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This study had the purpose of documenting the hemodynamic correlates of effective arterial elastance (Ea; i.e., an accurate estimate of hydraulic load) in mitral stenosis (MS) patients. The main hypothesis tested was that Ea relates to the total vascular resistance (R)-to-pulse interval duration (T) ratio (R/T) in MS patients both before and after successful balloon mitral valvotomy (BMV). High-fidelity aortic pressure recordings were obtained in 10 patients (40 +/- 12 yr) before and 15 min after BMV. Ea value was calculated as the ratio of the steady-state end-systolic aortic pressure (ESAP) to stroke volume (thermodilution). Ea increased after BMV (from 1.55 +/- 0.63 to 1.83 +/- 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linear relationship between Ea and R/T: Ea = 1.09R/T - 0.01 mmHg/ml, r = 0.99, P = 0.0001. This ultimately depended on the powerful link between ESAP and mean aortic pressure [MAP; r = 0.99, 95% confidence interval for the difference (MAP - ESAP) from -18.5 to +4.5 mmHg]. Ea was also related to total arterial compliance (area method) and to wave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, and this was likely to be explained by decreased arterial compliance. The present study indicated that Ea depended mainly on the steady component of hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.
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PMID:Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy. 933 14

We studied the response in left ventricular (LV) internal dimensions and posterior wall thickness during the performance of sudden strenuous exercise without warm-up (SSE) and sudden strenuous exercise with warm-up (SSEw) in 15 healthy, untrained college-aged males (26 +/- 5.0 yr). Measurements of left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), stroke dimension (SD = LVEDD-LVESD), fractional shortening (FS = SD/EDD) and posterior wall thickness (PWT) were obtained from continuous 2-D targeted on M-mode echocardiography. Continuous EKG and blood pressure were obtained at rest and during the final 10 s of SSE (30 s of upright leg cycle ergometry of 400 W at 80 rpm). SSEw was preceded by warm-up exercise (6 min of graded leg cycle exercise of 2-min stages initial load 30 W, increasing in 30-W increments at 60 rpm, followed immediately by SSE). Our findings revealed that there were no significant differences in the LV internal dimensions (LVEDD, LVESD, FS, PWT), HR max, RPP max, ECG, and MAP max between SSE and SSEw. Sudden strenuous exercise without warm-up is not associated with a reduced LV function. The results of this study are contradictory to previous findings that have suggested that SSE is associated with transient global left ventricular (LV) dysfunction.
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PMID:Cardiovascular response to sudden strenuous exercise: an exercise echocardiographic study. 934 59

Cytosolic Ca2+ overload has been proposed as a main cause of neuronal injury during cerebral ischemia. SNX-111, a synthetic product of the naturally occurring omega-conotoxin MVIIA, is a novel, presynaptic N-type Ca2+ channel antagonist and has been reported to be neuroprotective against cerebral ischemia. We studied the neuroprotective effects of SNX-111 in a rabbit model of focal cerebral ischemia. New Zealand white male rabbits (2.5-3.5 kg) were given 1 mg/kg/h i.v. SNX-111 (n=8) or normal saline (n=8) 10 min after onset of a 2-h period of transient focal cerebral ischemia induced by occlusion of the left middle cerebral, anterior cerebral and internal carotid arteries followed by 4 h reperfusion. SNX-111 significantly attenuated overall cortical ischemic neuronal damage by 44% (saline, 38.7+/-3.0%; SNX-111, 21.5+/-6.0%, P<0.05) and regions of hyperintensity on T2-weighted MRI by 30% (saline, 70.6+/-4.0%; SNX-111, 49.3+/-11.0%, P<0.05). No significant difference in (regional cerebral blood flow) rCBF or MAP (mean arterial blood pressure) was found between SNX-111- and saline-treated rabbits suggesting that neuroprotection is due to a cellular effect. We conclude that SNX-111 reduces ischemic injury in this model. Its use as a clinical neuroprotective agent for cerebrovascular surgery or stroke should be investigated further.
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PMID:SNX-111, a novel, presynaptic N-type calcium channel antagonist, is neuroprotective against focal cerebral ischemia in rabbits. 945 74

Total intravenous anaesthesia (TIVA) using propofol, gamma-hydroxybutyrate (GHB) or midazolam in combination with sufentanil was investigated in 45 patients undergoing coronary artery bypass grafting (CABG). Anaesthesia was induced with sufentanil, etomidate and pancuronium. After endotracheal intubation, anaesthesia was continued with sufentanil (2 micrograms kg-1 h-1) for all patients. Patients were randomized to receive supplementary propofol (2 mg kg-1 h-1, n = 15), gamma-hydroxybutyrate (20 mg kg-1 h-1, n = 15) or midazolam (0.06 mg kg-1 h-1, n = 15). Haemodynamic measurements were performed after induction and at various times in the pre-bypass period. In the propofol group, a significant decrease in heart rate (HR 12% +/- 3%), cardiac index (CI 23% +/- 4%), mean arterial pressure (MAP 16% +/- 3%) and left ventricular stroke work index (LVSWI 17% +/- 4%) occurred until sternotomy was performed. With the exception of cardiac index, both midazolam and gamma-hydroxybutyrate produced similar haemodynamic effects: cardiac index was temporarily decreased (19% +/- 4%) by midazolam and remained unchanged after gamma-hydroxybutyrate. In both groups, sternotomy was followed by temporary hypertension, associated with a significant rise in systemic vascular resistance. No electrocardiographical signs of ischaemia were observed in any patient. In the case of propofol and midazolam, gamma-hydroxybutyrate showed adequate haemodynamic stability especially after induction of anaesthesia and may also be a suitable agent for total intravenous anaesthesia in patients with coronary artery disease. However, during sternotomy, supplementary administration of opioids was required.
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PMID:Total intravenous anaesthesia using propofol, gamma-hydroxybutyrate or midazolam in combination with sufentanil for patients undergoing coronary artery bypass surgery. 946 94

The effects of hypoxemia and hypercapnia in acute cardiovascular response to periodic non-obstructive apneas were explored in seven preinstrumented, sedated paralyzed and ventilated pigs under three conditions: room air breathing (RA), O2 supplementation (O2), and supplementation with O2 and CO2 (CO2). EEG monitoring showed no arousal under any conditions. RA apneas increased mean arterial pressure (MAP, from baseline 95.9 +/- 4.5 to late apnea 124.4 +/- 7.8 Torr, P < 0.01), left ventricular end-diastolic pressure, end-diastolic and end-systolic myocardial fiber lengths and systemic vascular resistance, but decreased cardiac output (CO, 3.09 +/- 0.34-2.37 +/- 0.26 L/min, P < 0.01), heart rate (HR, 115.1 +/- 7.5-102.0 +/- 7.8 bpm, P < 0.01), and stroke volume (SV, 29.6 +/- 0.7 21.1 +/- 1.8 ml, P < 0.01). 02 apneas produced similar decreases in HR (114.0 +/- 11.8-105.4 +/- 8.7 bpm, P < 0.05) as with RA apneas, but smaller increases in MAP (94.5 +/- 1.8-103.4 +/- 2.8 Torr, P < 0.01) and in the variables of pre- and after-load. CO and SV remained unchanged with O2 apneas. CO2 was associated with higher MAP, CO, and HR at baseline relative to RA, but similar cardiovascular response during apneas in direction and magnitude to those of O2 apneas. We conclude that in this model hypoxemia is a major but not the sole determinant of the pressor response during apneas. Hypercapnia cannot explain the pressor response seen when hypoxemia is abolished. The HR fall during apneas is independent of hypoxemia, hypercapnia and the pressor response.
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PMID:Role of hypoxemia and hypercapnia in acute cardiovascular response to periodic apneas in sedated pigs. 962 31

We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.
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PMID:Does labetalol predispose to pulmonary edema in severe pregnancy-induced hypertensive disease? 964 12

To prevent hypercalcemia in the treatment of secondary hyperparathyroidism, low calcium (L-Ca) dialysate is advocated. However, changes in ionized calcium (i-Ca) levels have a pivotal role in myocardial contraction and could influence blood pressure stability during dialysis. Recently, our group found in patients with normal cardiac function a significant decrease in blood pressure (decrease in systolic blood pressure [DSBP]: -13 mm Hg and decrease in mean arterial pressure [DMAP]: -7 mm Hg) during dialysis with L-Ca dialysate compared with high calcium (H-Ca) dialysate, and this was mainly related to a decreased left ventricular contractility with use of L-Ca dialysate. On the basis of these data, it could be expected that changes in i-Ca levels during dialysis are of more clinical importance in cardiac-compromised patients (CCpts), New York Heart Association classifications III and IV. In this study, the effects of L-Ca dialysate (1.25 mmol/L) and H-Ca dialysate (1.75 mmol/L) on arterial blood pressure parameters (systolic [SBP], diastolic [DBP], and mean arterial blood pressure [MAP]), heart rate, stroke distance (SDist), and minute distance (MDist) during 3 hours of a standardized ultrafiltration/hemodialysis (UF+HD) in nine CCpts was investigated. i-Ca levels increased significantly with H-Ca dialysate UF+HD, whereas there was no change with L-Ca dialysate. SBP, DBP, and MAP decreased statistically and clinically significantly during UF+HD with L-Ca dialysate and were significantly lower with the use of L-Ca dialysate compared with H-Ca dialysate. SDist and MDist decreased significantly with L-Ca dialysate, whereas there were no changes in SDist and MDist with H-Ca dialysate. The predialysis and postdialysis index of systemic vascular resistance (SVRI) was similar between L-Ca dialysate and H-Ca dialysate use. Between the two groups, there were no significant differences in changes in SVRI. From this study, we can conclude that changes in i-Ca levels are a very important determinant of the blood pressure response during UF+HD in CCpts, and this response is mediated by changes in myocardial contractility.
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PMID:Effect of dialysate calcium concentrations on intradialytic blood pressure course in cardiac-compromised patients. 966 33

The ratio of effective arterial elastance (Ea) to left ventricular elastance (Ees) is an indicator of the coupling between ventricular properties and arterial load properties. Another criterion for the coupling between an energy source and its load is the principle of economical fuel consumption, or mechanical efficiency, which is defined as the ratio of stroke work (SW) to myocardial oxygen consumption per beat (MVO2). It has been revealed that SW of ventricular contraction is maximized when Ea/Ees = 1, while mechanical efficiency is maximized when Ea/Ees = 0.5. The purpose of the present study was to investigate the ventriculo-arterial coupling during hypertension, and the effects of nicardipine on this relationship in surgical patients using Ea/Ees and SW/MVO2 as indicators. Anaesthesia was maintained with isoflurane, nitrous oxide, and fentanyl. Radial artery pressure was displayed on a polygraph, and left ventricular end-systolic and end-diastolic volumes were determined by use of transoesophageal echocardiography. Ees was calculated as MAP/(ESVI-4), where MAP is mean arterial pressure and ESVI is end-systolic volume index. Ea was calculated as the ratio of MAP to stroke volume index (SVI). Stroke work index (SWI) was calculated as the product of MAP and SVI. MVO2 was assessed by estimating the ventricular pressure-volume area index (PVAI), which is expressed as the sum of SWI and the end-systolic potential energy index. Before (baseline), and 3, 10, 20, and 30 min after i.v. nicardipine (30 micrograms kg-1), Ea/Ees and SWI/PVAI were determined in 14 surgical patients with intraoperative hypertension. Before nicardipine (during hypertension), Ea was almost equal to Ees, whereas Ea/Ees was significantly reduced to about 0.5-0.6 at 3, 10, and 20 min after nicardipine. SWI/PVAI was maximized and significantly greater than the baseline value at 3 min after nicardipine. These results suggest that, during hypertension, ventricular and arterial properties were so matched as to maximize SW at the expense of the work efficiency, whereas mechanical efficiency of ventricular contraction was maximized after nicardipine.
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PMID:Effects of nicardipine on ventriculo-arterial coupling in humans. 981 19

Cardiovascular instability continues to be one of the primary clinical problems in hemodialysis. Acetate buffer in dialysate is one of the factors that may induce hypotension. Since uremia may have a direct effect on the regulation of the cardiovascular system, the present study was designed to investigate the separate effects of uremia and acetate hemodialysis on blood pressure in anesthesized dogs, as well as the hemodynamic parameters determined by invasive cardiovascular monitoring. Animals were separated into four groups: (1) group I, hemodialysis with acetate in controls; (2) group II, hemodialysis with acetate in uremic dogs; (3) group III, hemodialysis with bicarbonate in controls; and (4) group IV, hemodialysis with bicarbonate in uremic dogs. Acute uremia was induced by bilateral ureteral ligation and a 90-minute hemodialysis (acetate or bicarbonate) procedure was performed 72 hours later. The results obtained in this study show that, compared with dogs with normal renal function, acute uremia resulted in an elevation in mean arterial pressure (MAP; 178 +/- 13 vs. 115 +/- 23 mm Hg, P < 0.01), which was associated with an increase in cardiac index (CI) and left ventricular stroke work index (LVSWI). In these dogs, the pulmonary capillary wedge pressure (PCWP; preload) and the systemic vascular resistance index (SVRI; afterload) were not different than controls. In uremic dogs, hemodialysis with acetate, but not with bicarbonate, decreased the MAP to values similar to controls. The decrease in MAP induced by acetate hemodialysis in uremic dogs was associated with a decrease in SVRI and PCWP. These results suggest that in dogs with acute uremia, acetate hemodialysis (HD) decreases myocardial contractility that was previously increased by a direct effect of uremia. In controls, acetate produced a moderate decrease in MAP that was the result of a mild decrease in CI and SVR. Since PCWP was not significantly decreased after acetate HD, the decrease in CI can be attributed to a mild decrease in myocardial performance. In conclusion, this study in dogs suggests that uremia enhances myocardial contractility directly. Acetate hemodialysis reduces this elevated myocardial contractility to normal values.
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PMID:Cardiovascular response to hemodialysis: the effects of uremia and dialysate buffer. 983 90

1. Metabolic and functional effects of ischaemic preconditioning (IP), pretreatment with carbachol (Ch) and combined interventions were studied in rat isolated working hearts subjected to 20 min global ischaemia (37 degrees C) and 40 min reperfusion. Prior to the ischaemic period, hearts were either perfused according to Langendorff (control group), ischaemically preconditioned by 5 min global ischaemia and 5 min reperfusion (IP group), perfused with 0.1 mumol/L Ch for 5 min and then with Ch-free Krebs'-Henseleit buffer for 5 min (Ch group) or perfused with 0.1 mumol/L Ch for 5 min and then subjected to IP (Ch + IP group). 2. Although Ch exerted slight negative chronotropic and inotropic effects during pre-ischaemic Langendorff perfusion, it did not affect myocardial contents of ATP and phosphocreatine (PCr) prior to sustained ischaemia. At the end of final reperfusion, the IP and Ch groups showed similar recovery of aortic output (67.5 +/- 5.0 and 56.8 +/- 5.4%, respectively), cardiac output (65.4 +/- 5.4 and 63.5 +/- 5.7%, respectively) and stroke volume (73.4 +/- 7.5 and 67.0 +/- 6.7%, respectively) expressed as a percentage of steady state values. These indices were higher than those in the control group (42.8 +/- 4.7, 53.8 +/- 4.3 and 56.1 +/- 5.6%, respectively; P < 0.05). The Ch + IP group exhibited complete recovery of all indices of pump function, including cardiac work, expressed as the cardiac output-mean aortic pressure (CO-MAP) product. 3. There were no differences in ATP recovery between the groups after reperfusion: the ATP content was, on average, 73.1 +/- 3.5% of the initial ATP content. However, all treated groups had enhanced PCr recovery and better preservation of total creatine (sigma Cr = PCr + Cr), an index of cell membrane integrity, than control. Metabolic efficacy of the pre-ischaemic interventions can be ranked as follows: IP < or = Ch < Ch + IP. In all groups, myocardial content of sigma Cr was positively correlated with percentage recovery of the CO-MAP product at the end of reperfusion (r = 0.79, P < 0.05). 4. The results demonstrate that Ch treatment combined with IP provides significantly greater postischaemic myocardial salvage. The similarity of the metabolic and functional effects of Ch treatment and IP strongly suggests muscarinic M2 acetylcholine receptor involvement in acute adaptation of rat heart to ischaemia/reperfusion stress.
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PMID:Metabolic and functional effects of carbachol and ischaemic preconditioning in rat isolated heart. 1002 66


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