Latitude of the study place and age of the patient are associated with incidence of mediastinitis and microbiology in open-heart surgery: a systematic review and meta-analysis.

OBJECTIVE: We aimed to summarize the pooled frequency of mediastinitis following open-heart surgery caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), and Gram-negative bacteria. DESIGN: This study was a systematic review and a meta-analysis of prospective and retrospective cohort studies. MATERIALS AND METHODS: We searched the literature, and a total of 97 cohort studies were identified. Random-effect model was used to synthesize the results. Heterogeneity between studies was examined by subgroup and meta-regression analyses, considering study and patient-level variables. Small-study effect was evaluated. RESULTS: Substantial heterogeneity was present. The estimated incidence of mediastinitis evaluated from 97 studies was 1.58% (95% confidence intervals [CI] 1.42, 1.75) and that of Gram-positive bacteria, Gram-negative bacteria, and MRSA bacteria evaluated from 63 studies was 0.90% (95% CI 0.81, 1.21), 0.24% (95% CI 0.18, 0.32), and 0.08% (95% CI 0.05, 0.12), respectively. A meta-regression pinpointed negative association between the frequency of mediastinitis and latitude of study place and positive association between the frequency of mediastinitis and the age of the patient at operation. Multivariate meta-regression showed that prospective cohort design and age of the patients and latitude of study place together or in combination accounted for 17% of heterogeneity for end point frequency of mediastinitis, 16.3% for Gram-positive bacteria, 14.7% for Gram-negative bacteria, and 23.3% for MRSA bacteria. CONCLUSION: Evidence from this study suggests the importance of latitude of study place and advanced age as risk factors of mediastinitis. Latitude is a marker of thermally regulated bacterial virulence and other local surgical practice. There is concern of increasing risk of mediastinitis and of MRSA in elderly patients undergoing sternotomy.

[Experiences with biological aortic valve at Ullevål hospital]. / Erfaringer med biologiske aortaklaffer ved Ullevål sykehus.

Biological valves have been used at Ullevål Hospital since 1993 in patients over the age of 70, and in younger patients when anticoagulation is contraindicated. We have used two different types of biological valves; Medtronic Freestyle, a non-stented valve made from pigs aortic root; and Carpentier-Edwards, made from calf pericardium. This valve is mounted in a metallic frame (stent), covered by dacron. Both valves are fixed in glutaraldehyde to diminish tissue antigenicity. 91 patients were operated with biological valves during the period 1993 till January 1998; 56 patients received the Carpentier-Edwards and 35 Freestyle. Postoperative complications have been few and time in the intensive care unit and total hospital stay is satisfactory despite the high age of this group of patients. The overall 30 days postoperative mortality was 4.4%. In conclusion, aortic stenosis and insufficiency can be operated with low mortality and short postoperative or intensive care stay. There was no significant difference between the two groups of patients.

[Pelvi-rectal abscesses. Diagnosis, treatment and follow-up by transrectal ultrasonography]. / Pelvirektale abscesser. Diagnostikk, behandling og oppfølging ved hjelp av transrektal ultralydundersøkelse.

Pelvirectal abscess usually presents with vague symptoms which may delay diagnosis and subsequent treatment. However, it is important to recognize this condition since these abscesses may interfere with the sphincter function or give rise to chronic fistulo-in-ano. We describe two patients in whom transrectal ultrasound was applied for diagnosis, and who were treated for a pelvirectal abscess. Both patients were admitted to our hospital because of tumour of the rectum. There were few symptoms and signs of infection. Transrectal ultrasound examination of the rectum made a significant contribution to early diagnosis. We also point out the advantage of transrectal ultrasound examination during follow-up, mainly because we were able to rule out malignant neoplasm by obtaining an ultrasound-guided specimen for histological examination.

[Rectal cancer. Staging with transrectal ultrasonography]. / Cancer recti. Vurdering av dybdevekst med transrektal ultrasonografi.

30 patients with carcinoma of the rectum were examined preoperatively with endoluminal rectal ultrasound and digital examination in order to assess the stage of the tumour. The results were compared with the histopathological findings in the resected specimens from 23 patients. The following operations were performed: 11 abdominoperineal rectal amputations, five low anterior resections and seven local excisions. Discrepancies between the ultrasonic and histological staging occurred in seven patients, six tumours were overstaged and one understaged ultrasonically. Digital assessment overstaged eight tumours and understaged two. The ultrasonic examination provided additional information in 12 patients.

[Intraoperative ultrasonography of the liver]. / Intraoperativ ultralydundersøkelse av lever.

Intraoperative ultrasound is the most recent diagnostic tool in liver surgery. It presents the surgeon with a technique that can provide detailed information about liver tumours and their topography prior to surgery. It also provides very good visualization of the vascular tree of the liver. This article gives a detailed description of the technique of intraoperative ultrasound of the liver. It also presents results from two groups of patients: 30 patients who underwent laparatomy for colorectal cancer (n = 16) or for liver tumours (n = 14) were examined by intraoperative ultrasound of the liver. The results were compared with the observations made by preoperative ultrasound examination. In seven patients the intraoperative ultrasound examination showed liver tumors that had not been detected preoperatively. The intraoperative ultrasound was decisive for the operative strategy in three of the patients treated for liver tumours. In one of the patients operated on for colorectal cancer, in whom the intraoperative ultrasound examination revealed a previously unrecognized metastasis, a liver resection is now planned. Our study confirms that intraoperative ultrasound is a valuable form of examination in patients treated for colorectal cancer and is important for deciding the surgical strategy for patients treated for liver tumours.

Frequency dependent myocardial potassium fluxes during beta adrenergic stimulation of intact pig hearts.

STUDY OBJECTIVE: The aim was to determine the frequency dependent myocardial potassium fluxes of intact pig hearts at control inotropy and during beta adrenergic stimulation. DESIGN - Atrial pacing rate was suddenly raised and decreased by 50 beats.min-1 at control inotropy and during infusion of isoprenaline, 2.5 nmol.min-1, into the left coronary artery. EXPERIMENTAL MATERIAL: Nine anaesthetised pigs (21-33 kg) were instrumented for electric pacing of the right atrium and metabolic and haemodynamic recordings. MEASUREMENTS AND MAIN RESULTS: Myocardial potassium balance was measured by PVC-valinomycin electrodes in the left atrial cavity and in a shunt (with flow meter) diverting blood from the coronary sinus to the right atrium. Isoprenaline raised net myocardial potassium flux following the change in pacing rate from 19(14-23) to 38(32-46) mumol.100 g-1.min-1 (median, 95% confidence interval, difference: p = 0.03). The corresponding myocardial potassium flux per beat increased from 0.38(0.29-0.45) to 0.80(0.63-0.97) mumol.100 g-1 (p = 0.03). Accumulated potassium flux increased from 9(8-11) to 17(11-27) mumol.100 g-1, respectively (p = 0.03). CONCLUSIONS: In intact hearts beta adrenergic stimulation doubles the frequency dependent myocardial potassium flux. This component constitutes 22-25% of the ouabain inhibitable potassium flux at both levels of inotropy.

Influence of angiotensin on total intravascular capacity in the anaesthetized pig.

The present study examined the influence of angiotensin on total intravascular capacity. In eight anaesthetized pigs, splenectomy, carotid sinus denervation and cervical vagotomy were performed. Blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that changes in total intravascular volume could be recorded as the inverse of changes in reservoir volume. Angiotensin administration at 0.2 microgram kg-1 min-1 i.v. for 5 min was associated with a decrease in total intravascular volume of 57 +/- 6 ml (P less than 0.05) and an increase in aortic pressure from 96 +/- 5 to 119 +/- 6 mmHg (P less than 0.05). With subsequent angiotensin administration in five of the animals, the responses were not attenuated. In five of the animals, angiotensin was associated with a decrease in intravascular volume of 72 +/- 8 ml (P less than 0.05) before abdominal evisceration and 33 +/- 13 ml (P less than 0.05) after evisceration. These responses were significantly different from each other. In four of these eviscerated animals, angiotensin was associated with a decrease in intravascular volume of 35 +/- 17 ml (P less than 0.05) before ligation of all four limbs and a decrease of 36 +/- 4 ml (P less than 0.05) after limb ligation. Thus, angiotensin acts directly to decrease total intravascular volume. The decrease is due to decreases in both splanchnic and extrasplanchnic volume. The extrasplanchnic volume decrement is not due to decreases in skeletal muscle or cutaneous tissue intravascular capacity in the limbs.

Regulation of splanchnic organ size during muscarinic receptor stimulation in the anaesthetized pig.

To determine the mechanisms responsible for changes in splanchnic organ size during muscarinic receptor stimulation, acetylcholine was infused at 5 micrograms kg-1 min-1 in 11 anaesthetized pigs which had previously undergone carotid denervation and cervical vagotomy. Blood pressure decreased by 42 +/- 4 mmHg (P less than 0.005), portal vein pressure decreased by 1.0 +/- 0.3 mmHg (P less than 0.01), IVC pressure increased by 0.2 +/- 0.1 mmHg (P less than 0.01), hepatic arterial flow increased by 10 +/- 6 ml min-1 (NS), portal vein flow decreased by 89 +/- 20 ml min-1 (P less than 0.005), splenic segment length (SSL) decreased by 0.52 +/- 0.11 mm (P less than 0.005) (control 12.49 +/- 1.27) (measured with ultrasonic crystals) and hepatic segment length (HSL) increased by 0.29 +/- 0.06 mm (P less than 0.005) (control 13.94 +/- 1.16). Aortic constriction to decrease the splanchnic distending pressure by an amount comparable to that achieved with the acetylcholine-associated decrease in portal flow caused a similar decrease in SSL and increase in HSL. Graded constriction of the portal vein or IVC, to increase SSL or HSL respectively, in the presence and absence of acetylcholine demonstrated no change in splenic or hepatic compliance with acetylcholine. Ligation of the splenic vasculature reduced the acetylcholine-associated HSL increase from 0.41 +/- 0.09 to 0.20 +/- 0.07 mm (P less than 0.05). Acetylcholine infused directly into the portal vein did not alter HSL. Atropine abolished all acetylcholine-associated haemodynamic changes. Thus, muscarinic receptor stimulation does not appear to act directly on splanchnic capacity vessels. Splenic dimension decreases due to a decrease in splanchnic flow and pressure, and hepatic dimension increases due to an increase in IVC pressure and redistribution of volume from the spleen.

In-vivo quantification of myocardial Na-K pump rate during beta-adrenergic stimulation of intact pig hearts.

Maintenance of adequate electrical activity of the heart depends critically on the ability of the Na-K pump to compensate for normal passive sodium and potassium fluxes. Using sudden injections of [3H]ouabain into the left coronary artery in anaesthetized open-chest pigs, we monitored transient changes in myocardial potassium balance by PVC-valinomycin mini-electrodes. When related to the number of pumps blocked and fractional inhibition, these data provided estimates of total Na-K pump capacity as well as actual pump rate and perturbations of the Na-K balance. Experiments were performed in hearts with and without intracoronary isoprenaline infusion (2.5 nmol min-1). After injection of 120 nmol [3H]ouabain into the left coronary artery, myocardial [3H]ouabain concentrations were 118 (74-178) and 103 (76-145) pmol g-1 and total concentrations of [3H]ouabain binding sites were 893 (752-1076) and 785 (691-877) pmol g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (differences not significant). The [3H]ouabain injection caused a net potassium release of 81 (56-132) and 43 (23-75) mumol 100 g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (n = 6-8; significance of difference, P = 0.03). Na-K pump rate estimated from mono-exponential release curves was 6363 (3942-10,858) K+ ions min-1 site-1 during beta-adrenoceptor stimulation and 2514 (1380-4322) in control (significance of difference, P = 0.03). This corresponds to 40 and 16%, respectively, of the maximum possible pump rate determined from ATP hydrolysis. Comparison of accumulated potassium release and relative Na-K pump rate indicates that catecholamines enhance the sensitivity of the Na-K pump for intracellular sodium.

Interplay among cardiac chambers. Left and right ventricular performance during changes in contractility, afterload and during simultaneous atrio-ventricular contraction.

1. Only a slight increase in stroke volume is observed during a selective left-sided inotropic stimulation of the in situ pig heart. Decreased left ventricular preload during left-sided inotropic stimulation reduces activation of the Frank-Starling mechanism and hence explains the rather small increase in stroke volume. We suggest that left-sided inotropic stimulation redistributes blood from the pulmonary circulation toward the systemic circulation causing a fall in pulmonary artery pressure and increased right ventricular output because of this afterload-reduction. 2. A rise in stroke volume during selective right-sided inotropic stimulation is not attenuated by a concomitant reduction in right ventricular preload. On the contrary, right ventricular preload rises in response to inotropic stimulation of the right atrium. Right-sided inotropic stimulation redistributes blood toward the pulmonary vascular bed and the left side of the heart. Left ventricular function is improved by this redistribution. 3. Both left ventricular end-systolic and end-diastolic volumes are better maintained by thoracic aortic occlusion during left-sided inotropic stimulation than at control inotropy. The concomitantly better preserved dimensions in the right ventricle can be explained by reduced pressure in the pulmonary circulation and a decrease in right-ward septal bulging. The rise in stroke volume by aortic occlusion during intravenous isoproterenol infusion is mainly due to a greater redistribution volume than at control inotropy. 4. Prolongation of the diastolic interval may reduce the end-diastolic pulmonary artery pressure to such an extent that right atrial contraction could eject blood into the pulmonary artery during late ventricular diastole.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors reducing left and right ventricular output during simultaneous atrioventricular activation in the pig heart.

Forward stroke volume fell by 26% (23-30%) (median and 95% confidence interval) when simultaneous atrioventricular (AV) pacing was induced at constant heart rate in 10 anaesthetized open-chest pigs. To assess the relative importance of factors which could cause this reduction in right and left ventricular (RV and LV) output, we compared cardiac dynamics when either ventricular filling or forward stroke volume was equally reduced by caval constriction and simultaneous AV pacing. We estimated the degree of ventricular filling by recording segment lengths (SL) in the free walls of both ventricles. Our analysis revealed that abolished active LV filling by the left atrium reduced forward stroke volume by 11% (8-14%). The remaining fall in output could be attributed to mitral regurgitation. In the right side of the heart the response was different. The drop in RV filling during simultaneous AV pacing accounted for approximately one-half of the fall in forward RV stroke volume. Estimates based on SL recordings demonstrated that forward RV stroke volume fell by 7% (2-25%) because of tricuspidal regurgitation. Pulmonary artery pressure was 4.5 (3.4-5.7) mmHg higher during simultaneous AV pacing than during caval constriction, representing a relative rise in afterload that reduced the RV stroke volume by 6-8%. Thus, reduced ventricular filling during simultaneous AV pacing accounted for approximately one-half of the drop in forward output from both ventricles. Slightly more than one-half of the reduction in forward LV stroke volume could be attributed to mitral regurgitation. In the right side of the heart tricuspidal regurgitation and a relative rise in pulmonary artery pressure each accounted for about one-quarter of the fall in forward RV output.

Significance of right atrial function during right sided inotropic stimulation of pig hearts in situ.

Cardiac adjustments to inotropic stimulation of the right side of the heart were examined in anaesthetised, open chest pigs by calcium chloride infusion (80 mumol.min-1) into the right coronary artery. At stable haemodynamic conditions and at constant heart rate, right ventricular (RV) pre-ejection segment length increased by 4.6 (2.7-7.2) % (median, 95 % confidence interval) (p less than 0.01), RV end diastolic pressure rose from 5.3 (3.4-7.7) to 6.0 (3.6-8.8) mm Hg (p less than 0.05), and stroke volume rose by 6.8 (4.2-10.8) % (p less than 0.001). When the effect of right atrial contraction on RV filling was excluded by simultaneous pacing of atria and ventricles, the RV pre-ejection segment length no longer increased, and stroke volume rose by only 3.5 (0.1-9.5) % (p less than 0.05) during right side inotropic stimulation. Right atrial inotropic stimulation improves right ventricular filling, and may cause redistribution of blood from the systemic to the pulmonary circulation. This redistribution would raise the pulmonary vascular pressures, and thereby also improve left ventricular filling. The improved right ventricular filling partly accounts for the rise in RV output.

Forward diastolic flow in pulmonary artery induced by right atrial contraction of pig hearts.

To study whether right atrial contraction can forward blood into the pulmonary artery during diastole, blood volume was expanded in anesthetized open-chest pigs until mean right atrial pressure was 13-20 mmHg (range). In the control situation, blood flow in the pulmonary artery was only observed during ventricular systole. Forward diastolic pulmonary artery flow, coinciding with right atrial contraction, was observed when diastolic pulmonary artery pressure was reduced during selectively increased left-side contractility, during bradycardia after propranolol injection (0.5 mg/kg body wt iv), and during the prolonged diastolic interval after spontaneously occurring atrial extrasystoles. The prolongation of the diastolic interval in all three series caused the diastolic pulmonary artery pressure to decline and the filling of the right atrium to increase, thus further stimulating the right atrial Frank-Starling mechanism. The diastolic blood flow in the pulmonary artery constituted 11% of the stroke volume during increased left-side inotropic stimulation, 8% during bradycardia, and 6% in beats preceded by a prolonged diastolic interval. Thus, in the normal heart, blood can be ejected into the pulmonary artery during right atrial contraction.

Temporal relationship of contractility and myocardial potassium balance following beta-adrenergic stimulation of the in situ pig heart.

Lower intracellular Na+ during beta-adrenergic stimulation provides an increased driving force for Na-Ca exchange, which might attenuate the inotropic response. Since (1) Na+ reduction is coupled to K+ uptake, and (2) K+ uptake lags behind the positive inotropic response to isoproterenol, we could examine the effect of Na-Ca exchange by comparing cardiac contractility and K+ balance following intracoronary isoproterenol infusion (0.6-0.8 microgram min-1). In 8 open-chest pigs, potassium concentrations were continuously measured by PVC-valinomycin mini-electrodes in arterial blood (a), and in myocardial venous blood in a shunt from the coronary sinus (cs) to the right atrium. Shunt flow, aortic flow, a left ventricular segment length and left ventricular pressure (LVP) were also continuously recorded. 64 (41-85)% (median and 95% confidence interval) of the LV dP/dt increase occurred within 1 min; thereafter contractility rose slowly. During the first minute of isoproterenol infusion, there was a small net myocardial K+ release, which then reversed to K+ accumulation. A maximum a-cs K+ concentration difference of 0.20 (0.09-0.39) mM occurred at 3.0 (2.0-4.25) min, falling to 0.05 (0.01-0.10) mM after 6.5 (3.75-8.75) min, at which point accumulated myocardial K+ uptake was 135 (27-219) mumol 100 g-1. Heart rate remained unchanged and intramural ECG indicated no sign of ischemia during the first 1.5 min of isoproterenol infusion. At 6.25 (5.0-8.0) min after stop of isoproterenol, LV dP/dt was 12 (9-24)% lower than before infusion (P less than 0.02) whereas myocardial K+ content remained higher than control. Thus, the monovalent cation shift succeeding the positive inotropic response was not associated with reduced contractility, but could explain the undershoot of LV dP/dt after stopping isoproterenol.

Myocardial potassium uptake and catecholamine release during cardiac sympathetic nerve stimulation.

To determine whether sympathetic nerve stimulation induces a significant potassium uptake in the myocardium, the changes in myocardial potassium balance, catecholamine release, lactate uptake, and oxygen consumption were recorded in eight anaesthetised open chest pigs during electrical stimulation of the right intermediate cardiac nerve at 10 Hz. Potassium concentrations were continuously measured by polyvinylchloride valinomycin minielectrodes in arterial and coronary sinus blood. Potassium concentration in coronary sinus blood fell to a nadir 0.42(0.21-0.61) mmol.litre-1 below control values (median and 95% confidence interval) and resulted in a peak potassium uptake of 65(38-102) mumol.min-1 100 g-1 after 2.5(2.0-3.0) min, which correlated (r = 0.94, p less than 0.001) with cardiac noradrenaline release. Accumulated myocardial potassium uptake amounted to 139(82-241) mumol.100 g-1 when a stable potassium concentration difference between arterial and coronary sinus blood was reached after 5.5(4.25-6.50) min. Cardiac contractility (LV dP/dt), myocardial oxygen consumption, and lactate uptake rose from control to peak potassium uptake (p less than 0.001) by 140%, 158%, and 92% respectively. Coronary sinus blood noradrenaline and adrenaline concentrations rose significantly (p less than 0.01) from 58(44-87) pg.ml-1 at control to 2208(1159-5627) pg.ml-1 at peak uptake and from 15(11-19) pg.ml-1 to 85(64-230) pg.ml-1 respectively. Arterial noradrenaline increased from 29(19-41) pg.ml-1 to 374(176-640) pg.ml-1 and arterial adrenaline rose from 15(11-23) pg.ml-1 to 31(24-52) pg.ml-1 (p less than 0.001). It is concluded that sympathetic nerve stimulation induces a substantial myocardial potassium uptake in a dose dependent relation to cardiac noradrenaline release and alters the contractile and metabolic state of the heart substantially with only minor changes in arterial catecholamine concentration.

Myocardial potassium uptake during alpha- and beta-adrenoceptor stimulation.

The changes in myocardial K+ balance during alpha- and beta-adrenoceptor stimulation were compared in 10 anesthetized open-chest pigs by intracoronary isoproterenol and phenylephrine infusions. K+ concentration was continuously recorded by polyvinyl chloride catheter-valinomycin minielectrodes in arterial and coronary sinus blood. The arterial-coronary sinus difference and accumulated myocardial K+ uptake were calculated after computerized data sampling. Isoproterenol (2.5 nmol/min ic) reduced coronary sinus K+ transiently to a nadir of 0.37 (0.23-0.53) mM (median and 95% confidence interval) below control. The accumulated K+ uptake amounted to 139 (63-215) mumol/100 g. After beta-blockade by propranolol, phenylephrine (100 nmol/min ic) induced a transient coronary sinus K+ lowering of 0.16 (0.13-0.21) mM and an accumulated K+ uptake of 30 (20-41) mumol/100 g, both values less than those of isoproterenol (P less than 0.001). Myocardial contractility increased only during isoproterenol infusion, arterial blood pressure rose slightly by phenylephrine, but changes in myocardial O2 extraction and lactate uptake did not indicate cardiac ischemia. We conclude that both alpha- and beta-adrenoceptor stimulation induce a myocardial K+ uptake presumably due to increased Na-K pump activity, the latter more efficiently.

Cardiac adjustments to left-side inotropic stimulation of in situ pig hearts.

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.

Cardiac end-diastolic dilation during acute blood pressure elevation is inotropy dependent.

To examine if the degree of left ventricular (LV) end-diastolic dilation during an acute blood pressure elevation is inotropy dependent, the descending thoracic aorta was occluded before and during a continuous isoproterenol infusion into the left coronary artery in 10 open-chest pigs. The increase in peak LV systolic pressure and in LV tension-time-index induced by aortic occlusion, were equal before and during the isoproterenol infusion. Left and right ventricular (RV) segment lengths were continuously recorded in the free walls of both ventricles, by an ultrasonic technique. A slight fall in LV end-diastolic segment length by the intracoronary isoproterenol infusion was corrected by an i.v. saline infusion. Left ventricular end-diastolic volume was therefore equal at both levels of inotropy when the aorta was occluded, and the heart rate was kept constant by right atrial pacing. At control inotropy, aortic occlusion induced a rise in LV end-diastolic segment length; 6.0 (4.0-8.2)% (median and 95% confidence interval), compared with the smaller (P less than 0.05) increase of 3.8 (2.6-5.5)% during isoproterenol infusion. The end-systolic segment length increased more (P less than 0.01) at control inotropy than during intracoronary isoproterenol infusion: 10.9 (6.9-14.4)% and 4.1 (1.5-7.4)%, respectively. In the RV, both end-diastolic and end-systolic segment length increased slightly during aortic occlusion but only at control inotropy. Thus during an acute blood pressure elevation, the end-diastolic and end-systolic ventricular volumes are better maintained at high than at control inotropy.

Conditions for increased cardiac output during occlusion of the descending thoracic aorta.

Previous studies have demonstrated that occlusion of the descending thoracic aorta (AO) at constant heart rate induces a rise in stroke volume during a continuous intravenous (i.v.) isoproterenol infusion, but no change in stroke volume during a selective inotropic stimulation of the left ventricle as achieved by an intracoronary (i.c.) isoproterenol infusion. To determine the mechanism for this difference in stroke volume response, the haemodynamic adjustments of both the right and the left ventricle to AO during continuous i.v. and i.c. isoproterenol infusion in anesthetized open-chest pigs were compared. The AO induced a similar rise in left ventricular systolic pressure and end-systolic segment length (measured by an ultrasonic technique) in both ventricles whether isoproterenol was infused i.v. or i.c., but stroke volume rose by 26.3 (11.9-38.1%) (median and 95% confidence interval) (P less than 0.01) during i.v., compared with 3.8 (-7.4-14.7)% (n.s.) during i.c. isoproterenol infusion (difference in response: P less than 0.01). End-diastolic segment length increased more by AO during i.v. than i.c. isoproterenol infusion; 7.8 (5.1-16.9)% vs. 5.7 (3.1-8.5)% (difference in response: P less than 0.01) in the left ventricle, and 5.9 (3.5-8.1)% vs. 1.0 (-1.5-3.3)% (difference in response: P less than 0.01) in the right ventricle. Redistribution of blood through the inferior caval vein measured immediately after AO, amounted to 130 (110-172) ml during i.v. and to 77 (52-89) ml during i.c. isoproterenol infusion (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)