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Effect of acute blood volume expansion on cardiac output, plasma dopamine beta-hydroxylase, and renal function in rats with chronic constriction of the ascending aorta.

To examine the effect of raised left atrial pressure (AP) on the relationship of cardiac output to renal function, we constricted the ascending aorta in rats (AC) and 1-6 months later tested their response to acute volume expansion (VE) with blood (2% body weight, iv). Sham-operated (SH) rats were controls. In AC rats heart weight increased 38%, but cardiac output was 47% lower. Statistically significant differences in the initial clearance periods were (AC vs. SH): venous pressure (VP) 8 +/- 2 vs. 3+/- 1 cm H2O; inulin clearance (CIN) 0.61 +/- 0.06 vs. 0.84 +/- 0.04 ml/min; sodium excretion (UNAV) 1.2 +/- 0.2 vs. 2.1 +/- 0.3 muequiv./min. Filtration fraction, fractional UNaV, mean arterial pressure (MAP), and plasma dopamine beta-hydroxylase (DBH) were the same in both groups. After VE, cardiac output increased proportionately more in AC (69% vs. 27%); however, the absolute increases were not different. UNaV increased proportionately more in AC rats, but the absolute increase was less (5.1 vs. 7.5 muequiv./min). Multiple variable regression analysis showed that UNaV correlated with CIN, MAP, and VP, with no difference between AC and SH animals. Cardiovascular-renal relationships were indistinguishable from previous descriptions of dogs and rats with chronic vena caval constriction. Modulation of renal function by left AP was not apparent. In both groups after the peak response to VE, UNaV decreased in association with decreased cardiac output and increased sympathetic nervous activity as indicated by raised DBH levels. After VE, VP remained high in AC but not in SH animals.

Animals↗

Echocardiographic diagnosis of partial pericardial constriction of the left ventricle.

In a patient with hemodynamic findings typical of severe, generalized pericardial constriction, echocardiography demonstrated partial constriction of the left ventricle; the patient had partial pericardiectomy 17 years earlier. Diagnosis was confirmed by angiocardiography and at surgery. Echocardiography suggested penetration of the myocardium at places by pericardial calcification; this finding was confirmed at surgery.

Angiocardiography↗

Ganglionic blockade in conscious dogs with chronic caval constriction.

Chronic constriction of the thoracic inferior vena cava decreases venous return and cardiac output, increases the secretion of renin and aldosterone, and produces sodium retention with ascites and edema formation. The arterial pressure is maintained at normotensive levels in this caval model by an increase in total peripheral resistance. The objective of the present study was to compare renal and hemodynamic responses to ganglionic blockade in the conscious thoracic caval dog to responses obtained in another low-output model, the chronic sodium-deplete dog, and also to the responses obtained in the normal sodium-replete dog. The control base-line pressures averaged 103 +/- 2, 110 +/- 3, and 110 +/- 3 mmHg, respectively, in the sodium-replete, sodium-deplete, and thoracic caval dogs (P greater than 0.05). Ganglionic blockade in the conscious dog with caval constriction resulted in a sustained 20- to 30-mmHg fall in the arterial pressure; a sustained fall of 20 mmHg occurred in the sodium-deplete dogs. In contrast, ganglionic blockade failed to decrease the blood pressure at any time in the normal sodium-replete animals. Effective renal blood flow and creatinine clearance failed to demonstrate sustained changes after ganglionic blockade in any group of dogs; renal sodium excretion increased only in the normal sodium-replete dogs. These results suggest an enhanced contribution of the sympathetic nervous system to blood pressure maintenance in both the sodium-deplete and the caval dogs. Although the data fail to demonstrate an important contribution of the adrenergic system in the chronic sodium retention in these two experimental models, decreases in renal perfusion pressure may have blunted any potential natriuresis in these animals following ganglionic blockade.

Animals↗

Renal response to atrial natriuretic factor in conscious dogs with caval constriction.

Constriction of the thoracic inferior vena cava to decrease venous return and atrial filling markedly elevates plasma renin activity (PRA) and plasma aldosterone concentration (PAC) and produces chronic sodium retention and ascites in the dog. Infusion of a synthetic atrial natriuretic factor into conscious dogs with caval constriction and ascites at doses of 175 and 350 ng X kg-1 X min-1 for 30 min each produced striking increases (P less than 0.05) in creatinine clearance, diuresis, and kaliuresis but failed to increase urinary sodium excretion. Infusions of atrial natriuretic factor at these doses into conscious normal dogs, however, produced a striking increase in sodium excretion from 41 +/- 14 and 55 +/- 19 mu eq/min to 150 +/- 58 and 181 +/- 49 mu eq/min (P less than 0.05 for both values). Creatinine clearance and urine flow also increased in these normal dogs, but potassium excretion remained unchanged during the infusion periods. Atrial natriuretic factor produced parallel suppression (P less than 0.05) of the elevated levels of PRA and PAC in the caval dogs but failed to significantly decrease either PRA or PAC in the normal animals. Arterial pressure, heart rate, and PAH clearance were unchanged in both groups of dogs during infusion of atrial natriuretic factor. These results suggest that the pattern of renal electrolyte excretion elicited in response to the acute infusion of atrial natriuretic factor is dependent, at least partially, on the preexisting status of the renal tubules to facilitate sodium reabsorption and potassium excretion. The results also are consistent with the concept that atrial natriuretic factor might function to tonically inhibit the renin-angiotensin-aldosterone system.

Aldosterone↗

Hypocapnia-induced constriction of the canine peripheral airways exhibits tachyphylaxis.

Hypocapnia-induced constriction of peripheral airways may be important in regulating the distribution of ventilation in pathological conditions. We studied the response of the peripheral lung to hypocapnia in anesthetized, paralyzed, mechanically ventilated dogs using the wedged bronchoscope technique to measure resistance of the collateral system (Rcs). A 5-min hypocapnic challenge produced a 161 +/- 19% (mean +/- SE) increase in Rcs. The magnitude of this response was not diminished with repeated challenge or by atropine sulfate (1 mg base/kg iv), chlorpheniramine maleate (5 mg base/kg iv), or indomethacin (5 mg/kg iv). The response was reduced by 75% by isoproterenol (5 micrograms/kg iv) (P less than 0.01) and reduced by 80% by nifedipine (20 micrograms/kg iv) (P less than 0.05). During 30-min exposure to hypocapnia the maximum constrictor response occurred at 4-5 min, after which the response attenuated to approximately 50% of the maximum response (mean = 53%, range 34-69%). Further 30-min challenges with hypocapnia resulted in significantly decreased peak responses, the third response being 50% of the first (P less than 0.001). The inability of indomethacin or propranolol to affect the tachyphylaxis or attenuation of the response suggests that neither cyclooxygenase products nor beta-adrenergic activity was involved. Hence, hypocapnia caused a prompt and marked constrictor response in the peripheral lung not associated with cholinergic mechanisms or those involving histamine H1-receptors or prostaglandins. With prolonged exposure to hypocapnia there was gradual attentuation of the constrictor response with continued exposure and tachyphylaxis to repeated exposure both of which would tend to diminish any compensatory effect of hypocapnic airway constriction on the distribution of ventilation.

Airway Resistance↗

Nonuniform expansion of constricted dog lungs.

The parenchymal marker technique was used to measure regional tidal volumes of samples of lung parenchyma in four open-chest supine dogs. Radiopaque markers that had been implanted in the lower lobe were tracked by biplane video fluoroscopy during sinusoidal volume oscillations at tidal volumes of approximately 20% of total lung capacity and frequencies of 1-40 breaths/min before and after methacholine was administered by aerosol. The volumes of tetrahedrons with apexes at four markers were computed, and sine waves were fit to the data for volume vs. time for each tetrahedron. The ratio of mean regional volume to mean airway pressure decreased by 10-45% after exposure to methacholine. Dynamic lung elastance and resistance of the constricted lungs were larger than control, and both were frequency dependent. Regional elastance and resistance varied considerably among tetrahedrons, and these were also frequency dependent. The data were fit by a model in which tissue elastance was uniform and nearly equal to elastance in the control state, but small-airway resistance was high and variable. We conclude that the lung contracts under bronchoconstriction but that the increased dynamic elastance and resistance of the constricted lung may be primarily the result of nonuniform increased airway resistance at the level of the terminal bronchioles.

Air Pressure↗

Limb constriction as a complication of intra-uterine vesico-amniotic shunt: fetoscopic release.

Complete fetal bladder outlet obstruction was first diagnosed in a fetus at 13.5 weeks. After sequential vesicocentesis had shown good renal function, a vesico-amniotic shunt was inserted at 17 weeks with a Rodeck catheter. The procedure was successful and amniotic fluid volume re-accumulated to normal levels. A detailed scan at 20 weeks showed that the distal free end of the catheter was wound round the left fetal thigh. As the fetus grew, there was progressive constriction of the fetal thigh by the catheter. By 29 weeks, Doppler blood flow changes to the left leg were apparent. Fetoscopic surgery was performed at 30 weeks to release the constriction. The catheter was divided successfully, but the divided end of the shunt subsequently retracted into the fetal abdomen, producing urinary ascites, bilateral hydroureter and hydronephrosis. The baby was delivered at 31.5 weeks in good condition. Endoscopic resection of anterior and posterior urethral valves was performed at 6 months of age. At 2 years, the child has normal renal function, growth parameters and developmental milestones. Mild indentation of the left thigh was still apparent, although there was no functional impairment.

Amniotic Fluid↗

Comorbidity of constrictive pericarditis and hemophilia A.

OBJECTIVE: To report a case of comorbidity of constrictive pericarditis and hemophilia A. CLINICAL PRESENTATION AND INTERVENTION: A 21-year-old male with hemophilia A was referred to our clinic and was examined with the subsequent evaluation of shortness of breath, leg edema and ascites. Clinical and laboratory examinations were performed. The results were consistent with constrictive pericarditis (CP), and the symptoms were completely relieved following institution of medical therapy. CONCLUSION: Because hemophilia A and pericarditis may be coincidentally present clinical conditions, avoidance of surgical procedures in hemophilic patients is preferable unless the resolution of the symptoms of pericarditis cannot be effected by medical therapy.

Adult↗

Constrictive pericarditis following coronary-artery bypass grafting in a patient with chronic asymptomatic pericardial disease.

Constrictive pericarditis is a rare complication of open-heart surgery. We describe a patient who was found at the time of coronary artery bypass surgery to have asymptomatic pericardial thickening and subsequently developed rapidly progressive constrictive pericarditis. At operation for pericardiectomy, the bypass graft to the posterior descending coronary artery was found to be strangled by fibrous tissue while the remaining two bypass grafts were patent. Following pericardiectomy, the patient made a good recovery.

Chronic Disease↗

Pericardial color Doppler flow in postpericardiotomy effusive constrictive pericarditis.

A laminar color Doppler flow was discovered in the pericardial space in a 35-year-old man with postpericardiotomy effusive constrictive pericarditis. The flow was detected by transesophageal color Doppler echocardiography. A further pulsed Doppler study revealed a to-and-fro flow, which was synchronized with the cardiac rhythm. We hypothesized that this flow was generated by the rhythmic cardiac contraction. It was then augmented by hard fibrous pericardium and became detectable by color Doppler echocardiography. Pericardial effusion is a frequent echocardiographic finding but little attention has been paid to the flow in it. The laminar flow in the pericardial space in our patient is related to his hard pericardium and can aid in making the diagnosis of effusive constrictive pericarditis. We suggest that flow in the pericardial space deserves more attention and may provide valuable diagnostic aid.

Adult↗

Effect of endogenous opioid blockade on fetal cardiovascular and sympathoadrenal responses to hypoxemia induced by umbilical cord constriction.

The cardiovascular and plasma catecholamine responses to hypoxemia following endogenous opioid blockade were evaluated in 18 late gestation fetal lambs (0.75-0.83 gestation) in utero. Hypoxemia was produced by progressive constriction of the umbilical cord with an inflatable silicone rubber cuff while fetal heart rate, blood pressure, and arterial blood gases were monitored. Fetal arterial blood samples were obtained for plasma catecholamine analysis using a radioenzymatic method. The animals were divided into 4 experimental groups. Control animals during normoxemia and following hypoxemia are represented by groups I and III, respectively. During umbilical constriction, arterial oxygen tension declined from 21.4 +/- 0.3 to 13.4 +/- 0.3 torr (p less than 0.001, mean +/- SE) and was accompanied by an increase in blood pressure (44 +/- 1 to 53 +/- 1 torr), decrease in heart rate (176 +/- 4 to 114 +/- 4 beats/min) and rise in plasma norepinephrine (437 +/- 90 to 3,410 +/- 617 pg/ml) and epinephrine (53 +/- 10 to 1,074 +/- 325 pg/ml). Naloxone infusion had no significant effect on the fetus during either normoxemic (group II) or hypoxemic conditions (group IV). Plasma catecholamines rose less in group IV than in hypoxemic control fetuses (norepinephrine: 2,407 +/- 406 vs. 3,410 +/- 617 pg/ml; epinephrine: 966 +/- 641 vs. 1,074 +/- 305 pg/ml), but the differences were not significant (p greater than 0.2). It is concluded that endogenous opioids do not play a major role in the modulation of cardiovascular and sympathoadrenal adaptations to moderate hypoxemia in the fetus.

Animals↗

Constriction of an extremity after amnioreduction in a TRAP-like sequence.

We present an unusual case of TRAP sequence (twin reversed arterial perfusion) with persistent polyhydramnios despite spontaneous thrombosis of the vena umbilicalis of the acardius. Serial amnioreduction was performed owing to considerable maternal discomfort and preterm labor. After three procedures, spontaneous abortion occurred. Unexpectedly, the normal twin had an apparently recent constriction of the right forearm. We hypothesize that limb constriction could be a rare but specific complication of aggressive amnioreduction.

Abortion, Spontaneous↗

Occult constrictive pericardial disease. Diagnosis by rapid volume expansion and correction by pericardiectomy.

Significant pericardial disease can exist without overt manifestations. Occult constrictive pericardial disease (OCPD) is identified by normal baseline hemodynamics and normal left ventricular systolic function with a characteristic response to rapid volume infusion. Following the intravenous administration of 1000 ml of normal saline over six to eight minutes, striking elevations of filling pressures are seen; however, diagnosis depends specifically upon a) the development of typical pressure pulse morphology of constriction, b) loss or reversal or respiratory variation of right atrial pressure, and c) precise diastolic equilibration of intracardiac pressures. Nineteen patients with OCPD have been identified in a five year period. Unexplained fatigue, dyspnea and chest pain was the uniform pattern of presentation. Eleven have undergone pericardiectomy resulting in a dramatic symptomatic improvement in all. Each demonstrated gross and/or microscopic evidence of pericardial disease. Recatheterization with volume infusion in five patients following pericardiectomy has revealed return to normal or near normal hemodynamics. This study describes the method for diagnosis of OCPD and recommends pericardiectomy for the management of disabling symptoms.

Adolescent↗

Echocardiographic features of the interventricular septum in chronic constrictive pericarditis.

Echocardiographic characteristics of the interventricular septum (IVS) have been studied in eight patients with chronic constrictive pericarditis (CP). Values of septal thickening (ST) were clearly below normal in all cases. Interventricular septal systolic motion (IVSSM) was normal in four cases, hypokinetic in three and paradoxical in one. In seven out of the eight patients, an early interventricular septal diastolic motion (IVSDM) consisting of a sudden anterior displacement followed by a brisk posterior rebound was recorded. The beginning of this anomalous movement was coincident with the pericardial knock in the phonocardiogram and its peak was coincident with the simultaneously recorded deep "y" trough in the jugular pulse tracing. The tendency toward normality of IVSDM observed after pericardiectomy in six out of seven patients suggests that this peculiar interventricular septal systolic motion may be a frequent and probably specific echocardiographic finding in constrictive pericarditis.

Adolescent↗

Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic constriction of the fetal ductus arteriosus. A possible mechanism for persistent pulmonary hypertension and transient tricuspid insufficiency in the newborn infant.

The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction.

Animals↗

Prenatal features of ductus arteriosus constriction and restrictive foramen ovale in d-transposition of the great arteries.

BACKGROUND: Although most neonates with d-transposition of the great arteries (TGA) have an uncomplicated preoperative course, some with a restrictive foramen ovale (FO), ductus arteriosus (DA) constriction, or pulmonary hypertension may be severely hypoxemic and even die shortly after birth. Our goal was to determine whether prenatal echocardiography can identify these high-risk fetuses with TGA. METHODS AND RESULTS: We reviewed the prenatal and postnatal echocardiograms and outcomes of 16 fetuses with TGA/intact ventricular septum or small ventricular septal defect. Of the 16 fetuses, 6 prenatally had an abnormal FO (fixed position, flat, and/or redundant septum primum). Five of the 6 had restrictive FO at birth. Five fetuses had DA narrowing at the pulmonary artery end in utero, and 6 had a small DA (diameter z score of <-2.0). Of 4 fetuses with the most diminutive DA, 2 also had an abnormal appearance of the FO, and both died immediately after birth. One other fetus had persistent pulmonary hypertension. Eight fetuses had abnormal Doppler flow pattern in the DA (continuous high-velocity flow, n=1; retrograde diastolic flow, n=7). CONCLUSIONS: Abnormal features of the FO, DA, or both are present in fetuses with TGA at high risk for postnatal hypoxemia. These features may result from the abnormal intrauterine hemodynamics in TGA. A combination of restrictive FO and DA constriction in TGA may be associated with early neonatal death.

Constriction, Pathologic↗

Chronic nonocclusive coronary artery constriction impairs ventricular function, myocardial structure, and cardiac contractile protein enzyme activity in rats.

To determine the effects of chronic nonocclusive coronary constriction on cardiac hemodynamics, structural integrity, and contractile protein enzyme activity, the left coronary artery was narrowed in rats, and measurements of ventricular performance, magnitude, and distribution of tissue damage and myofibrillar Mg2+ and Ca2+ myosin ATPase activities were evaluated 1 month later. In the presence of coronary artery stenosis averaging 58%, three levels of involvement of global cardiac performance were identified, and the rats were divided accordingly. In the first group, only left ventricular end-diastolic pressure (LVEDP) was increased; in the second group, LVEDP and left ventricular +dP/dt and/or -dP/dt were affected; and in the third group, LVEDP, left ventricular +dP/dt and -dP/dt, and right ventricular end-diastolic pressure were impaired. Thus, left ventricular moderate dysfunction, severe dysfunction, and failure occurred with coronary narrowing. On a structural basis, coronary constriction resulted in an ongoing process characterized by acute myocytolytic necrosis and foci of replacement fibrosis in different stages of healing. The number of these lesion profiles in the left ventricular myocardium increased 4.7-, 4.4-, and 8.3-fold in rats with moderate dysfunction, severe dysfunction, and failure, respectively. Biochemically, Mg(2+)-ATPase activity of myofibrils increased biventricularly when moderate dysfunction was present. However, this parameter decreased with the appearance of severe dysfunction, reaching control values in ventricular failure. Ca2+ myosin ATPase activity was reduced in the left ventricle of rats with severe dysfunction and failure, whereas it was elevated in the right ventricle of rats with severe dysfunction. In conclusion, a fixed lesion of the left main coronary artery with a modest reduction in vessel luminal diameter generates a conditioned state of the heart characterized by a continuous loss of myocytes and replacement scarring, which, in combination with alterations in contractile protein enzyme activity, may be responsible for a number of abnormalities in cardiac dynamics ranging from moderate dysfunction to pump failure.

Adenosine Triphosphatases↗

Lumen loss in transplant coronary artery disease is a biphasic process involving early intimal thickening and late constrictive remodeling: results from a 5-year serial intravascular ultrasound study.

BACKGROUND: Coronary artery disease is the major cause of late cardiac allograft failure. However, few data exist regarding the natural history of changes in intimal and external elastic membrane (EEM) areas after heart transplantation. METHODS AND RESULTS: In 38 transplant recipients, serial intravascular ultrasound examinations were performed 3.7+/-2.2 weeks after transplantation and annually thereafter for 5 years. In 59 coronary arteries, we compared 135 matched segments among serial studies. In each segment, intravascular ultrasound images were digitized at 1-mm intervals, and mean values of EEM and lumen and intimal areas were analyzed. In the first year after transplantation, the intimal area increased significantly from 1.8+/-1.6 to 3.0+/-2.1 mm(2) (P<0.001). Subsequently, the annual increase in intimal area decreased. EEM area did not change during the first year; however, between years 1 and 3, significant expansion of EEM area occurred (15.4+/-4.6 to 17.2+/-5.4 mm(2), P<0.001). Thereafter, EEM area decreased significantly from 17.2+/-5.4 mm(2) (year 3) to 15.1+/-4.9 mm(2) (year 5, P=0.01). Different mechanisms of lumen loss were observed during 2 phases after transplantation: early lumen loss primarily caused by intimal thickening and late lumen loss caused by EEM area constriction. CONCLUSIONS: This serial ultrasound study revealed that most of the intimal thickening occurred during the first year after heart transplantation. Changes in the EEM area showed a biphasic response, consisting of early expansion and late constriction. Thus, different mechanisms of lumen loss were observed during the early and late phases after transplantation.

Adult↗