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PubMed1993

Accurate preoperative diagnosis of pericardial constriction using cine computed tomography.

OBJECTIVES: The purpose of this study was to determine the accuracy of cine computed tomography in the diagnosis of constrictive pericarditis. BACKGROUND: Constrictive pericarditis is characterized by abnormalities of both cardiac structure and function. Accurate diagnosis requires detection of both a thickened pericardium and abnormal ventricular diastolic filling. At present, no one diagnostic technique has demonstrated sufficient accuracy in this setting. Cine computed tomography is a relatively new cardiac imaging mode with very high time and spatial resolution that has the potential to accurately diagnose constrictive pericarditis. METHODS: Twelve consecutive patients were retrospectively identified who had catheterization findings suggestive of constrictive physiology, had undergone a cine computed tomographic examination and had pathologic data that delineated the status of the pericardium. Group 1 (with constrictive pericarditis; n = 5) had surgical confirmation of thickened pericardium and improved clinically after pericardiectomy. Group 2 (no constrictive pericarditis; n = 7) had cardiomyopathy with normal pericardium. Seven normal volunteers (Group 3) were also studied. Cine computed tomograms were obtained for the entire heart (8-mm slices, 17 frames/s, nonionic contrast medium). Pericardial thickness was measured at 10 degrees intervals at three ventricular levels in each subject. The rapidity of diastolic filling was assessed by calculating the percent filling fraction in early diastole. RESULTS: Pericardial thickness was 10 +/- 2 mm (mean +/- SD) in Group 1, 2 +/- 1 mm in Group 2 and 1 +/- 1 mm in Group 3 (p < 0.05, constrictive pericarditis vs. no constrictive pericarditis). Left ventricular filling fraction was 83 +/- 6% in Group 1, 62 +/- 9% in Group 2 and 44 +/- 5% in Group 3. Right ventricular filling fraction was 93 +/- 5% in Group 1, 62 +/- 14% in Group 2 and 35 +/- 6% in Group 3 (p < 0.05, Group 1 vs. Groups 2 and 3). Both indexes provided a clear-cut distinction between patients with and without constriction. CONCLUSIONS: Cine computed tomography simultaneously provides both anatomic and physiologic data that allow accurate preoperative diagnosis of pericardial constriction.

Adult↗
PubMed1986

Effect of aortic constriction on the oxygen supply-consumption balance in partially ischaemic myocardium.

A study was carried out to determine the effect of distal aortic constriction on the regional oxygen supply-consumption balance in ischaemic and non-ischaemic myocardium. Left anterior descending coronary artery flow was reduced by 50% in anaesthetised mongrel dogs, and half these animals were subjected to distal ascending aortic constriction (ventricular systolic-aortic systolic pressure gradient 50 mm Hg). Blood flows were determined using radioactive microspheres, and arterial and venous oxygen saturations were determined using microspectrophotometry. When left anterior descending artery flow was decreased by 50% tissue flow, as measured by microspheres in the ischaemic region in both control and aortic constricted animals, decreased. Aortic constriction increased flow in the non-ischaemic zone compared with the same region in control animals. The arteriovenous oxygen content difference increased similarly in the ischaemic region in control and aortic constricted animals compared with their respective non-ischaemic zones. Aortic constriction decreased this difference in the non-ischaemic region compared with these same regions in control animals. Oxygen consumption in the non-ischaemic and ischaemic regions of aortic constricted animals was higher than in control animals. The oxygen supply to consumption ratio was lower in the ischaemic zone in both control and aortic constricted animals than in their respective non-ischaemic regions. Aortic constriction does not appear to alter the oxygen supply-consumption balance in the ischaemic myocardium compared with control animals. Thus the increased work performed by the heart in response to the aortic constriction is adequately matched by an increased flow even in the flow restricted region.

Animals↗
PubMed1975

Muscle load and constriction of the rabbit ear artery.

This isolated, perfused ear artery of the rabbit has been used to examine the effect of alterations in muscle load on the construction of arteries. The equilibrium muscle load, taken as the difference in wall stress between the relaxed and constricted artery at the same external radius, was varied by changing the transmural pressure and by constricting the artery. 2. The equilibrium muscle load increased initially and then declined with decreasing external radius when the transmural pressure was kept constant. The maximum muscle load was reached when the relaxed external radius had been reduced by 11% at 80 mmHg and by 4-5% (relative to the radius at 80 mmHg) at 160 mmHg. 3. Arteries from young rabbits (3-6 months in age) which were partially constricted by adrenaline or spontaneous activity responded better to 60 sec of 4 Hz field stimulation at transmural pressures above 100 mmHg than did relaxed arteries. Neither field stimulation nor high concentrations of noradrenaline ( is greater than 800 ng/ml.) were able to constrict most arteries effectively at pressures above 160-170 mmHg unless partial constriction was present. The partial constriction reduced the load placed on the muscle by the same transmural pressure. Constrictio n during field stimulation was due largely to the release of neurotransmitter. 4. Ear arteries from young and older rabbits differed little in their ability to constrict against different transmural pressures. The one major difference was a lesser maximum constriction of arteries from older rabbits (18-24 months in age). However, arteries from older rabbits constricted well at the higher transmural pressures only because wall thickening largely compensated for a decreased ability of the muscle to develop active tension. 5. It is concluded that a decrease in internal radius to wall thickness ratio by either sufficient partial vasoconstriction or by wall thickening favours constriction of arteries because the load placed on the muscle by the same transmural pressure is reduced. Wall thickening may be an important compensatory reaction for deteriorating muscle contraction.

Animals↗
PubMed1992

Constrictive pericarditis and restrictive cardiomyopathy: evaluation with MR imaging.

Twenty-nine patients who were referred with the possible diagnosis of constrictive pericarditis underwent electrocardiographically gated transverse spin-echo magnetic resonance (MR) imaging to determine the accuracy of spin-echo MR imaging for the diagnosis of constrictive pericarditis and to compare the morphologic features of constrictive pericarditis with those of restrictive cardiomyopathy as seen on spin-echo MR images. Constrictive pericarditis was verified by means of surgery and/or catheterization in 17 patients. The sensitivity, specificity, and accuracy of MR imaging in the diagnosis of constrictive pericarditis were 88%, 100%, and 93%, respectively. Thickened pericardium was observed in 88% of patients with proved constrictive pericarditis. Pericardial thickening was not identified in patients with restrictive myocarditis (n = 4). The most frequent site of pericardial thickening was over the right ventricle. In constrictive pericarditis, the signal intensity of the thickened pericardium was similar or decreased compared with that of the myocardium. Indirect findings of impaired right ventricular diastolic filling (eg, dilatation of the inferior vena cava and right atrium) were identified in constrictive pericarditis and restrictive cardiomyopathy. MR imaging can serve as a noninvasive examination for the definitive diagnosis of constrictive pericarditis and can help distinguish between constrictive pericarditis and restrictive cardiomyopathy on the basis of pericardial thickness.

Cardiomyopathy, Restrictive↗
PubMed1991

Exposure of neonatal rats to carbon monoxide alters cardiac adaptation to aortic constriction.

We tested the hypothesis that a 32-day exposure of newborn rats to 500 ppm carbon monoxide (CO) would alter the adaptive response of the heart to aortic constriction in adulthood. At 110 days of age aortic constriction or sham operations were performed, and hearts were studied 28 days later. Aortic constriction increased left ventricular (LV) mass by 40% over the control value of 611 +/- 27 mg; this adaptive response was not altered by CO exposure. Aortic constriction and CO exposure increased right ventricular (RV) mass by 10 and 11%, respectively, over the control value of 185 +/- 10 mg. The effects of both experimental procedures on RV mass were additive (23%). Peak LV pressure development (dP/dtmax) in vitro increased 29% after aortic constriction in the nonexposed rats. CO exposure blunted the increase in peak LV systolic pressure due to aortic constriction. Maximum positive and negative dP/dtmax decreased by 19% after aortic constriction and were unaffected by CO exposure. The percentage of alpha-myosin heavy chain (MHC) in the ventricles was 94 +/- 2% in the control group and was decreased to 81 +/- 3% by aortic constriction. In contrast, the percentage of alpha-MHC was 87 +/- 2% for CO-exposed rats and was not significantly altered after aortic constriction. In vitro coronary flow was increased 18% in hearts of adult rats exposed to CO as neonates. Exposure of neonatal rats to CO induced chronic adaptations in the myocardium, some of which became evident in adulthood only when hearts were challenged by aortic constriction.

Adaptation, Physiological↗
PubMed1984

Analysis of the vagal reflex tracheal constriction in the dog.

We devised a preparation for measuring the vagal reflex tracheal constriction following the bronchoconstriction induced by histamine inhaled in the bronchial side in dogs. Properties of the vagal reflex tracheal constriction were investigated using this preparation. Histamine inhaled in the bronchial side caused the tracheal constriction following the bronchoconstriction. The tracheal constriction was inhibited by section of the bilateral superior laryngeal nerves or vagal cooling, respectively, but was not completely blocked. The combination of section of the bilateral superior laryngeal nerves and vagal cooling abolished the tracheal constriction. An i.v. administration of pentobarbital reduced both bronchoconstriction and tracheal constriction. These findings indicate that the tracheal constriction observed in the present study is mediated by the vagal reflex arc and that the extravagal pathway consisting of the recurrent and superior laryngeal nerves plays a role in a part of the afferent pathway of the vagal reflex airway responses. When the bronchoconstriction was completely abolished by isoproterenol inhaled in the bronchial side, the reflex tracheal constriction still existed. Transient inflation and deflation of the lungs caused reflex tracheal dilatation and constriction, respectively. We conclude that the vagal reflex airway constriction is due to complex effects which may be mediated by plural sensory receptors in the airways.

Animals↗
PubMedDate not supplied

Rate of the myogenic response increases with the constriction level in rabbit femoral arteries.

The myogenic response forms an important aspect of blood flow regulation and is usually quantified by the steady-state relation between pressure and diameter. The aim of the present study is to analyze the dynamics of the myogenic response. In six isolated rabbit femoral arteries, the time course of the active part of the diameter response to a pressure step from 95 to 110 cm H2O (from 9.5 to 11 kPa), at two levels of norepinephrine (NE)-induced constriction, was fitted to a monoexponential curve to obtain the time constant. The NE concentrations used in the superfusion solution were between 0.8 and 1.5 microM for high constriction and between 0.2 and 0.6 microM for low constriction. Acetylcholine (1 microM in perfusion) was used to check endothelial function. The respective median values of the time constants with and without endothelium, are 13.2 and 15.5 sec (NS) for the high level of constriction and 49.5 and 58.5 sec (NS) for the low constriction level. Time constants at the two constriction levels were significantly different (p = 0.002). In seven separate experiments using 40 mM KCl, in the superfusion fluid, to constrict femoral arteries to the same level as during the high level of NE constriction, it was found that the amplitude of the myogenic response was much smaller, compared with the norepinephrine experiments, and the time constant was significantly longer (median: 80.8 sec). We conclude that the dynamics of the myogenic response in the rabbit femoral artery is independent of the endothelium, but is dependent on the constriction level and type of constricting agent.

Animals↗
PubMed1989

Doppler assessment of the pulsatility index of the middle cerebral artery during constriction of the fetal ductus arteriosus after indomethacin therapy.

To investigate the effects of constriction of the ductus arteriosus on the pulsatility index of the middle cerebral artery, maximum velocity waveforms were obtained in 13 fetuses (one set of twins) whose mothers were treated with indomethacin for preterm labor (n = 9) or polyhydramnios (n = 3). Eleven of the fetuses manifested ductal constriction within 48 hours of therapy, whereas two fetuses had constriction after 1 week of therapy. Six of the 13 fetuses also manifested tricuspid insufficiency in association with constriction of the ductus arteriosus. All abnormal cardiac changes resolved in utero after discontinuation of indomethacin. No difference in the pulsatility index values of the middle cerebral artery was observed in the fetuses with ductal constriction but without tricuspid regurgitation (n = 7) when the values were compared with those obtained in absence of ductal constriction (1.87 +/- 0.37 vs. 1.88 +/- 0.33). In the fetuses that manifested both ductal constriction and tricuspid insufficiency (n = 6), the pulsatility index values in the middle cerebral artery were significantly lower in the presence of ductal constriction when compared with the values obtained in the absence of ductal constriction (2.22 +/- 0.26 vs. 1.57 +/- 0.34). These results indicate that a response to indomethacin sufficient to cause both ductal constriction and tricuspid insufficiency decreases the pulsatility index of the middle cerebral artery.

Blood Circulation↗
PubMed1991

Effects of actinomycin D on airway constriction induced by tachykinins and capsaicin in guinea-pigs.

The effects of actinomycin D on airway constriction induced by tachykinins was studied in guinea-pigs in vitro and in vivo. Actinomycin D significantly inhibited the constriction of isolated guinea-pig trachea induced by neurokinin A (NKA) and eledoisin. Conversely, substance P (SP)- and physalaemine-induced constrictions were not affected by actinomycin D. The same selectivity in the inhibitory action of actinomycin D against tachykinins was also observed in in vivo. Actinomycin D given i.v. specifically inhibited the increase in airway resistance induced by NKA. I.v. injection of NKA caused not only airway constriction but also transient systemic hypotension. Interestingly, actinomycin D injected i.v. inhibited only airway constriction and the systemic hypotension induced by NKA was not affected. These results clearly suggest that actinomycin D specifically inhibits NKA-induced airway constriction in guinea-pigs. Actinomycin D also had an inhibitory action on the airway constriction induced by capsaicin. In the case of capsaicin-induced constriction, actinomycin D was more effective on the later phase of constriction than on the acute phase. The airway constriction induced by capsaicin is thought to be mediated by the release of SP and NKA from sensory nerve endings, and the persistent increase in airway resistance induced by capsaicin is thought to be due mainly to NKA.

Airway Resistance↗
PubMed1997

Dopamine constricts porcine pial veins.

Dopamine has been shown to induce pial arterial relaxation and constriction in several species. Its mode of action on pial veins, however, remains unclarified. The vasomotor effect of dopamine on porcine pial veins was, therefore, examined using an in vitro tissue bath technique. The results indicated that dopamine constricted exclusively isolated ring segments of pial veins in the presence or absence of active muscle tone. The constriction induced by dopamine was not affected by N(omega)-nitro-L-arginine (L-NNA, 2 x 10(-5) M) or indomethacin (10(-5) M). Only in few preparations was the constriction induced by maximum concentration of dopamine potentiated by L-NNA, suggesting that dopamine at high concentrations may release NO or a NO-related substance. In the presence of L-NNA (2 x 10(-5) M), dopamine-induced constriction was inhibited by phentolamine and yohimbine (but not prazosin) in a concentration-dependent manner with maximum inhibition at 10(-6) M. SKF38393 and 6-bromo-APB (selective dopamine D1 receptor agonists) and LY171555 (a selective dopamine D2 receptor agonist) also induced pial venous constriction exclusively in the presence of L-NNA. The constriction was not affected by phentolamine (10(-6) M). The order of potency for these agonists in the presence of phentolamine, propranolol, guanethidine and L-NNA was: 6-bromo-APB > SKF38393 > dopamine > LY171555. The dopamine-induced constriction in the presence of phentolamine was further inhibited by both SCH23390 (a selective dopamine D1 receptor antagonist) and sulpiride (a selective dopamine D2 receptor antagonist), but was not affected by dopamine D3 or D4 receptor antagonists. These results indicate that dopamine at low and high concentrations induces exclusively constriction of isolated porcine pial veins. The constriction is mediated by postsynaptic alpha2-adrenoceptors, and dopamine D1 and D2 receptors.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2003

Myogenic constriction is increased in mesenteric resistance arteries from rats with chronic heart failure: instantaneous counteraction by acute AT1 receptor blockade.

(1) Increased vascular resistance in chronic heart failure (CHF) has been attributed to stimulated neurohumoral systems. However, local mechanisms may also importantly contribute to set arterial tone. Our aim, therefore, was to test whether pressure-induced myogenic constriction of resistance arteries in vitro--devoid of acute effects of circulating factors--is increased in CHF and to explore underlying mechanisms. (2) At 12 weeks after coronary ligation-induced myocardial infarction or SHAM-operations in rats, we studied isolated mesenteric arteries for myogenic constriction, determined as the active constriction (% of passive diameter) in response to stepwise increase in intraluminal pressure (20 - 160 mmHg), in the absence and presence of inhibitors of potentially involved modulators of myogenic constriction. (3) We found that myogenic constriction in mesenteric arteries from CHF rats was markedly increased compared to SHAM over the whole pressure range, the difference being most pronounced at 60 mmHg (24+/-2 versus 4+/-3%, respectively, P<0.001). (4) Both removal of the endothelium as well as inhibition of NO production (L-N(G)-monomethylarginine, 100 micro M) significantly increased myogenic constriction (+16 and +25%, respectively), the increase being similar in CHF- and SHAM-arteries (P=NS). Neither endothelin type A (ET(A))-receptor blockade (BQ123, 1 micro M) nor inhibition of perivascular (sympathetic) nerve conduction (tetrodotoxin, 100 nM) affected the myogenic response in either group. (5) Interestingly, increased myogenic constriction in CHF was fully reversed after angiotensin II type I (AT(1))-receptor blockade (candesartan, 100 nM; losartan, 10 micro M), which was without effect in SHAM. In contrast, neither angiotensin-converting enzyme (ACE) inhibition (lisinopril, 1 micro M; captopril, 10 micro M) or AT(2)-receptor blockade (PD123319, 1 micro M), nor inhibition of superoxide production (superoxide dismutase, 50 U ml(-1)), TXA(2)-receptor blockade (SQ29,548, 1 micro M) or inhibition of cyclooxygenase-derived prostaglandins (indomethacin, 10 micro M) affected myogenic constriction. (6) Sensitivity of mesenteric arteries to angiotensin II (10 nM - 100 micro M) was increased (P<0.05) in CHF (pD(2) 7.1+/-0.4) compared to SHAM (pD(2) 6.2+/-0.3), while the sensitivity to KCl and phenylephrine was not different. (7) Our results demonstrate increased myogenic constriction in small mesenteric arteries of rats with CHF, potentially making it an important target for therapy in counteracting increased vascular resistance in CHF. Our results further suggest active and instantaneous participation of AT(1)-receptors in increased myogenic constriction in CHF, involving increased sensitivity of AT(1)-receptors rather than apparent ACE-mediated local angiotensin II production.

Angiotensin II↗
PubMed2000

Role of protein kinase C in angiotensin II-induced constriction of renal microvessels.

UNLABELLED: Role of protein kinase C in angiotensin II-induced constriction of renal microvessels. BACKGROUND: Although angiotensin II (Ang II) exerts its action through multiple vasomotor mechanisms, the contribution of phosphoinositol hydrolysis products to Ang II-induced renal vasoconstriction remains undetermined. METHODS: The role of protein kinase C (PKC) in Ang II-induced afferent (AFF) and efferent (EFF) arteriolar constriction was examined using the isolated perfused hydronephrotic rat kidney. RESULTS: Ang II (0.3 nmol/L)-induced EFF constriction was refractory to inhibition of voltage-dependent calcium channels by pranidipine (1 micromol/L, 19 +/- 2% reversal) but was completely reversed by a PKC inhibitor, chelerythrine (1 micromol/L, 96 +/- 2% reversal). Furthermore, direct PKC activation by phorbol myristate acetate (PMA; 1 micromol/L) caused prominent EFF constriction, and this constriction was inhibited by manganese and free calcium medium. In contrast, Ang II-induced AFF constriction was completely abolished by pranidipine (98 +/- 4% reversal) and was partially inhibited by chelerythrine (55 +/- 3% reversal). Although PMA elicited marked AFF constriction, this constriction was insensitive to the calcium antagonist, but was totally inhibited by manganese or free calcium medium. CONCLUSIONS: PKC plays an obligatory role in Ang II-induced EFF constriction that requires extracellular calcium entry through nonselective cation channels. In contrast, in concert with our recent findings demonstrating a complete dilation by thapsigargin, Ang II-induced AFF constriction is mainly mediated by inositol trisphosphate (IP3) and voltage-dependent calcium channel pathways, but could not be attributed to the PKC-activated calcium entry pathway (for example, nonselective cation channels). Rather, Ang II-stimulated PKC may cross-talk to the IP3/voltage-dependent calcium channel pathway and could modulate the vasoconstrictor mechanism of the AFF. Thus, the role of PKC during Ang II stimulation differs in AFF and EFF, which may constitute segmental heterogeneity in the renal microvasculature.

Angiotensin II↗
PubMed2002

Cerebrovascular alterations in pressure and protein kinase C-mediated constriction in Dahl salt-sensitive rats.

BACKGROUND: Dahl salt-sensitive (DSS) rats fed an 8.7% sodium chloride diet from weaning spontaneously developed hypertension and a 50% mortality rate by 5 weeks. Before death the rats exhibited behavioural signs of stroke and disruption of the blood-brain barrier. OBJECTIVES: To test the hypothesis that rats exhibiting stroke had middle cerebral arteries (MCAs) that had lost the ability to constrict in response to pressure, and to assess whether this defect was associated with abnormalities in protein kinase C (PKC)-mediated constriction. METHODS: MCAs were sampled from DSS rats before and after stroke and from Dahl salt-resistant (DSR) rats fed 8.7% NaCl. Constrictions in response to a 100 mmHg pressure step and to PKC activation by phorbol dibutyrate (PDB) (0.1 micromol/l) in the presence of nifedipine (3 micromol/l) were measured. RESULTS: MCAs from DSS rats after stroke constricted in response to vasopressin but were unable to constrict in response to pressure or PDB in the presence of nifedipine, whereas those from DSS rats before stroke and from DSR rats constricted in response to all the stimuli. The PKC inhibitors, chelerythrine (12 micromol/l) and bisindolylmaleimide (5 micromol/l) inhibited constrictions in response to pressure and to PDB in the presence of nifedipine. CONCLUSIONS: Constriction of the MCA in response to pressure is dependent on functional PKC signalling. Development of stroke in DSS rats fed a high-salt diet is associated with an inability of the MCAs to constrict in response to pressure, possibly because of the presence of an incompetent PKC system. The inability to constrict in response to pressure may cause blood flow abnormalities that contribute to disruption of the blood-brain barrier in these rats.

Animals↗
PubMed1997

Arteriolar constriction in skeletal muscle during vascular stunning: role of mast cells.

Striated muscle becomes stunned during reperfusion after sublethal ischemia. Resistance vessel tone and reactivity are altered in stunned muscle tissues. The hypothesis that adenosine-regulated mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles was tested. The hamster cremaster muscle was subjected to 1 h of ischemia followed by reperfusion. Resistance arterioles constricted during reperfusion (74% of maximal diameter at baseline vs. 42% of maximal diameter after 30 min of reperfusion; P < 0.01). Mast cells degranulated in reperfusion concomitant with arteriolar constriction. Stimulation of mast cell degranulation in control animals with compound 48/80 or cold superfusate (21 degrees C) caused vasoconstriction that mimicked that seen in reperfusion. The mast cell stabilizer cromolyn blocked degranulation and constriction. If mast cell granules were depleted by applying compound 48/80 before inducing ischemia, then arterioles failed to constrict during reperfusion. Adenosine A3-antagonist BW-A1433 abolished constriction. These findings suggest that arterioles constrict in reperfusion due to adenosine-regulated mast cell degranulation. Vasodilation in response to sodium nitroprusside and acetylcholine was normal in stunned, constricted arterioles. However, the dose-response curves to adenosine were shifted to the left in arterioles constricted by either stunning, compound 48/80, exposure to cold superfusate, or cromolyn compared with control vessels. Depletion of granular components via stunning, compound 48/80, cold superfusate, or inhibition of secretion with cromolyn results in unopposed A1- or A2-mediated vasodilation in response to adenosine, whereas the dilatory effects of adenosine are blunted by simultaneous release of vasoconstrictors from mast cells in control animals. In summary, it was found that mast cell degranulation occurs during reperfusion and leads to constriction of resistance arterioles and altered vascular reactivity to adenosine. Adenosine is released in ischemia and stimulates mast cell degranulation via the A3 receptor located on mast cells during reperfusion.

Acetylcholine↗
PubMed1995

Effects of aortic constriction during experimental acute right ventricular pressure loading. Further insights into diastolic and systolic ventricular interaction.

BACKGROUND: Acute right ventricular (RV) hypertension may result in hemodynamic collapse. The associated reduction in left ventricular (LV) end-diastolic volume is thought to result from reduced RV output (secondary to RV ischemia) and adverse direct ventricular interaction. Aortic constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an increased coronary perfusion pressure. We hypothesized that altered ventricular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. METHODS AND RESULTS: We instrumented nine dogs with ultrasonic dimension crystals to measure RV segment length, septum-to-RV free wall and septum-to-LV free wall diameters, and LV anterioposterior diameter. Catheter-tipped manometers were used to measure LV and RV pressures. Pericardial pressure was measured with flat, liquid-containing balloon transducers. Inflatable cuff constrictors were placed on the pulmonary artery (PA) and aorta, and a flow probe was placed on the PA. The right coronary artery (RCA) was perfused independently by a roller pump calibrated for flow. During moderate PA constriction, while RCA pressure was maintained at control level, RCA flow did not change significantly (15.8 +/- 6.2 to 16.9 +/- 11.5 mL/min) and was similar during severe PA constriction (18.6 +/- 9.8 mL/min). During severe PA constriction, RV stroke volume decreased from a control value of 10.3 +/- 4.9 to 2.3 +/- 1.4 mL/beat (P < .05). When aortic constriction was added while RCA pressure was maintained at control level, there was an increase in RV stroke volume to 4.5 +/- 2.0 mL/beat (P < .05) with no associated change in RCA flow (17.8 +/- 9.5 mL/min). However, pressure-dimension loops clearly demonstrated changes in diastolic and systolic ventricular interaction; with aortic constriction, there was a large increase in the transeptal pressure gradient associated with a rightward septal shift. During either isolated severe PA constriction or simultaneous severe PA and aortic constriction, RCA flow was increased until RCA pressure was approximately equal to that in the aorta. This produced an increase in RCA flow of 50% (P < .05); however, this increase in coronary flow was ineffective in improving any measure of RV function. CONCLUSIONS: In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.

Animals↗
PubMed2003

Coronary myogenic constriction antagonizes EDHF-mediated dilation: role of KCa channels.

In hypertension, pressure-induced myogenic constriction and impaired endothelium-derived hyperpolarizing factor (EDHF)-mediated dilation may contribute to increased vasomotor tone. Myogenic constriction as well as EDHF-mediated dilation may share common signaling mechanisms, and both may control KCa channel activity to set arterial tone. To investigate a potential relation between the 2 mechanisms, we studied coronary arteries of Sprague-Dawley rats for individual myogenic constriction compared with EDHF-mediated dilation of the same artery. EDHF-mediated dilation was measured as the maximal dilation to acetylcholine (100 micromol/L) after preconstriction, resistant to NO inhibition (NG-methyl-l-arginine acetate salt, L-NMMA, 100 micromol/L), and prostaglandin inhibition (indomethacin, 10 micromol/L) but abolished by charybdotoxin (100 nmol/L) plus apamin (500 nmol/L). Individual coronary myogenic constriction at an intraluminal pressure of 70 mm Hg (n=9) ranged from 6% to 44% (24+/-4%). EDHF-mediated dilation ranged from 18% to 84% (42+/-7%). Elevating pressure to 130 mm Hg (n=8) increased myogenic constriction by 2-fold (P<0.01) and decreased EDHF-mediated dilation by 2.6-fold (P<0.01). Interestingly, individual myogenic constriction inversely correlated to individual EDHF-mediated dilation (r=-0.75, P<0.001, n=17). Pretreatment with the KCa channel opener NS1619 (30 micromol/L) prevented coronary myogenic constriction and increased EDHF-mediated dilation by 2.2-fold (P<0.01), whereas the KATP channel opener cromakalim (3 micromol/L) had no effect on EDHF-mediated dilation. For comparison, in mesenteric arteries (at 70 mm Hg) low myogenic constriction (2+/-1%) was associated with high EDHF-mediated dilation (93+/-2%), and pretreatment with NS1619 had no effect. Our results demonstrate that myogenic constriction in coronary arteries antagonizes EDHF-mediated dilation. Activation of KCa channels with NS1619 reduces myogenic constriction and profoundly increases EDHF-mediated dilation, specifically in coronary arteries, suggesting a potential therapeutic impact to reduce coronary risk in hypertension.

Animals↗
PubMed2003

Inhibition of in vivo constriction of fetal ductus arteriosus by endothelin receptor blockade in rats.

The fetal ductus can be constricted by drugs, including cyclooxygenase inhibitors (indomethacin), nitric oxide synthesis antagonists [N-nitro-L-arginine monomethyl ester (L-NAME)], and glucocorticoid hormones (dexamethasone). Constriction of the fetal ductus by endothelin (ET) 1 was reported in an in vitro study. We studied the preventive effect of a dual ET receptor antagonist (bosentan) and a selective ET-A blocker (CI-1020) on pharmacologic fetal ductal constriction in rats. Near-term pregnant Wistar rats at d 21 and preterm rats at d 19 were used. The fetal ductus was constricted by four medications: orogastric administration of indomethacin (10 mg/kg) on fetal d 21, orogastric indomethacin 1 mg/kg combined with muscular injection of L-NAME (10 mg/kg) on fetal d 21, and muscular injection of L-NAME or dexamethasone (1 mg/kg) on fetal d 19. Bosentan (0.1, 1, 10, or 100 mg/kg) was injected intraperitoneally either simultaneously with indomethacin, L-NAME, or dexamethasone, or 4 h after administration of 10 mg/kg indomethacin. CI-1020 (0.01, 0.1, 1, or 10 mg/kg) was injected intraperitoneally simultaneously with indomethacin. After maternal atlas dislocation, cesarean section, fetal whole-body freezing, and cutting on the freezing microtome, measurements were made of the inner diameters of the ductus, main pulmonary artery, and ascending aorta. Bosentan blocked fetal ductal constriction by indomethacin, indomethacin plus L-NAME in the near-term rats, and constriction by L-NAME and dexamethasone in the preterm rats dose dependently. Fetal ductal constriction was nearly completely blocked by simultaneously administered 100 mg/kg of bosentan or 10 mg/kg of CI-1020. Dual ET receptor antagonist (bosentan) and selective ET-A blocker (CI-1020) prevent constriction of the fetal ductus arteriosus induced by ductus-constricting agents in rats, indicating that ET and ET-A receptors are essential in fetal ductal constriction.

Animals↗
PubMed1992

The role of microvascular damage in photodynamic therapy: the effect of treatment on vessel constriction, permeability, and leukocyte adhesion.

Intravital microscopy of the rat cremaster muscle was used to evaluate changes in vessel constriction, vessel permeability, and leukocyte adhesion during and after photodynamic therapy (PDT). Animals were given Photofrin doses of 0-25 mg/kg i.v. 24 h before treatment. Cremaster muscles were exposed to 135 J/cm2 light at 630 nm. Animals given 5 mg/kg Photofrin showed no vessel constriction or increase in vessel permeability to albumin. Doses of 10 and 25 mg/kg Photofrin caused a dose-related constriction of arterioles which was observed within the first minutes of illumination at the higher drug dose. After the initial constriction, arteriole response to PDT was biphasic in nature, with some vessels relaxing to nearly control levels while others remained fully constricted. Constriction of venules occurred only at the highest porphyrin dose studied (25 mg/kg) and was delayed in comparison to arteriole constriction. Photofrin doses which produced arteriole constriction also caused an increase in venule permeability to albumin, which occurred shortly after the start of light treatment and was progressive with time. Leakage began at specific sites along the venule wall but became uniform along the entire length of the venule by 1 h after treatment. Changes in the adherence of polymorphonuclear leukocytes to venule endothelium were also observed with PDT. Photofrin doses of 25 mg/kg and 45 J/cm2 light were sufficient to cause polymorphonuclear leukocytes to become adherent to the vessel wall. A second group of animals was given indomethacin trihydrate to examine the involvement of cyclooxygenase products such as thromboxane in vessel response to PDT. Animals given 5 mg/kg indomethacin intraarterially 1 h before light treatment showed no constriction of arterioles or venules at all Photofrin and light doses studied. No increases in venule permeability to albumin were seen in this group of animals. This suggests that cyclooxygenase products including thromboxane are important in causing vessel constriction and changes in permeability during PDT. The initiating event which causes the release of these vasoactive agents remains unknown.

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