (peak D) flow velocity of > or =18% distinguished constriction with 79% sensitivity and 91% specificity. Using tissue Doppler echocardiography, a peak early velocity of longitudinal expansion (peak Ea) of > or =8.0 cm/s differentiated patients with constriction from restriction with 89% sensitivity and 100% specificity. A slope of > or =100 cm/s for the first aliasing contour in color M-mode flow propagation predicted patients with constriction with 74% sensitivity and 91% specificity. Thus, the newer methods of tissue Doppler echocardiography and color M-mode flow propagation are equivalent and complimentary with Doppler respiratory variation in distinguishing between constrictive pericarditis and restrictive cardiomyopathy. The additive role of the new methods needs to be established in difficult cases of constrictive pericarditis where respiratory variation may be absent or decreased.

Adult↗
PubMed1984

Diagnosis of constrictive pericarditis by two-dimensional echocardiography: studies in a new experimental model and in patients.

The purpose of this study was to determine the value of two-dimensional echocardiography in detecting constrictive pericarditis. Serial two-dimensional echocardiography was performed in eight closed chest conscious dogs with experimental constrictive pericarditis, using a new model that creates constrictive pericarditis by the introduction of a pericardial irritant mixture. Constrictive pericarditis was confirmed in these dogs by cardiac catheterization and pathologic examination. Four patients with constrictive pericarditis and three patients with restrictive cardiomyopathy (amyloidosis) were also studied. Analysis of short-axis two-dimensional echocardiograms was performed to determine the frame by frame change in left ventricular cavity areas throughout diastole. Curves of diastolic left ventricular cavity area change versus percent duration of diastole were constructed for each animal and human subject. Pericardial thickness was measured at various gain settings on two-dimensional and M-mode echocardiograms and at post-mortem examination. In dogs with constrictive pericarditis, the echocardiograms seriously overestimated and correlated poorly with pathologic measurements of pericardial thickness. In dogs after constrictive pericarditis developed, 69 +/- 11% (mean +/- SD) (range 50 to 84) of cavity area change occurred in the initial 30% of diastole compared with 35 +/- 7% (range 20 to 45) in control two-dimensional echocardiograms (p less than 0.001). Four patients with constrictive pericarditis showed similar accelerated cavity expansion in early diastole, but three patients with cardiac amyloidosis showed more variable left ventricular diastolic expansion rates. It is concluded that two-dimensional echocardiograms can demonstrate characteristic diastolic filling abnormalities in constrictive pericarditis, but cannot accurately measure pericardial thickness.

Amyloidosis↗
PubMed1999

Left ventricular systolic and diastolic function after pericardiectomy in patients with constrictive pericarditis: Doppler echocardiographic findings and correlation with clinical status.

OBJECTIVES: The study assessed changes in left ventricular systolic and diastolic function after pericardiectomy in patients with constrictive pericarditis and correlated postoperative Doppler echocardiographic findings with clinical status. BACKGROUND: Despite the efficacy of pericardiectomy, some patients with constrictive pericarditis fail to improve postoperatively. Data on serial evaluation of systolic and diastolic function after pericardiectomy and its relation to clinical status are not available. METHODS: From 1985 to 1995, a total of 58 patients with constrictive pericarditis underwent pericardiectomy and had at least one follow-up Doppler echocardiographic study with a respirometer: 23 patients had one examination within 3 months postoperatively, 19 had a study within 3 months and another one more than 3 months postoperatively, and 16 had one study more than 3 months postoperatively. RESULTS: In the early postoperative period, diastolic function was normal in 17 patients (40.5%), restrictive in 17 (40.5%), and constrictive in 8 (19%). Among 19 patients who had serial Doppler echocardiography, in 2 patients with restrictive physiology and 5 with constrictive physiology the results had become normal, and 1 patient who had had constrictive physiology had restrictive findings. In late follow-up, left ventricular end-diastolic diameter increased compared with preoperative measurement (p = 0.0009). Diastolic filling pattern at late follow-up was normal in 20 patients (57%), restrictive in 12 (34%) and constrictive in 3 (9%). There was a significant relationship between diastolic filling patterns and symptomatic status (chi2 = 20.9, p < 0.0001). Patients with persistent abnormal diastolic filling on Doppler echocardiography had had symptoms for a longer time preoperatively than did patients with normal diastolic physiology (p = 0.0471). CONCLUSIONS: Diastolic filling characteristics remain abnormal in a substantial number of patients with constrictive pericarditis after pericardiectomy. These abnormalities may resolve gradually but can persist. Diastolic filling abnormalities after pericardiectomy correlate well with clinical symptoms and tend to occur in patients who have had symptoms longer preoperatively. This finding supports the recommendation that pericardiectomy be performed promptly in symptomatic patients with constrictive pericarditis.

Adolescent↗
PubMed1975

Cardiac tamponade, constrictive pericarditis and pericardial resection in rheumatoid arthritis.

Four patients with rheumatoid constrictive pericarditis and two patients with rheumatoid cardiac tamponade are presented, and 60 previously reported cases with these two complications are reviewed. Rheumatoid arthritis was moderate to severe in 84% of the patients with cardiac tamponade and in 74% of the patients with constrictive pericarditis. However, both these complications were also seen in patients who had only mild arthritis and in two previously reported cases constrictive pericarditis actually preceded the onset of rheumatoid arthritis. The duration of rheumatoid arthritis had no bearing on the development of these complications. In 75% of patients with cardiac tamponade, and in 66% of cases with constrictive pericarditis, subcutaneous nodules were present. In those cases where the rheumatoid factor was measured it was positive in 92% with cardiac tamponade and in 84% with constrictive pericarditis. In 63% of patients with cardiac tamponade and in 70% of cases with constrictive pericarditis a history of pericardial type of pain was obtained and/or a pericardial rub heard. The diagnosis of cardiac tamponade and constrictive pericarditis was made clinically and in doubtful cases confirmed by cardiac screening and intracardiac pressure recordings. The low sugar content in the pericardial fluid in the absence of infection or malignancy was an important clue to the rheumatoid etiology of the effusion. In the majority of the cases histological appearances of the pericardial tissue showed non-specific fibrous reaction and infiltration with plasma cells and lymphocytes. Only in five of the cases, including one from the present series, were typical rheumatoid granulomatous lesions demonstrated. Treatment with corticosteroids neither prevented the occurrence nor led to amelioration of either cardiac constriction or tamponade. Pericardial resection was life saving, producing both symptomatic and objective involvement of the cardiac function. In the present series of six cases two patients developed aortic incompetence. In one of these it was due to rheumatoid granulomatous valve disease and in the other due to non-specific aortic valvulitis. The combination of constrictive pericarditis and granulomatous aortic valve disease has not been previously recorded.

Adult↗
PubMed2001

Renal fibrosis in diabetic and aortic-constricted hypertensive rats.

To assess if the renal damage observed in rats with diabetes and hypertension is due to hemodynamic or metabolic changes, a progressive aortic constriction between the two renal arteries has been done in streptozotocin-induced diabetic rats (constriction + diabetes group) and in nondiabetic rats (constriction group). This model allows us to study two kidneys subjected to different perfusion pressure (PP) in the same metabolic environment. One-month-old rats (100-120 g body wt) were subjected to the aortic constriction procedure. Three months after constriction, glomerular filtration rate and renal plasma flow were similar in both kidneys of the two groups. PP was greater in the kidney placed over the ligature [constriction high-pressure kidney (CH) or constriction + diabetic high-pressure kidney (DH)] than in the one placed below the ligature [constriction low pressure (CL) or constriction + diabetic low pressure (DL)]. Proteinuria was higher in the CH than in the CL kidneys (512 +/- 61 vs. 361 +/- 38 microg/30 min, respectively) and much higher in the DH kidney (770 +/- 106 microg/30 min). Renal fibrosis was measured in tissue sections stained with Syrius red using a computer-assisted image analysis system. DH and DL kidneys showed higher corpuscular cross-sectional and capillary tuft areas than the CH and CL ones. The DH kidney showed slight mesangial expansion and thickening of the capillary walls, which were more pronounced in the former. Most renal corpuscles from CH and DH groups were nearly normal in morphology appearance, and only in some instances a slight increment in mesangium was observed. Transforming growth factor-beta1 (TGF-beta1) immunostaining revealed that DH kidneys showed the highest glomerular expression. We concluded that 1) diabetic animals develop glomerular but not interstitial fibrosis to a greater extent than nondiabetic animals and that this lesion principally occurs in the hypertensive kidney (DH), and 2) increased TGF-beta expression is associated with diabetic renal damage.

Animals↗
PubMed1997

Phasic coronary flow characteristics in patients with constrictive pericarditis: comparison with restrictive cardiomyopathy.

BACKGROUND: Phasic coronary flow characteristics have been reported in patients with aortic valve disease and hypertrophic cardiomyopathy. The purpose of this study was to assess the differences in coronary flow characteristics between patients with constrictive pericarditis and those with restrictive cardiomyopathy. METHODS AND RESULTS: The study populations consisted of 7 case patients with constrictive pericarditis, 8 with restrictive cardiomyopathy, and 11 control subjects with chest pain and normal coronary arteries. Five minutes after injection of 3 mg of isosorbide dinitrate, phasic coronary flow velocity patterns were analyzed in the proximal segment of the angiographically normal left anterior descending coronary artery at rest using a 0.014-in, 15-MHz Doppler guidewire. Coronary flow reserve was obtained from the ratio of adenosine-induced (0.14 mg x kg(-1) x min(-1) I.V.) hyperemic/baseline time-averaged peak velocity. Although in case patients with constrictive pericarditis and restrictive cardiomyopathy maximal hyperemic time-averaged peak velocity (21+/-8 and 31+/-17 versus 60+/-19 cm/s, respectively; P<.001) and coronary flow reserve (1.3+/-0.4 and 1.6+/-0.6 versus 3.6+/-0.4, respectively, P<.001) were significantly lower than in control subjects, there were no significant differences in these indexes between the two groups of case patients. Velocity half-time of diastolic flow velocity corrected by square root(RR), which indicates deceleration of diastolic flow, in the groups of case patients with constrictive pericarditis and restrictive cardiomyopathy was significantly less than that in control subjects (6.2+/-2.6 and 10.6+/-1.5 versus 16.9+/-2.7, respectively; P<.001); this was also significantly smaller in constrictive pericarditis than restrictive cardiomyopathy (P<.001). This index <9.5 could distinguish constrictive pericarditis from restrictive cardiomyopathy with a sensitivity of 86% and a specificity of 88%. Furthermore, time from the beginning of diastole to diastolic peak velocity corrected by square root(RR) indicating acceleration of diastolic flow velocity in constrictive pericarditis was significantly less than that in restrictive cardiomyopathy and control subjects (2.8+/-1.2 versus 4.8+/-0.8 and 4.4+/-0.6, respectively; P<.001). CONCLUSIONS: Although coronary flow reserve is limited in both constrictive pericarditis and restrictive cardiomyopathy because of restriction of hyperemic response, rapid acceleration and more rapid deceleration of diastolic flow velocity are more characteristic in constrictive pericarditis than in restrictive cardiomyopathy.

Adult↗
PubMed2000

Reversal of hypercapnia induces KATP channel and NO-independent constriction of basilar artery in rabbits with acute metabolic alkalosis.

The mechanism of hypocapnic constriction of the cerebral vasculature under conditions of altered acid-base balance has not been investigated. As K(ATP) channels and NO have been implicated in hypocapnic constriction, this study investigated their roles in the constriction due to lowered pCO(2) in hypercapnic rabbits with acute metabolic alkalosis. Metabolic alkalosis was induced acutely following ketamine/xylazine injection. Lowering blood pCO(2) from initial baseline hypercapnic levels to near normocapnic and hypocapnic levels constricted basilar artery by 10.2+/-0.8% (4) and 16.2+/-0.6% (44), respectively (means+/-S.E., n), as determined in an in situ cranial window preparation. The constrictions were maintained for 4-5 h and return of pCO(2) to hypercapnic levels relaxed the constriction. Changing the suffusate pH to either the pH of the cerebral spinal fluid observed during initial baseline hypercapnia or following lowered pCO(2) did not alter the magnitude of constriction due to lowered pCO(2). Neither 0.3 mM N(G)-monomethyl-L-arginine monoacetate, an NO synthase inhibitor, nor 10 microM glibenclamide, a K(ATP) channel blocker, altered the magnitude of hypocapnic constriction. These results demonstrated that under conditions of acute metabolic alkalosis and accompanying compensatory hypercapnia, subsequent pCO(2) reduction induces prolonged constriction of the basilar artery that is independent of (1) cerebral spinal fluid pH over a physiologic range, and (2) NO and K(ATP) channels.

ATP-Binding Cassette Transporters↗
PubMed1999

Roles of oxygen radicals and elastase in citric acid-induced airway constriction of guinea-pigs.

Antioxidants attenuate noncholinergic airway constriction. To further investigate the relationship between tachykinin-mediated airway constriction and oxygen radicals, we explored citric acid-induced bronchial constriction in 48 young Hartley strain guinea-pigs, divided into six groups: control; citric acid; hexa(sulphobutyl)fullerenes + citric acid; hexa(sulphobutyl)fullerenes + phosphoramidon + citric acid; dimethylthiourea (DMTU) + citric acid; and DMTU + phosphoramidon + citric acid. Hexa(sulphobutyl)fullerenes and DMTU are scavengers of oxygen radicals while phosphoramidon is an inhibitor of the major degradation enzyme for tachykinins. Animals were anaesthetized, paralyzed, and artificially ventilated. Each animal was given 50 breaths of 4 ml saline or citric acid aerosol. We measured dynamic respiratory compliance (Crs), forced expiratory volume in 0.1 (FEV0.1), and maximal expiratory flow at 30% total lung capacity (Vmax30) to evaluate the degree of airway constriction. Citric acid, but not saline, aerosol inhalation caused marked decreases in Crs, FEV0.1 and Vmax30, indicating marked airway constriction. This constriction was significantly attenuated by either hexa(sulphobutyl)fullerenes or by DMTU. In addition, phosphoramidon significantly reversed the attenuating action of hexa(sulphobutyl)fullerenes, but not that of DMTU. Citric acid aerosol inhalation caused increases in both lucigenin- and t-butyl hydroperoxide-initiated chemiluminescence counts, indicating citric acid-induced increase in oxygen radicals and decrease in antioxidants in bronchoalveolar lavage fluid. These alterations were significantly suppressed by either hexa(sulphobutyl)fullerenes or DMTU. An elastase inhibitor eglin-c also significantly attenuated citric acid-induced airway constriction, indicating the contributing role of elastase in this type of constriction. We conclude that both oxygen radicals and elastase play an important role in tachykinin-mediated, citric acid-induced airway constriction.

Animals↗
PubMed1987

Halothane relaxes previously constricted isolated porcine coronary artery segments more than isoflurane.

Coronary vasodilation by halothane and isoflurane were compared using in vitro tension recording. Porcine left anterior descending coronary arterial segments (1.5-2.0 mm o.d.) were constricted with either K+ (30 mM) or prostanoid U44069 (6 X 10(-7) M) in the absence of other drugs or anesthetics. Following stabilization of constriction, arteries were exposed to halothane or isoflurane at 0.5, 1.0, 1.5, 2.0, and 3.0% concentrations. K+ (30 mM) induced constriction was reduced by halothane at 1.5, 2.0, and 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced at 0.5, 1.0, 1.5, 2.0, and 3.0%. K+ (30 mM) induced constriction was reduced by isoflurane only at 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced by isoflurane only at 2.0 and 3.0%. U44069 induced constriction was more susceptible than K+ induced constriction to relaxation by halothane or isoflurane. Halothane was more potent than isoflurane as a direct relaxant of porcine epicardial left anterior descending arterial segments previously constricted with K+ (30 mM) or U44069 (6 X 10(-7) M).

Animals↗
PubMed2000

Inhibitory effects of halothane, isoflurane, sevoflurane, and pentobarbital on the constriction induced by hypocapnia and bicarbonate in isolated canine cerebral arteries.

The effects of halothane, isoflurane, sevoflurane (0.5, 1 and 2 MAC) and pentobarbital (10(-5) M, 10(-4) M and 3 x 10(-4) M) on hypocapnia- and bicarbonate-induced constriction of isolated dog middle cerebral arteries were investigated in vitro. The isometric tension of isolated cerebral arterial rings was measured in an organ bath containing Krebs bicarbonate solution, aerated with 5% CO2 and 95% O2. Hypocapnia, induced by replacing the bathing solution with one that had been equilibrated with 2.5% CO2 and 97.5% O2, produced a sustained vasoconstriction (268 +/- 36 mg, mean +/- SEM). Exposure of arterial rings to a bathing solution that contained double the concentration of NaHCO3 (50 mM) elicited a phasic constriction followed by a gradual decrease in tension (309 +/- 34 mg). Although halothane, isoflurane, and sevoflurane attenuated both hypocapnia- and bicarbonate-induced constrictions in a dose-dependent manner, the inhibition of these constrictions was greater in rings treated with halothane than in those treated with isoflurane or sevoflurane when compared at equipotent concentrations. These alkaline-induced constrictions were attenuated by pentobarbital only at the highest concentration of 3 x 10(-4) M. Halothane (1 and 2 MAC) attenuated the constriction induced by hypocapnia to a greater extent than that induced by 15 mM KCl, whereas pentobarbital (10(-4) M and 3 x 10(-4) M) attenuated hypocapnia-induced constriction less than KCl-induced constriction. These results indicate that alkaline-induced constriction is more vulnerable to halothane than other volatile anesthetics and pentobarbital. The mechanisms of the inhibitory effects of halothane and pentobarbital on alkaline-induced cerebral vasoconstriction seem to differ; the inhibitory effect of pentobarbital, but not of halothane may be, in part, ascribed to its inhibitory effect on the Ca++ influx.

Anesthetics, Inhalation↗
PubMed2005

Constriction velocities of renal afferent and efferent arterioles of mice are not related to SMB expression.

BACKGROUND: Constriction of renal arterioles contributes significantly to the control of perfusion and glomerular filtration. Afferent but not efferent arterioles express smooth muscle myosin heavy chain B (SMB) (with a 5'-insert of seven amino acids). The aim of the present study was to investigate (1) the constriction characteristics of afferent and efferent arterioles under physiologic load and (2) whether expression of SMB may causally contribute to these constriction characteristics. METHODS: We compared constriction parameters [constriction amplitude, maximal rate of constriction velocity ("dc/dt(max)"), and time to half-maximal constriction (t(1/2)) of in vitro perfused renal afferent and efferent arterioles of wild-type (smb(+/+)] and homozygous SMB knockout [smb(-/-)] mice upon stimulation with angiotensin II (Ang II) (10(-8) mol/L) and potassium chloride (KCl) (100 mmol/L). SMB expression was investigated by double-labeling immunofluorescence. RESULTS: Contraction amplitude and dc/dt(max) of mouse afferent arterioles upon Ang II stimulation were significantly greater compared to efferent arterioles. However, constriction amplitudes, dc/dt(max), and t(1/2) of afferent as well as efferent arterioles upon Ang II stimulation were similar in smb(+/+) and smb(-/-) mice. Constriction amplitudes upon KCl stimulation of afferent arterioles were similar in both smb(+/+) and smb(-/-) mice. Furthermore, KCl-induced dc/dt(max) and t(1/2) of afferent arterioles were similar in both smb(+/+) and smb(-/-) mice. SMB expression could be detected in afferent but not efferent arterioles in smb(+/+) mice. No SMB expression in either arteriole could be observed in smb(-/-) mice. CONCLUSION: Our results suggest that the presence of different alternatively 5'-spliced smooth muscle-myosin heavy chain (SM-MHC) isoforms does not dominate the different contractile features of physiologically loaded renal afferent or efferent arterioles.

Alternative Splicing↗
PubMed1969

The re-distribution of cytochrome oxidase, noradrenaline and adenosine triphosphate in adrenergic nerves constricted at two points.

1. The experiments correlate certain changes in the ultrastructure of cat hypogastric nerves constricted at two points with the distribution of a mitochondrial enzyme (cytochrome oxidase), noradrenaline (stored in some of the vesicles with an electron dense core, i.e. granular vesicles) and adenosine triphosphate (ATP) (present in noradrenaline storage granules, mitochondria and the soluble fraction of the axon).2. Noradrenaline (NA) and granular vesicles accumulated proximal but not distal to both constrictions. The total amount of NA and the concentration of granular vesicles above the first constriction was greater than that present in a similar piece of normal nerve, indicating that the cell body was continuing to produce the transmitter despite injury to its axon. The granular vesicles proximal to the first constriction were found in swollen or distorted axons and in new axonal outgrowths. It was concluded that the movement of NA in these constricted nerves was only centrifugal in direction.3. Mitochondria and cytochrome oxidase accumulated on both sides of the two constrictions, indicating a bi-directional movement of mitochondria in the damaged axons. The possibility that some of the increase in the cytochrome oxidase could be related to an increase in the number of mitochondria in cells other than neurones is considered.4. The adenosine triphosphate content increased on both sides of the two constrictions. This increase developed more slowly and was less marked than that of the other two substances.5. It was concluded that (a) there was a close correlation between the behaviour of noradrenaline and granular vesicles and between cytochrome oxidase and mitochondria, (b) the dense cored vesicles and the mitochondria moved independently of one another and at different rates after constriction of non-myelinated axons, (c) while some of the changes may be attributed to an obstruction to the free movement of axoplasm others may be due to an active reaction to axonal injury, and (d) localized intraaxonal synthesis of noradrenaline and cytochrome oxidase did not occur between the two constrictions.

Adenosine Triphosphate↗
PubMed1995

Inhibition of arteriole alpha 2- but not alpha 1-adrenoceptor constriction by acidosis and hypoxia in vitro.

We have found that hypoxia and acidosis inhibit constriction by alpha 2D-adrenoceptors but not by alpha 1D-adrenoceptors on arterioles of rat skeletal muscle, facilitating local metabolic control of blood flow. When activated by full agonists like norepinephrine, this alpha 2D-constriction relies on Ca2+ influx through dihydropyridine-sensitive, voltage-operated Ca2+ channels (VOC), while alpha 1D-constriction does not. The purpose of the present study was to examine the dose sensitivity of this selective metabolic inhibition of alpha 2D-constriction and determine whether inhibition of VOCs is involved. Changes in lumen diameter of microcannulated arterioles isolated from rat skeletal muscle (107 +/- 3 microns control diam) were measured by videomicroscopy for bath-added agents. Decreases in pH (7.4-7.0) or PO2 (70 to 10 mmHg) caused graded inhibition of alpha 2D-adrenoceptor constriction (UK-14304 plus prazosin); the half-maximum inhibitory concentration for acidosis was 7.1 and for PO2 was 24 mmHg. alpha 1D-Adrenoceptor constriction by the respective full and partial alpha 1-agonists, phenylephrine (PE) and St-587 (both plus rauwolscine), was unaffected. Because St-587 but not PE constriction was dependent on VOC activation, the sensitivity of alpha 2D- but not alpha 1D-constriction to acidosis and hypoxia appeared to be independent of reliance on VOCs. This was examined directly; contractile sensitivity to KCl and the VOC agonist, SDZ-202-791, was unaffected by pH 7.0 or PO2 10 mmHg. These data suggest that alpha 2D-constriction is sensitive to inhibition by hypoxia and acidosis through a mechanism that does not involve direct blockade of dihydropyridine-sensitive Ca2+ channels.

Acidosis↗
PubMed1993

Inhibition of neutral endopeptidase augments anaphylactic constriction of guinea pig tracheal smooth muscle.

To determine whether tachykinins participate in antigen-induced constriction of tracheal smooth muscle, we examined the effects of a neutral endopeptidase inhibitor, phosphoramidon, the tachykinin antagonist (D-Pro4, D-Trp7,9,10)-substance P(4-11), and capsaicin-induced tachykinin depletion on the responses to antigen in tracheal rings from ovalbumin-sensitized guinea pigs. In these preparations, the antigen (ovalbumin, 0.1 microgram/ml) produced reproducible and durable constriction of tracheal smooth muscle. Incubation with phosphoramidon (10 min, 10 microM) prior to antigen challenge significantly augmented the magnitude of ovalbumin-induced constriction by 22% after 30 min and by 31% after 45 min. The addition of phosphoramidon at the plateau level of antigen-induced constriction produced a similar, significant increase in the magnitude of the constriction. Following incubation with tachykinin antagonist (D-Pro4,D-Trp7,9,10)-substance P(4-11) (5 microM), the contractile response of the tracheal rings to the antigen was not altered. Furthermore, the addition of phosphoramidon (10 microM) did not significantly affect this contraction. Similarly, neither tachykinin antagonist nor phosphoramidon altered the ovalbumin-induced constriction of the tracheal rings from capsaicin-treated guinea pigs. Based on these findings, we hypothesize that tachykinins or similar broncho-constricting neutral endopeptidase substrates were released from tachykinin-containing nerve endings during immediate hypersensitivity reaction in airways, manifesting a modest and delayed constrictive effect. Following alteration of endopeptidase activity, these substances could modulate the anaphylactic constriction of the airway smooth muscle.

Anaphylaxis↗
PubMed1993

Endothelium-dependent relaxation competes with alpha 1- and alpha 2-adrenergic constriction in the canine epicardial coronary microcirculation.

BACKGROUND: The purpose of this study was to determine whether endothelium-dependent relaxation competes with alpha 1- and alpha 2-adrenergic coronary microvascular constriction in the beating heart in vivo. METHODS AND RESULTS: Coronary microvascular diameters were measured using stroboscopic epi-illumination and intravital microscopy during fluorescein microangiography in open-chested dogs (n = 20). Both alpha 1- and alpha 2-adrenergic receptors were selectively activated by intracoronary infusions of norepinephrine (0.05 and 0.2 microgram.kg-1 x min-1) in the presence of the alpha 2-adrenergic antagonist rauwolscine (0.2 mg/kg) or the alpha 1-adrenergic antagonist prazosin (0.75 mg/kg) during beta-adrenergic blockade (1 mg/kg propranolol). Microvascular diameters during selective alpha-adrenergic receptor activation were measured under baseline conditions and after inhibition of endogenous nitric oxide synthesis by an analogue of L-arginine, either NG-nitro-L-arginine (L-NA, 30 mg/kg) or NG-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg). Under baseline conditions, alpha 1-adrenergic activation constricted small arteries (vessels with diameters between 100 and 300 microns) (4 +/- 1% and 5 +/- 1% decrease in diameter for the low and high doses of norepinephrine, respectively, both p < 0.05) but did not change the diameter of arterioles (vessels with diameters < 100 microns). In contrast, alpha 2-adrenergic activation by the lower but not the higher dose of norepinephrine induced constriction of arterioles (6 +/- 2% and 3 +/- 4% decrease in diameter, p < 0.05 and NS, respectively) but not small arteries. Inhibition of nitric oxide synthase activity by either L-NA or L-NAME produced constriction of small coronary arteries (9 +/- 2% decrease in diameter, p < 0.01) and arterioles (6 +/- 1% decrease in diameter, p < 0.05). The dilatation of small arteries and arterioles by acetylcholine (0.05 microgram-1 x kg-1 x min-1 intracoronary infusion; 10 +/- 1% increase in diameter under baseline conditions, p < 0.05) was abolished by either analogue. Both alpha 1- and alpha 2-adrenergic coronary microvascular constriction were markedly potentiated after L-NA or L-NAME. alpha 1-Adrenergic constriction was unmasked in arterioles (7 +/- 3% and 10 +/- 4% decrease in diameter, p < 0.05), although it was not significantly increased in small arteries. Conversely, alpha 2-adrenergic constriction was unmasked in small arteries (8 +/- 1% and 6 +/- 2% decrease in diameter, both p < 0.05) and potentiated in arterioles (12 +/- 1% and 8 +/- 4% decrease in diameter, both p < 0.05). After L-NA or L-NAME, microvessels retained the ability to dilate to sodium nitroprusside (0.1 microgram.kg-1 x min-1 intracoronary infusion; 10 +/- 2% increase in diameter, p < 0.05). alpha-Adrenergic constriction was not accentuated by increased tone alone, since it was either attenuated or converted to dilatation during a similar degree of preconstriction by the endothelium-independent vasoconstrictor angiotensin II (p < 0.05 for both alpha 1- and alpha 2-adrenergic activation). CONCLUSIONS: These data confirm that alpha-adrenergic receptors are widespread in the coronary microcirculation, with the baseline functional responses to alpha 1-adrenergic activation predominating in small arteries and those to alpha 2-adrenergic activation predominating in arterioles. Furthermore, coronary microvascular constriction caused by both alpha 1- and alpha 2-adrenergic receptor activation is significantly modulated by endothelium-dependent relaxation, being markedly potentiated by inhibition of nitric oxide synthase activity. The data imply that alpha-adrenergic activation will assume considerable importance as a determinant of coronary microvascular resistance in pathophysiological situations associated with coronary endothelial impairment.

Animals↗
PubMed1991

Effect of reduced blood flow on alpha 1- and alpha 2-adrenoceptor constriction of rat skeletal muscle microvessels.

Adrenergic constriction of skeletal muscle arterioles, particularly small terminal arterioles, is opposed by decreased blood flow or increased metabolic rate. Our previous studies indicate that neural constriction of large arterioles, which have both postjunctional alpha 1- and alpha 2-adrenoceptors, is mediated by alpha 1-receptors; small arterioles depend on alpha 2-receptors. Also, alpha 2, but not alpha 1, constriction is reduced by acidosis. Differential sensitivity of alpha 1 versus alpha 2 constriction to metabolic signals such as H+ may underlie the sensitivity of arteriolar adrenergic constriction to metabolic inhibition. To examine this hypothesis, we studied the effect of reduced perfusion on alpha 1- versus alpha 2-mediated constriction of large arterioles and venules. Intravital microscopy of rat cremaster skeletal muscle was used to obtain concentration-response curves for phenylephrine (alpha 1-agonist) and UK-14,304 (alpha 2-agonist). Thirty percent reduction in cremasteric artery flow by venous outflow obstruction had no effect on baseline diameter, indicating no effect on "intrinsic tone." Reduced perfusion also had no effect on arteriolar or venular sensitivity to phenylephrine or venular sensitivity to UK-14,304 but significantly attenuated arteriolar response to UK-14,304. To examine a possible mechanism for the selective inhibition of alpha 2 constriction by acidosis, we determined the effect of acidosis on the partial alpha 1-agonist St587. Like alpha 2 constriction, St587-mediated constriction of arterioles was reduced during acidosis and was attenuated by nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed2003

Stroke development in stroke-prone spontaneously hypertensive rats alters the ability of cerebrovascular muscle to utilize internal Ca2+ to elicit constriction.

BACKGROUND AND PURPOSE: The ability of middle cerebral arteries (MCAs) to utilize intracellular smooth muscle (SM) Ca2+ to produce constriction in response to pressure and agonists was assessed in relation to hemorrhagic stroke development in Wistar-Kyoto stroke-prone (SHRSP) and stroke-resistant (srSHR) spontaneously hypertensive rats. METHODS: MCAs were studied with the use of a pressure myograph at 100 mm Hg. RESULTS: MCAs from srSHR and prestroke SHRSP exhibited pressure-dependent constriction and constricted in response to vasopressin or serotonin in the presence of nifedipine or the absence of [Ca2+]o. MCAs from poststroke SHRSP lost the latter functions and could only constrict in response to vasopressin/serotonin in Krebs' solution containing Ca2+ in the absence of nifedipine. This indicated that the SM could not utilize internal Ca2+ for constriction and maintained constriction by Ca2+ entry through L-type channels. The MCAs of poststroke SHRSP could not constrict to [K+]o-induced depolarization, suggesting that the agonist-induced opening of the L-type channels occurred by mechanisms other than SM depolarization. Depletion of the sarcoplasmic SM Ca2+ stores of MCAs from srSHR with cyclopiazonic acid did not prevent pressure-dependent constriction. CONCLUSIONS: Stroke in SHRSP produced a defect in the ability of MCAs to constrict in response to vasopressin or serotonin via the use of an intracellular source of Ca2+. This could be promoted by an inability of the SM to release intracellular Ca2+, by the depletion of internal Ca2+ stores, or by a decrease in the contractile sensitivity to Ca2+ released from the internal stores.

Animals↗