Atrial natriuretic peptide in liver cirrhosis with mild ascites

To clarify the involvement of atrial natriuretic peptide (ANP) in the pathogenesis of liver cirrhosis, we measured plasma ANP in patients with various stages of cirrhosis and in age-matched normal subjects. Urinary cyclic guanosine monophosphate (cGMP) was also measured as a marker of active biological ANP. In addition, effects of exogenous synthetic human ANP (0.5 Μg/kg) on renal functions were examined in normal subjects and in cirrhotics without ascites or with mild ascites. Plasma ANP levels were not significantly different among these 3 groups. Urinary cGMP concentrations were significantly higher in both cirrhotics without ascites and cirrhotics with mild ascites, (340 pmol/ml, P<0.05 and 496 pmol/ml, P<0.01 respectively) than normal subjects (95 pmol/ml). In normal subjects, marked increases in urinary volume (UV), sodium excretion (UNaV), fraction excretion of sodium (FENa) and free water clearance (CH₂O) were induced after ANP infusion, and significant recoveries were subsequently observed in these parameters. However, in cirrhotics, the responses to ANP infusion of UV, FENa and CH₂O were far less dramatic. The response of UV, UNaV and FENa in cirrhotics with mild ascites was delayed compared to cirrhotics without ascites. These results suggest that the blunted natriuretic responsiveness to ANP is contributory to the pathogenesis of initial sodium retention in cirrhotics. This study was presented in part in the 25th annual meeting of the Japanese Association for the Study of the Liver, June, 1, 1989 Kanazawa, Japan.     

Brain natriuretic peptide increases acutely and much more prominently than atrial natriuretic peptide during coronary angioplasty

BACKGROUND: Increased levels of plasma brain natriuretic peptide (BNP) are observed in patients with congestive heart failure, hypertension, left ventricular hypertrophy, and acute myocardial infarction. However, there are no data on serial changes in plasma levels of BNP in patients undergoing coronary angioplasty. HYPOTHESIS: The study was undertaken to examine plasma concentrations of BNP together with those of atrial natriuretic peptide (ANP) in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). METHODS: Plasma concentrations of BNP and ANP were examined in 13 patients with stable angina pectoris and good left ventricular function undergoing PTCA. Blood samples were taken from the femoral vein at baseline, after the first balloon inflation, after the end of the procedure, and 4 h thereafter. RESULTS: Plasma BNP levels were 14 +/- 4 at baseline, 22 +/- 10 after the first balloon inflation, 28 +/- 12 at the end of the procedure, and 15 +/- 4 pgr/ml 4 h thereafter (F = 13.05, p < 0.00001). Plasma ANP levels were 80 +/- 15, 86 +/- 14, 90 +/- 24, and 75 +/- 6 fmol/l (F = 5.95, p = 0.002), respectively. The increase of BNP at the end of the procedure was related to the increase of ANP (r = 0.78, p = 0.002). CONCLUSION: Plasma BNP levels increase acutely and much more prominently than those of plasma ANP during coronary angioplasty; however, plasma BNP levels return to baseline values shortly after the end of the procedure.     

Alternations in atrial natriuretic peptide release after DC cardioversion of non-valvular chronic atrial fibrillation

The response of atrial natriuretic peptide (ANP) release tohaemodynamic influences after cardioversion of atrial fibrillationhas not been fully examined. We measured plasma concentrationsof ANP and assessed haemodynamic changes 60–120 min afterDC cardioversion in 22 patients with non-valvular chronic atrialfibrillation. Passive leg elevation to enhance volume expansionwas performed 60 min after DC cardioversion. Sinus rhythm wasrestored in 18 of the 22 patients (successful DC cardioversiongroup). The control group consisted of seven patients with non-valvularchronic atrial fibrillation who did not undergo DC cardioversion(atrial fibrillation control group). In the successful DC cardioversiongroup, the mean pulmonary artery wedge pressure decreased significantly15 min after cardioversion (P<0.05) and then remained unchanged.Plasma concentrations of ANP also decreased significantly 15min after cardioversion (P<0.05). Furthermore, there wasan additional significant decrease in ANP levels for up to 60min after cardioversion (P<0.05 from 15 min). Passive legelevation for 15 min led to an increase in the mean pulmonaryartery wedge pressure (P<0.01) and right atrial pressure(P<0.05), but did not result in increased plasma concentrationsof ANP (47.1 ± 27.6 vs 43.9 ± 34.4 pg. ml^–1,mean ± SD, P=ns). In the atrial fibrillation controlgroup, passive leg elevation increased the mean pulmonary arterywedge pressure (P<0.01), the mean right atrial pressure (P<0.05)and plasma concentrations of ANP (139.9 ± 85.8 vs 1681±108.2, P<0.05). In summary, after successful DC cardioversionof non-valvular chronic atrial fibrillation, plasma concentrationsof ANP decreased in conjunction with decreased mean pulmonaryartery wedge pressure. The response of ANP release to volumeexpansion, however, appears to be dysregulated in this patientpopulation.     

Effect of sildenafil citrate (Viagra) on coronary flow in normal subjects

BACKGROUND: The purpose of this study was to evaluate the effect of sildenafil citrate (Viagra) on coronary function in normal subjects. METHODS: The study assessed mean blood pressure, left anterior descending coronary artery (LAD) flow, and echocardiographic variables before and 30 and 60 minutes after taking 50 mg of sildenafil citrate. The mean velocity of LAD flow was assessed with Doppler flow imaging. The study subjects were 6 healthy male volunteers (mean age 37 years). RESULTS: The mean velocity of LAD flow increased 60 minutes after taking sildenafil citrate, but there were no other changes. Two volunteers felt mild flashing and one had mild headache during the study. CONCLUSION: Sildenafil citrate caused vasodilatation in a normal coronary artery without systemic pressure drops. These results suggest that the agent itself did not have negative effects on the heart in normal subjects.     

Release of atrial natriuretic peptide in relation to metabolic changes during myocardial ischaemia induced by coronary angioplasty

The inter-relationships between ischaemia-induced metabolicchanges and atrial natriuretic peptide (ANP) release were studiedin 18 patients undergoing elective percutaneous transluminalcoronary angioplasty (PTC A). Transcardiac differences in ANP,lactate, pH, pCO₂ and O₂ saturation were analysed before andafter balloon inflation. The patients were divided into ischaemiaand non-ischaemia groups on the basis of the change in lactateextraction ratio during balloon inflation. The ischaemia group(patients with a decrease in lactate extraction ratio) showedan increase of 27±15 pg. ml^–1 in the transcardiacANP difference, whereas a decrease of 27±17pg.ml^–1occurred in the non-ischaemia group (no decrease in lactateextraction ratio). The change between the two patient groupswas statistically significant (P<0.05). Metabolic ‘pre-conditioning’was not observed in patients with successive dilatations, thereforedata from all the dilatations were combined and evaluated byregression analysis. A correlation coefficient of 0.40 (P<0.05)was obtained between the PTCA-induced changes in transcardiacANP and lactate differences. We conclude that transient myocardialischaemia induced by PTCA increases circulating ANP concentrationsin patients with signs of metabolic ischaemia, but not in thosewithout.     

Atrial natriuretic peptide in children with pneumonia

Atrial natriuretic peptide (ANP) has known natriuretic, diuretic, and vasodilatatory effects. It is synthesized and stored in the atrial cells. Stretching of the atrial muscle fibers during an increase in venous return sets a response of ANP release into the blood stream. High levels of ANP were measured in a number of lung diseases. Pneumonia in children is frequently accompanied by the hyponatremia of the syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH). High levels of ANP were found among patients with SIADH. Our objective was to determine if ANP plasma levels are altered in children with pneumonia, and to evaluate a possible correlation between severity of pneumonia and ANP levels. Blood samples from 28 children diagnosed with pneumonia were collected. Plasma ANP levels were determined by radioimmunoassay and compared to levels in 25 children without pneumonia. ANP levels in the pneumonia group (mean +/- SD, 16.02 +/- 11.69 pg/ml) increased significantly (P < 0.01) compared to levels in the control group (mean +/- SD, 7.44 +/- 9.29 pg/ml). Children in the pneumonia group also exhibited low levels of plasma sodium (mean +/- SD, 134.88 +/- 2.5 mmol/l) compared to levels in children without pneumonia (mean +/- SD, 139.77 +/- 4.15 mmol/l) (P < 0.01). There was no correlation between ANP plasma levels and severity of pneumonia. In conclusion, ANP levels in children with pneumonia, as in other lung diseases, are increased. High ANP levels may play a role in maintaining water and electrolyte equilibrium during a state of inappropriate ADH secretion accompanying pneumonia.     

Clinical, adrenergic and heart endocrine measures in chronic atrial fibrillation as predictors of conversion and maintenance of sinus rhythm after direct current cardioversion

The aim of this study was to evaluate clinical, adrenergic andendocrine factors that could predict sinus rhythm maintenanceafter direct current cardioversion in chronic atrial fibrillation. Nineteen patients with chronic non-rheumatic atrial fibrillation(mean duration 6±5 months) were studied. They were exercised24 h before cardioversion at maximum effort with the Naughtonprotocol. Heart rate and blood pressure at rest and exercisewere recorded and blood samples were taken for the assessmentof adrenergic activity, by measuring cyclic adenosine monophosphate,heart endocrine function, atrial natriuretic peptide and itssecond messenger, cyclic guanosine monophosphate. Fifteen ofthe 19 patients were initially converted to sinus rhythm (eightpatients with external and seven patients with internal DC shocks).After 3 months eight patients remained in sinus rhythm and 11had relapsed, most of them within the first month. On exercisethe chronotropic response was lower in the group who remainedin sinus rhythm than in the group in atrial fibrillation (peakheart rate 147±11 beats.min^–1 vs 165±24beats.min^–1 p=0·02). During exercise, the systolicblood pressure in the sinus group reached higher values thanin the group who relapsed (192±17 mmHg vs 176±18mmHg, p=0·03). Cyclic adenosine monophosphate increasedsignificantly from rest to peak exercise in the sinus rhythmgroup (from 23±9 pmol.ml^–1 to 31±15 mol.ml^–1,p=0·02) while it remained unchanged in the atrial fibrillationgroup (25±10 pmol.ml^–1 to 24±8 pmol.ml^–1,p=0·02). For all 19 patients the differ ence in cyclicadenosine monophosphate between rest and exercise was negativelycorrelated with maximum heart rate (r=0·58, p=0·009).Atrial natriuretic peptide increased from rest to peak exercisein the sinus rhythm group (from l29±58 fmol.ml^–1to 140±66fmol.ml^–1 while it remained unchangedin the group in which atrial fibrillation persisted or recurred(from 112±58 fmol.ml^–1 to 111±53 fmol.ml^–1p=0· A significant correlation between atrial natriureticpeptide and cyclic guanosine monophosphate levels at exercisebefore cardioversion was found for the sinus rhythm group only(r=0·76, p=0·02). In patients with non-rheumatic chronic atrial fibrillation evaluationof clinical parameters such as heart rate and blood pressurechanges during maximal exercise can be useful in the choiceof suitable therapy. An inadequate increase in plasma cyclic-adenosinemonophosphate and atrial natriuretic peptide on exercise couldpredict patients with more severe underlying disease, wherecardioversion should not be recommended.     

Atrial natriuretic peptide in atrial fibrillation before and after electrical cardioversion therapy

In eight patients with atrial fibrillation of less than 3 monthsduration and without congestive heart failure the plasma concentrationof atrial natriuretic peptide was determined one day before,the day after and again 30 days after electrical cardioversiontherapy. The pretreatment plasma concentration of the peptidewas 99 pg mg^–1 (23–480, median and range). The dayafter cardioversion to sinus rhythm the peptide concentrationhad normalized to 36 pg ml^–1 (18–151). The plasmaconcentration of atrial natriuretic peptide remained stablein all but one patient for a period of 30 days (46 pg ml^–1,16–695) (P = 0·03). In conclusion, the plasma concentration of atrial natriureticpeptide in patients with atrial fibrillation was significantlyreduced after electrical cardioversion to sinus rhythm and remainedstable for a period of 30 days.     

Coronary revascularization directed by results of coronary doppler flow measurements

We present a case where Doppler coronary flow velocity and Doppler reserve measurement directed the decision to proceed with coronary artery revascularization. Measurement of coronary Doppler flow velocity and flow reserve can be useful to help evaluate angiographic “intermediate lesions.” The following case involves an indeterminate lesion. A patient was felt likely to have a high-grade stenosis which could not be adequately visualized angiographically because of overlapping vessels. Largely based on the flow velocity and reserve data, the patient was referred for coronary artery bypass grafting.     

Standardization of plasma brain natriuretic peptide concentrations in older Japanese-relationship to latent renal dysfunction and ischemic heart disease

OBJECTIVES: To determine the contributors to elevating plasma brain natriuretic peptide (BNP) concentrations in older people with normal systolic function. To investigate the relationship between cyclic guanosine monophosphate (cGMP) and BNP in older people with and without ischemic heart disease (IHD). DESIGN: Observational study. SETTING: Hospitalized patients in Nagoya University Hospital from November 1997 to May 2000. PARTICIPANTS: Younger patients (<65) without IHD (n = 31), older patients (> or=65) without IHD (n = 37), and older patients with stable IHD (n = 32). All participants showed 45% or greater of their left ventricular ejection fraction (LVEF). MEASUREMENTS: LVEF, peak atrial velocity/peak early velocity (A/E) ratio at the mitral valve, and left ventricular mass volume were measured using transthoracic echocardiogram. Plasma BNP level, cGMP, and serum creatinine (Scr) were measured. Creatinine clearance (CLcr) was calculated based on 24-hour urine collection. RESULTS: Plasma BNP levels in older people with and without IHD were significantly greater than in younger patients (mean +/- standard deviation = 76.4 +/- 96.0 (P <.001), 165.2 +/- 200.6 (P <.001), and 8.1 +/- 7.0, respectively). By simple regression analysis, in the groups without IHD, the logarithm of plasma BNP (Log BNP) concentrations had a significant positive relationship with age (R = 0.657, P <.001), Scr (R = 0.449, P <.001), and A/E ratio (R = 0.326, P =.003) and a significant negative relationship with CLcr (R = -0.663, P <.001). A stepwise multiple regression analysis with Log BNP level as the dependent variable and age, Scr, CLcr, and A/E ratio as independent variables showed that CLcr was a significant independent contributor in groups without IHD (R = -0.766, P <.001). In this analysis, the regression coefficient of the intercept was 2.006, and that of CLcr was -0.010. The cGMP/BNP ratio in older subjects with stable IHD tended to be lower than in those without IHD (P =.063). CONCLUSIONS: Elevated BNP levels in older patients with normal systolic function may be in part due to latent renal dysfunction, despite normal Scr levels. In healthy older people, it is important to exclude the effects of latent renal function in assessing cardiac function according to BNP level. In older subjects with stable IHD, the cGMP/BNP ratio tended to be lower than in those without IHD. This may be a reflection of a poor response of cGMP to BNP.     

Atrial natriuretic peptide in alcoholic cirrhosis

Sodium retention in cirrhosis could result from a deficiency of atrial natriuretic peptide (ANP) or end-organ resistance to ANP. Venous levels of α-human ANP (αhANP) measured in 19 alcoholic cirrhotics by radio-immunoassay were in the higher end of the normal range (29.7 pg/ml, s.d. = 17.2) and tended to increase with development of ascites or varices. Arterial levels of αhANP were not related to right atrial pressure but were related inversely to pulse rate. There was significant splanchnic (mean = 37.2%, s.d. = 19.5) and non-splanchnic clearance (mean = 30.3%, s.d. = 17.1) of αhANP. The percentage extraction of αhANP across the splanchnic bed (%E ANP splanchnic) was not related to portal pressure, effective hepatic plasma flow or degree of intrahepatic shunting. The %E ANP splanchnic increased as functional liver cell mass (antipyrine clearance) decreased (r= 0.592, P= 0.034). Despite increased splanchnic clearance, αhANP levels increased with a fall in functional liver cell mass presumably due to increased release. Renal sodium retention in cirrhosis does not involve a deficiency of αhANP but increased end-organ resistance needs to be excluded.     

Flow velocity and predictors of a suboptimal coronary flow velocity reserve after coronary balloon angioplasty.

AIMS: This study was conducted to analyse flow velocity parameters and predictors of a suboptimal coronary flow reserve (<2.5) following balloon angioplasty. METHODS: Two hundred and twenty-five patients underwent sequential intracoronary Doppler as part of the DEBATE I study. Of these, 183, with complete angiography and Doppler at the 6-month follow-up, were included. Univariate and multivariate logistic analysis was performed to identify independent predictors of post-procedural suboptimal coronary flow reserve, defined as coronary flow reserve <2.5. RESULTS: Forty-eight per cent (n=88) of the patients achieved a suboptimal coronary flow reserve. These patients had higher baseline velocities (cm.s(-1)) before balloon angioplasty (18+/-9 vs 14+/-6, P=0.004), after balloon angioplasty (22+/-11 vs 14+/-5, P<0.001) and at follow-up (19+/-9 vs 16+/-6, P=0.011) than the optimal coronary flow reserve group. Although the suboptimal group had lower hyperaemic velocities (cm.s(-1)) after balloon angioplasty than the optimal group (42+/-17 vs 49+/-16, P=0.008), these velocities became similar at follow-up. Increasing age (odds ratio, OR 1.071, P=0.0002), female gender (OR 2.52, P=0.014) and increasing pre-procedural baseline average peak velocities (OR 1.056, P<0.001) were found to be independent predictors of a suboptimal coronary flow reserve following balloon angioplasty. CONCLUSION: A suboptimal coronary flow reserve was associated with (1) a chronically elevated baseline average peak velocity (2) a transient deficit in the hyperaemic average peak velocity (3) the elderly, and female gender.     

Quantitative contrast echocardiographic assessment of collateral derived myocardial perfusion during elective coronary angioplasty

OBJECTIVE—To determine whether myocardial contrast echocardiography can be used to quantify collateral derived myocardial flow in humans.
METHODS—In 25 patients undergoing coronary angioplasty, a collateral flow index (CFI) was determined using intracoronary wedge pressure distal to the stenosis to be dilated, with simultaneous mean aortic pressure measurements. During balloon occlusion, echo contrast was injected into both main coronary arteries simultaneously. Echocardiography of the collateral receiving myocardial area was performed. The time course of myocardial contrast enhancement in images acquired at end diastole was quantified by measuring pixel intensities (256 grey units) within a region of interest. Perfusion variables, such as background subtracted peak pixel intensity and contrast transit rate, were obtained from a fitted γ variate curve.
RESULTS—16 patients had a left anterior descending coronary artery stenosis, four had a left circumflex coronary artery stenosis, and five had a right coronary artery stenosis. The mean (SD) CFI was 19 (12)% (range 0-47%). Mean contrast transit rate was 11 (8) seconds. In 17 patients, a significant collateral contrast effect was observed (defined as peak pixel intensity more than the mean + 2 SD of background). Peak pixel intensity was linearly related to CFI in patients with a significant contrast effect (p = 0.002, r = 0.69) as well as in all patients (p = 0.0003, r = 0.66).
CONCLUSIONS—Collateral derived perfusion of myocardial areas at risk can be demonstrated using intracoronary echo contrast injections. The peak echo contrast effect is directly related to the magnitude of collateral flow.


Keywords: collateral circulation; quantitative myocardial contrast echocardiography; intracoronary pressure; myocardial perfusion     

Effect of Rotational Coronary Atherectomy on Peripheral Endothelin-1, Atrial Natriuretic Peptide, and Cyclic Adenosine Monophosphate Plasma Levels

We investigated the effects of coronary rotational atherectomy (PTCRA) on plasma levels of endothelin-1 (ET-1), atrial natriuretic peptide (ANP), and cyclic adenosine monophosphate (cAMP). We studied 14 patients undergoing PTCRA and compared them with 14 patients undergoing plain balloon angioplasty. Blood samples were taken from the femoral vein at baseline, after the end of the atherectomy, after the first balloon inflation, after the end of the procedure, and 4 hours later. ET-1 increased in the angioplasty group from 6.3 ± 3.2 pmol/L at baseline to 8.5 ± 3.9 pmol/L at the end of the procedure (F = 3.83, P = .02), whereas it did not change in the PTCRA group. ANP increased in the PTCRA group from 78.1 ± 15.7 pmol/L at baseline to 89.7 ± 24.0 pmol/L at the end of the procedure (F = 6.75, P = .0001), whereas it did not change in the angioplasty group. cAMP decreased in the PTCRA group, whereas it did not change in the angioplasty group. In conclusion, ET-1 increases less, ANP increases more, and cAMP decreases more during atherectomy than during plain balloon angioplasty.     

Atrial natriuretic peptide response to postural changes in patients with left atrial hypertension

Plasma atrial natriuretic peptide (ANP), cyclic guanosine monophosphate(GMP) and renin activity (PRA) were measured in 13 patientswith mitral stenosis 24 h before and 48 h after balloon valvotomyresulting in a fall in LA pressure from 23.4 ± 2.2 to10.5 ± 0.8 mmHg (P<0.01). Before treatment, plasmaANP was higher during ambulation (128.1 ± 18.5 pg ml^–1)than in the supine posture (93.3± 15.0 pg ml^–1;P<0.01) and did not diminish after return to the erect posture(86.4± 14.1 pg ml^–1). A physiological responsewas restored after valvotomy with ANP plasma levels of 49.2± 7.8pg ml^–1 in the initial ambulant period, 63.1± 12.6 pg ml^–1 in the supine posture and 44.6 ±8.7 pg ml^–1 in the final erect posture. Postural variationsof cyclic GMP were parallel to those of ANP. In contrast, LAhypertension did not abolish PRA postural response. During thethree successive periods of ambulation, supine posture and erectposture PRA was 5.4± 10, 2.8 ± 0.6 and 5.5±1.2ng h^–1 ml^–1, respectively, before treatment,whereas after treatment the values measured were 10.3 ±2.9, 2.3 ± 0.7 and 7.0 ± 2.5 ngh^–1 ml^–1respectively. Variations of plasma ANP, cyclic GMP and PRA inresponse to postural changes were also studied in 10 healthyvolunteers and in 12 uraemic patients with high plasma ANP.Similar physiological results were obtained in these two controlgroups, suggesting that the dysregulation of ANP response inpatients with high LA pressure was not related to the high valuesof plasma ANP. In conclusion, persistent elevation of plasmaANP in response to postural changes appears to be the consequenceof LA hypertension.     

Early changes in coronary flow physiology after balloon angioplasty or stenting: a 24-hour Doppler flow velocity study.

To evaluate early changes in myocardial microcirculation after balloon or stent coronary angioplasty, we studied 57 patients undergoing coronary angioplasty with a Doppler-tipped guidewire, with (n = 26) or without stenting. Postprocedural quantitative coronary angiography and coronary flow velocity were measured after 10 min and 24 hr. As compared to stenting, no stenting was associated with a higher postprocedural stenosis rate (21% +/- 13% vs. 12% +/- 10%; P < 0.05), smaller coronary velocity reserve (CVR; 2.2 +/- 0.4 vs. 2.5 +/- 0.7; P = 0.04), and smaller relative CVR (0.8 +/- 0.2 vs. 1.1 +/- 0.3; P = 0.001). At 24 hr, CVR and relative CVR in the unstented group increased to the level in the stented group, mainly because of a decrease in basal average peak velocity (APV). Overall, there was a significant negative linear relation between CVR and APV variations during the 24-hr period. In the subgroups with persistent abnormalities, CVR variation was closely related to the basal APV/reference APV ratio. In conclusion, coronary reserve normalization can occur within 24 hr after coronary angioplasty and is closely dependent on postangioplasty APV. Myocardial distal resistances should be considered when interpreting postangioplasty CVR.     

Atrial natriuretic peptide response to ionic and nonionic contrast left ventriculography

Atrial natriuretic peptide (ANP) levels were measured prior to and at 1 and 5 minutes postcontrast left ventriculography with an ionic contrast agent (diatrizoate), and a nonionic agent (iopamidol) and the results were compared. Since ionic contrast agents have been found to cause an increase in left ventricular end-diastolic pressure (LVEDP) and nonionic agents have been found to have less of an effect on LVEDP, we investigated the response of ANP levels, which have been found to increase secondary to increased LVEDP (atrial pressure), with both agents. A group of 38 patients who were scheduled for left heart catheterization for suspected coronary artery disease was included (19 in each group) and blood samples for ANP levels were drawn from the left ventricles. At the same time, heart rate, LVEDP, and left ventricular systolic pressure (LVSP) were also measured. It was found that the LVEDP increased significantly for both agents at 1 minute postventriculography, but no further change occurred at 5 min. Heart rate increased significantly in the diatrizoate group at 1 minute with a return of heart rate to preventriculography levels at 5 min, while the ANP level and LVSP remained unchanged at 1 minute postventriculography with both agents but increased significantly at 5 min in the diatrizoate group only. This difference in ANP response is not correlated with the LVEDP. The response of ANP may be related to heart rate and/or LVSP.     

Atrial natriuretic factor: Physiologic actions and implications in congestive heart failure

Summary Atrial natriuretic factor (ANF) represents a newly recognized hormone of cardiac origin. This peptide is synthesized by the myocardial cells of both atria and released by atrial stretch. The hormone promotes sodium and water excretion by the kidney, inhibits the renin-angiotensin-aldosterone system, and reduces systemic arterial pressure. Specific receptors for ANF are present in the kidney, adrenal glands, vascular smooth muscle, platelets and central nervous system. Congrestive heart failure is characterized by increased circulating levels of ANF; however, there appears to be an attenuation in the renal response to the hormone.Recent investigations have reported the effect of systemic administration of synthetic ANF to normal individuals and those with congestive heart failure. The hormone may promote a significant natriuresis and diuresis in addition to reducing arterial pressure and inhibiting renin and aldosterone secretion. Substantial questions remain as to the full physiologic significance and therapeutic potential of this hormone.     

Influence of the ischemic coronary bed on collateral blood flow

Summary The purpose of this study was to determine the influence of the resistance of the terminal vascular bed of an occluded coronary artery on collateral blood flow and collateral resistance. In 6 anesthetized dogs, left anterior descending coronary artery (LAD) was ligated, cannulated, and the terminal vascular bed was occluded by latex microspheres (diameter: 25). Retrograde flow was measured using a new technique, which allowed control of outflow pressure of retrograde flow (PRF) at the LAD cannula. When retrograde flow was interrupted, pressure in the occluded vessel represented collateral perfusion pressure (CPP) within the border zone of the ischemic vessel. Collateral resistance was determined dividing the pressure difference across the collateral bed (CPP-PRF) by retrograde flow. Variation of PRF was used as a model for changes in resistance of the ischemic bed. Retrograde flow fell when PRF was increased from 11.0±3.0 ml×min^–1×100 g^–1 (PRF=0) to 8.3±2.4 (p<0.01) (PRF=24.6±6 mm Hg). For the same PRF range, collateral resistance fell from 9.68±2.96 to 8.30±2.50 mm Hg×ml^–1×min×100 g (p<0.01). These results indicate that the vascular resistance of the terminal ischemic bed may considerably influence collateral blood flow and resistance.This study was supported in part by DFG grant Er 100/3-1