Biomedical subjects

J D Schipke

Publications and source records attributed to J D Schipke.

At least 19 recordsLinked to original sources

PubMed2000

Does ischemic preconditioning require reperfusion before index ischemia?

BACKGROUND: Ischemic preconditioning (IP) is initiated through one or several short bouts of ischemia and reperfusion which precede a prolonged ischemia. To test whether a reperfusion must precede the prolonged index ischemia, a series without reperfusion (intraischemic preconditioning: IIP) and a series with gradual onset of ischemia, i.e. ramp ischemia (RI), which is possibly related to the development of hibernation, was compared to conventional IP (CIP). METHOD: Experiments were performed an 27 blood-perfused rabbit hearts (Langendorff apparatus) that were randomized into one of four series: (1) control (n = 7): 60 min normal flow - 60 min low flow (10%) ischemia - 60 min reperfusion. (2) CIP (n = 7): 4 times 5 min zero flow with 10 min reperfusion each - 60 min low flow (10%) - ischemia 60 min reperfusion. (3) IIP (n = 7): 50 min normal flow - 10 min no flow - 60min low flow (10%) ischemia -4 60min reperfusion. (4) RI (n=6): gradual reduction to 10% flow during 60min - 60min low flow (10%) ischemia - 60min reperfusion. At the end of each protocol, the infarcted area was assessed. RESULTS: The infarct area in control hearts was 6.7+/-1.4% (means+/-SEM) of LV total area, in CIP hearts 2.6+/-0.8%, in IIP hearts 3.1+/-0.5%, and in RI hearts 3.0+/-0.3% (all p<0.05 vs. control). The differences between the three protection protocols were statistically not significant, and no protective protocol reduced post-ischemic myocardial dysfunction. CONCLUSION: The preconditioning effect (infarct size reduction) appears not to depend on intermittent reperfusion. Thus, the protective mechanism of IP develops during the initial ischemia that precedes the index ischemia. Alternatively, low-flow ischemia is effectively a sort of reperfusion.

Animals↗

PubMed1998

Effect of implantable cardioverter/defibrillator lead placement in the right ventricle on defibrillation energy requirements. A combined experimental and clinical study.

OBJECTIVES: The effect of implantable cardioverter/defibrillator (ICD) lead placement in the right ventricle (RV) on defibrillation efficacy has not been thoroughly investigated. Therefore, the goal of this combined experimental and clinical study was to evaluate the effect of a septal and a non-septal position of the right ventricular endocardial spring lead on defibrillation energy. METHODS: In 12 isoflurane-anaesthetized swine and subsequently in 8 patients who underwent ICD implantation, two different positions of the distal spring lead in the RV were investigated in randomized order: non-septal position (free wall of the RV) and septal position (interventricular septum). For each position, separate 50% probability determinations of energy (E50), peak voltage (V50) and peak current (A50) were calculated using the three reversal up/down defibrillation procedure. The E50, V50, A50 and impedance (I) were averaged and compared using the two-sided t-test for paired samples. RESULTS: Both the experimental study and the clinical study demonstrated that placing the distal defibrillation lead near to the septum rather than near to the ventricular free wall resulted both in the swine and in the patients in significantly lower E50-31.6%/ - 37.1%, V50-16.1%/-20.9% and A50 -10.0%/ - 24.2%, respectively. Defibrillation impedances were significantly reduced only in the experimental study. CONCLUSIONS: Defibrillation efficacy depends on the position of the distal spring electrode in the RV. A septal position significantly reduces the energy requirements compared to a non-septal position. The decrease in energy requirements might be explained by an increase in current flow through the septum and the posterolateral wall of the left ventricle. reserved

Animals↗

PubMed1998

Pharmacologic heart rate reduction: effect of a novel, specific bradycardic agent on the heart.

Because heart rate (HR) is a major determinant of myocardial oxygen consumption (MVO2) a decrease in HR could prevent ischemia or reduce its consequences. We examined the effects of a novel bradycardic agent of the benzazepinone type, DK-AH 269 (DK), on ventricular function and perfusion in 12 isolated, blood-perfused rabbit hearts. HR was significantly reduced by 1mumol/L DK (160 +/- 28 vs. 124 +/- 23 min-1); diastole lengthened from 235 +/- 69 to 334 +/- 85 ms. Aortic flow tended to fall after DK (50.0 +/- 29.6 vs. 35.6 +/- 21.5 ml/min), but stroke volume remained unchanged (0.29 +/- 0.16 vs. 0.28 +/- 0.17 ml) following DK. Peak left-ventricular pressure (LVPmax) (106 +/- 29 vs. 92 +/- 35 mmHg) and dp/dtmax (1482 +/- 582 vs. 1247 +/- 644 mmHg/s) were decreased. dp/dtmin, as a measure of early relaxation, was also decreased (-1361 +/- 362 vs, -1125 +/- 488 mmHg/s), whereas the end-diastolic pressure (LVPed) was increased (20 +/- 12 vs. 25 +/- 17 mmHg). Coronary blood flow (CBF) per beat was not affected by DK: 0.07 +/- 0.02 vs. 0.07 +/- 0.02 ml. However, the coronary resistance increased with DK from 0.76 +/- 0.29 to 1.13 +/- 0.66 mmHg/(ml/min/100 g). The MVO2 was decreased (6.8 +/- 3.4 vs. 5.9 +/- 2.8 ml/min/100 g). The relation between subendocardial and subepicardial flow (colored microspheres) was unchanged after DK (1.12 +/- 0.22 vs. 1.13 +/- 0.16). Using electrical pacing to restore the control HR, dp/dtmax, LVPed, and MVO2 were nearly restored to predrug levels. In contrast, stroke volume, LVPmax, dp/dtmin and CBF per beat were less than control. In summary: DK effectively reduces heart rate and increases diastole. In parallel with the moderately reduced contractile function, MVO2 is reduced whereas CBF per beat is preserved. These results suggest that this novel bradycardic agent could be useful in treating unwanted tachycardia in the experimental setting, postoperative tachycardia in patients with heart disease or be useful even in treating coronary heart disease.

Animals↗

PubMed1998

Basal metabolism does not account for high O2 consumption in stunned myocardium.

Myocardial O2 consumption (MVo2) in stunned myocardium is relatively high compared with the reduced ventricular function. The mechanism of this "oxygen paradox" could occur at different levels: basal metabolism, excitation-contraction coupling, and energy production. In one previously reported series on 12 isolated, blood-perfused rabbit hearts, left ventricular systolic and diastolic function in stunned myocardium were significantly decreased compared with control, whereas total MVo2 was not. The MVo2 for the unloaded contraction was overproportionately high for the decreased function in stunned myocardium, and contractile efficiency was clearly deteriorated. To assess whether the basal metabolism specifically is elevated in stunned myocardium, a second series (n = 14) with a similar protocol was performed in this study. Basal MVo2 after KCl arrest (0.5 +/- 0.3 ml.min-1.100 g-1) was significantly lower than that measured after KCl arrest (1.2 +/- 0.5 ml.min-1.100 g-1) in an additional series on nonischemic hearts (n = 8). Our conclusion is that basal MVo2 in stunned myocardium is not elevated. Thus this O2-consuming portion of total MVo2 is not responsible for the inefficiency in stunned myocardium. Instead, a "metabolic stunning" occurs at the level of both excitation-contraction coupling and force development by the contractile apparatus.

Animals↗

PubMed1997

Different responses of non-ischemic and post-ischemic myocardium towards Ca2+ sensitization.

We tested whether decreased Ca2+ sensitivity is a major cause for dysfunctional stunned myocardium. The experiments employed a novel Ca2+ sensitizing agent: the thiadiazinone derivative EMD 60 263. Experiments were done on 14 isolated, blood-perfused rabbit hearts. After control, seven hearts were subjected to 20 min no-flow ischemia, and then allowed to recover during 30 min reperfusion. Thereafter, EMD 60 263 was administered (3, 10 and 30 microm). For comparison, the effect of the same doses was investigated in seven non-ischemic hearts. At the low dose, the agent improved ventricular systolic function in the post-ischemic group significantly (LVPmax: 65+/-13 v 91+/-17 mmHg; dP/dtmax: 845+/-235 v 1300+/-350 mmHg/s), and non-significantly in the non-ischemic group (LVPmax: 115+/-35 v 132+/-39 mmHg; dP/dtmax: 1415+/-545 v 1885+/-720 mmHg/s). Early relaxation (dP/dtmin) was slightly improved in both groups (800+/-225 v 1050+/-220 mmHg/s post-ischemic; 1120+/-315 v 1205+/-285 mmHg/s non-ischemic). Heart rate was increased (151+/-35 v 175+/-45 beats/min) in the post-ischemic group and was unaffected in the non-ischemic group. At the higher dose, systolic ventricular function in the post-ischemic group was further improved (LVPmax: 109+/-17 mmHg, dP/dtmax: 1330+/-180 mmHg/s), but tended to decrease in the non-ischemic group (LVPmax: 121+/-40 mmHg, dP/dtmax: 1605+/-680 mmHg/s). This dose decreased heart rate in both groups (133+/-34 and 134+/-23 beats/min). 30 microm EMD 60 263 had deleterious effects in both groups. The different responses towards Ca2+ sensitization suggest that a decrease in Ca2+ sensitivity might play a role in dysfunctional stunned myocardium. Therefore, Ca2+ sensitizing agents of the thiadiazinone type could be useful to recruit a positive inotropic reserve in stunned myocardium.

Action Potentials↗

PubMed1996

Cardiac efficiency during coronary occlusion and during reperfusion after emergency revascularization under cardioprotection.

Myocardial infarction in consequence of a coronary artery occlusion presents a serious problem. It is the aim of any emergency revascularization to minimize the ischemia-induced damage or to salvage reversibly injured myocardium. In experiments on 8 anesthetized pigs, myocardial protection by orthograde perfusion with a high-volume cardioplegic solution was studied under controlled conditions. The left anterior descending artery (LAD) was occluded for 60 min. Then cardiopulmonary bypass was instituted and cardioplegia induced by 8 min perfusion of Bretschneider HTK solution into the aortic root. After 15 min global ischemia, the LAD was "revascularized' and 150 min reperfusion followed. Except for the early relaxation (dP/dtmin) and mean thickening velocity in the ischemic myocardium, all variables remained essentially unchanged during LAD occlusion. During the entire reperfusion, heart rate was significantly increased compared to control: 93 +/- 23 vs. 126 +/- 20/min. Left-ventricular (LV) peak pressure was significantly decreased at the end of the reperfusion, 104 +/- 33 and 77 +/- 22 mmHg, as was dP/dtmax:2155 +/- 655 vs. 1720 +/- 895 mmHg/s. Cardiac output was insignificantly decreased at the end of reperfusion, 2.6 +/- 0.6 vs. 2.4 +/- 0.5 L/min, whereas stroke-work index exhibited a significant deterioration: 1.2 +/- 0.6 vs. 0.5 +/- 0.3 mmHg.ml/kg. LV dP/dtmin was significantly impaired after ischemia and at the end of reperfusion, -1575 +/- 385 vs. -855 +/- 310 mmHg/s, while LV end-diastolic pressure exhibited only a moderate increase: 8 +/- 5 vs. 9 +/- 3 mmHg. MVO2, in turn, remained almost constant throughout the protocol for each of two methods by which it was predicted. The results show that global work, MVO2, and external efficiency were unchanged during early and late occlusion compared to control. During the entire reperfusion the myocardium was stunned, i.e. cardiac work was decreased at maintained MVO2. Thus, external efficiency was decreased. From these results we conclude that in reperfused myocardium after cardioplegic arrest, the oxygen is only inefficiently converted to develop force.

Analysis of Variance↗

PubMed1996

Haemodynamic and energetic properties of stunned myocardium in rabbit hearts.

OBJECTIVE: To amplify the description of myocardial stunning. DESIGN: Control versus 30 min after a 20 min no flow ischaemia. EXPERIMENTAL ANIMALS: 15 isolated rabbit hearts perfused with erythrocyte suspension. MAIN OUTCOME MEASURES: Left ventricular systolic function in terms of aortic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end systolic pressure-volume relation (ESPVR); early relaxation from dP/dtmin and rate of left ventricular pressure decay (tau). Passive properties: ventricular and myocardial stiffness. Coronary resistance from coronary blood flow and perfusion pressure. Total myocardial oxygen consumption (MVo2tot). Total mechanical energy via pressure-volume area (PVA). Contractile efficiency (Econ) and MVo2 of the unloaded contracting heart (MVo2unl). External mechanical efficiency (Eext) from stroke work and MVo2tot. RESULTS: Systolic variables in stunned myocardium were significantly decreased (mean (SD)): aortic flow: 38 (13) v 9 (11) ml/min; LVPmax: 112 (19) v 74 (18) mm Hg; dP/dtmax: 1475 (400) v 1075 (275) mm Hg/s. ESPVR was not significantly decreased, at 138 (73) v 125 (58) mm Hg/ml, but the volume axis intercept was shifted rightward: 0.30 (0.37) v 0.65 (0.25) ml. Likewise, early relaxation was impaired: dP/dtmin (-1275 (250) v -975 (250) mm Hg/s) and tau (37 (7) v 46 (10) ms). LVPed was significantly decreased at 19 (12) v 12 (7) mm Hg, and both the ventricular (end diastolic pressure-volume relation) and the myocardial stiffness (constant k) were increased by 75% and 31%, respectively. Coronary resistance increased non-significantly from 0.83 (0.31) to 1.04 (0.41) mm Hg/(ml/min/100 g). Decreases in PVA (570 (280) v 270 (200) mm Hg.ml/100 g), MVo2tot (40 (9) v 34 (8) microliters/beat/100 g), and MVo2unl (26 (9) v 22 (6) microliters/beat/100 g) did not reach significance, in contrast to significant decreases in Econ (31 (18) v 14 (7)%) and Eext (0.75 (0.29) v 0.18 (0.25) arbitrary units). CONCLUSIONS: Ventricular systolic function is decreased after brief episodes of ischaemia. The decrease in diastolic function probably amplifies the systolic deterioration during myocardial stunning. Passive diastolic properties are also changed, shown by increases in both ventricular and myocardial stiffness. The increase in coronary resistance indicates stunning at the vascular level which could limit oxygen supply. With maintained MVo2tot during stunning, external efficiency is decreased. Possible candidates for this metabolic stunning are inadequate excitation-contraction coupling and disturbed O2 utilisation by the contractile apparatus.

Animals↗

PubMed1996

Analysis of respiratory water--a new method for evaluation of myocardial energy metabolism.

Aerobic ATP synthesis via oxidative phosphorylation causes a proportional production of respiratory water. Thus the amount of respiratory water produced at a given time should be a reliable measure of the current ATP demand of the mammalian myocardium. Respiratory water from isolated rabbit hearts was labeled by using the stable oxygen isotope 18O. The hearts were perfused according to the method of Langendorff (O. Langendorff. Pfluegers Arch. 61: 291-332, 1895) with 18O2-equilibrated Krebs-Henseleit solution. Control hearts were exclusively perfused with carbogen-equilibrated Krebs-Henseleit solution. Myocardial tissue was then lyophilized; the extracted water and samples from the coronary venous effluent were converted to CO2 by using the guanidine hydrochloride technique. The delta 18O values within the CO2 samples were determined by mass spectrometry and related to the standard mean ocean water (SMOW) scale. Compared with control hearts, the 18O-labeled hearts exhibited a significant increase of delta 18O values from tissue water (-47.50 +/- 0.64 vs. -40.35 +/- 2.05% SMOW; P < 0.05). The values were also significantly increased in the coronary venous effluent after a perfusion time of only 50 s (-47.50 +/- 0.64 vs. -43.66 +/- 0.91% SMOW; P < 0.05). Thus this first adaptation of the guanidine hydrochloride technique on microliter samples of myocardial tissue water and coronary venous effluent demonstrates that this method can be used to evaluate both respiratory activity and the kinetics of cardiac metabolic processes.

Adenosine Triphosphate↗

PubMed1996

Delayed recompression after SCUBA diving-induced barotrauma: a case report.

During a SCUBA course, a woman (26 yr) ascended from shallow water (< or = 8 m) in panic on 2 successive days. She suffered moderate symptoms of gas embolism (pain in the upper chest and in both knees), very likely owing to a pulmonary barotrauma. The woman remained untreated for 3 d until her return flight during which symptoms worsened. After another 24 d, she entered the hyperbaric center in Duisburg, Germany, where she was successfully treated by recompression with hyperbaric oxygenation (to 0.6 MPa on day 1, and to 0.28 MPa on days 2 and 3).

Adult↗

PubMed1996

[Effect of a new bradycardic substance on the isolated rabbit heart].

Beside wall tension and contractility, heart rate is a major determinant of myocardial oxygen consumption. Therefore, a decrease in heart rate could prevent ischemia or reduce its consequences. We examined the effect of a new bradycardic agent of the benzazepinone-type (DK-AH 269) on eight isolated, saline-perfused rabbit hearts, bradycardia resulted from a specific blockade of i(f)-channels in sinus node cells. After control measurements (C), the substance was added in three increasing concentrations (D1: 10(-8) M, D2: 10(-7) M, D3: 10(-6) M). We observed a dose-dependent reduction in heart rate (C: 206 +/- 25, D1: 195 +/- 30, D2: 77 +/- 41, D3: 154 +/- 48/min). In the highest dosage, the duration of diastole was increased by 100%. To characterize systolic function, we measured stroke volume (SV), peak left ventricular pressure (LVPmax) and its first derivative (dP/dtmax). Aortic flow was slightly decreased whereas SV increased to 108% of control after initial reduction at the two lower dosages. LVPmax remained unchanged, and dP/dtmax was dose-dependently reduced to 91, 81, and 70% of control (C: 1885 +/- 376, D1: 1721 +/- 525, D2: 1526 +/- 504, D3: 1327 +/- 337 mm Hg/s); dP/dtmin as a measure of early relaxation was also reduced. The coronary flow per beat did not change compared with control in the presence of the two lower doses of DK-AH 269, but was significantly increased with the highest dose (C: 0.29 +/- 0.06, D1: 0.28 +/- 0.07, D2: 0.29 +/- 0.09, D3: 0.34 +/- 0.11 ml). The myocardial oxygen demand was dose-dependently decreased (C: 10.4 +/- 2.5, D1: 9.6 +/- 2.5, D2: 8.8 +/- 2.6, D3: 7.9 +/- 2.4 ml/min/100 g). The relation between subendocardial and subepicardial flow, assessed with colored microspheres, exhibited no changes in the presence of the highest dose of DK-AH 269 (C: 1.28 +/- 0.09, D3: 1.27 +/- 0.08). DK-AH 269 reduced heart rate in isolated rabbit hearts and increased the duration of diastole. Whereas systolic function was primarily left unchanged, coronary flow per beat and oxygen consumption were decreased. According to our results, this new bradycardic agent could be useful in treating coronary heart disease.

Animals↗

PubMed1995

Utilization of oxygen by the contractile apparatus is disturbed during reperfusion of post-ischaemic myocardium.

UNLABELLED: Post-ischaemic ventricular function remains depressed (= myocardial stunning) despite nearly normal coronary blood flow during reperfusion. In order to illuminate the causes of this phenomenon, we studied the relationship between ventricular function and myocardial oxygen consumption (MVO2tot) in experiments on 15 isolated rabbit hearts perfused with erythrocyte suspension (hct = 30%). Left ventricular systolic function was assessed by measuring aortic flow (ml.min-1), peak systolic pressure (LVPmax), dP/dtmax, and early relaxation in terms of dP/dtmin during control and 30 min after the onset of reperfusion, following 20 min global no-flow ischaemia. The pressure-volume area was calculated as a measure of total mechanical energy. The external mechanical efficiency (Eext) was assessed from stroke work and MVO2tot. Both contractile efficiency (Econ = inverse slope of the MVO2-PVA relationship) and MVO2 of the unloaded contracting heart (MVO2unl = basal MVO2 + MVO2 for excitation-contraction coupling) were calculated using pressure-volume area and MVO2tot. RESULTS: At matched heart rate (149 +/- 30 vs 147 +/- 31 min-1; mean +/- SD) and end-diastolic volume (1.3 +/- 0.2 ml), the systolic variables were significantly decreased in the stunned myocardium: aortic flow: 38 +/- 13 vs 9 +/- 11 ml.min-1, LVPmax: 112 +/- 19 vs 74 +/- 18 mmHg, and dP/dtmax: 1475 +/- 400 vs 1075 +/- 275 mmHg.s-1. Likewise, dP/dtmin was significantly impaired (-1275 +/- 250 vs -975 +/- 250). The decrease in pressure-volume area (570 +/- 280 vs 270 +/- 200 mmHg.ml.100 g-1) was not statistically significant. In contrast, both Eext (0.75 +/- 0.29 vs 0.18 +/- 0.26 arbitrary units) and Econ (31 +/- 18 vs 14 +/- 7%) were significantly decreased, whereas MVO2tot (40 +/- 9 vs 34 +/- 8 microliters.beat-1.100 g-1) and MVO2unl (26 +/- 9 vs 22 +/- 6 microliters.beat-1.100 g-1) were not. SUMMARY: Ventricular function after brief episodes of ischaemia is decreased whereas MVO2tot is maintained, i.e. external efficiency is decreased. MVO2 for the unloaded contraction remained unchanged, indicating that MVO2 for excitation-contraction coupling is inappropriately high for the depressed contractile state. The decreased contractile efficiency indicates further that O2 utilization of the contractile apparatus is disturbed during reperfusion.

Animals↗

PubMed1995

[The value of CKMB and myoglobin determinations during reperfusion after regional myocardial ischemia in the anesthesized pig].

The efficacy of a revascularization treatment after acute coronary artery occlusion can be evaluated by different diagnoses. The ECG and the time-course of, for example, the CK isoenzyme MB are widely used as quick, objective, and almost noninvasive tools. In addition, the assessment of functional recovery of the postischemic myocardium or the evaluation of the magnitude of irreversibly injured myocardium is essential for therapeutic strategies. In the present study, myoglobin that is not yet routinely established, is compared with CKMB to answer the following questions: do measurements of serum-CKMB and serum-myoglobin reliably demonstrate 1) the success of a revascularization treatment? 2) the functional recovery of the postischemic myocardium? 3) the magnitude of irreversibly injured myocardium? To answer these questions, the left anterior descending coronary arteries of 17 anesthetized pigs were occluded for 60 min and reperfused for 180 min after successful "revascularization". The major findings of this study on anesthetized pigs are: 1) The time-course of both the CKMB activity and the myoglobin concentration exhibit the successful revascularization. 2) The CKMB maximum does not exhibit the recovery of the ventricular function, whereas the myoglobin maximum moderately correlated with the contractile state (dP/dtmax) at the end of reperfusion and significantly with the recovery of dP/dtmax during reperfusion. Recovery of the regional function (= mean thickening velocity) within the 180 min reperfusion is predicted neither by CKMB nor myoglobin analysis. 3) Both investigated markers correlate closely with the magnitude of the irreversibly injured myocardium.

Animals↗

PubMed1995

Comparison between the effects of a novel Ca++ sensitizer and a phosphodiesterase inhibitor on stunned myocardium.

Inotropic agents are used widely for pharmacological bridging of the failing heart either until recovery after surgical intervention or until transplantation. EMD 57033 is a novel specific Ca++ sensitizing agent with purportedly minor phosphodiesterase (PDE) III-inhibiting properties. It acts as an inotropic agent without raising intracellular Ca++ levels. In turn, the PDE III-inhibitor enoximone has been used for several years to treat low cardiac output syndrome. However, little is known about its effects on postischemic reperfused (stunned) myocardium. We investigated the effects of EMD 57033 (EMD; 30 microM) and enoximone (E20 micrograms/ml) on stunned myocardium. The experiments were performed on 16 isolated rabbit hearts perfused with an erythrocyte suspension (hematocrit = 30%; [Ca++] = 2.5 mM). Hearts were reperfused after a 20 min no-flow ischemia. Measurements were performed at control, 30 min after the onset of reperfusion, and after administration of one of the drugs. Both agents significantly improved the depressed systolic function [left ventricular pressure (LVP)max from 61 +/- 12 to 93 +/- 18 mmHg, and its derived pressure (dP/dt)max from 860 +/- 220 to 1340 +/- 300 mmHg/s and LVPmax from 78 +/- 9 to 83 +/- 15 mmHg, and its derivative dP/dtmax from 1040 +/- 230 to 1385 +/- 300 mmHg/s, respectively] and early relaxation (dP/dtmin from 810 +/- 250 to 1260 +/- 345 mmHg/s and from 1000 +/- 200 to 1135 +/- 295 mmHg/s, respectively) that occurred during postischemic reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

[Minimal interval length for safe determination of brief heart rate variability].

UNLABELLED: After heart rate variability (HRV) had been established in the clinic, the question about the minimum interval length for analyzing electrocardiograms emerged. Respiration rate, heart rate and heart rate variability were analyzed in 25 sport divers during 6 min intervals at control, immersion, submersion and while SCUBA diving. Thereafter, the interval length was systematically shortened to 1 min. RESULTS: Respiration rate was significantly reduced during submersion and diving. Heart rate, in turn, remained essentially unchanged during the four experimental steps. The HRV measures in the time domain (standard deviation, coefficient of variation, RMSSD and pNN50) exhibited significant changes during immersion, submersion and diving compared to control conditions. The spectral density in the low frequency range was increased compared to control, the increase being significant during diving. Immersion, submersion and diving, thus, present strong stimuli for the autonomic nervous system. The length of the HRV measures of the time domain could be shortened to 3 min without significant loss of information, except for pNN50. Reduction of the respiration rate during diving considerably shifted the respiratory arrhythmia from the high to the low frequency range. Such shifts deserve special attention interpreting HRV measures from the frequency domain. The interval length for the measures in the frequency domain could only be shortened to 5 min. CONCLUSION: Measures from the time domain, in particular standard deviation and co-efficient of variation, seem to be superior to measures from the frequency domain in analyzing short-term HRV.

Adult↗

PubMed1993

Regional blood flow and contractile function: are they matched in normal, ischemic and reperfused myocardium?

One central hypothesis of cardiovascular physiology has been a balance between myocardial blood flow and contractile function during natural conditions, i.e. supply and demand are matched. This hypothesis was derived from studies relating total coronary blood flow to global ventricular function. The present article examines the relationship between myocardial blood flow and function on a regional level. In normal myocardium, considerable heterogeneity of blood flow exists, indicating similar heterogeneity of metabolic demand and potentially also function. However, when the degree of metabolic coupling between flow and function is questioned, there is no evidence whether or not flow and function are matched on a regional level. One closely related hypothesis of cardiovascular pathology has been an imbalance or mismatch between supply and demand during ischemia. Because myocardial function rapidly declines during early ischemia, residual, regional myocardial blood flow and function may be once again matched on a lower level. Such low-level supply-demand balance may persist over prolonged periods of ischemia and permit the myocardium to remain viable, i.e. the myocardium can "hibernate." Analyzing myocardial blood flow and function on a regional level has generated new insight into strategies of adaptation to the adverse situation of reduced blood flow. Whereas in hibernating (ischemic) myocardium, regional myocardial blood flow and function are matched, flow and function appear to be unmatched in reperfused, dysfunctional, i.e. 'stunned' myocardium. "Stunned myocardium" appears once more as a result of a strategy of adaptation, as the preceding ischemia did not induce irreversible myocardial damage but preserved the ischemic myocardium viable, although functionally impaired.

Adaptation, Physiological↗

PubMed1993

Diastolic dysfunction of stunned myocardium.

The prolonged regional contractile failure of reperfused myocardium has usually been characterized in terms of systolic function, while only few reports on its diastolic function are available. None of these studies considered changes in the isovolumic diastole and the subsequent filling phase separately. Therefore, in the present study, the velocities of wall excursion during systole (Vsys), isovolumic diastole (Viso) and filling phase (Vfill) were determined in 12 anesthetized dogs. Additionally, post-ejection thickening (Pejt), a marker of left ventricular asynchrony, was determined. Measurements were performed under control conditions, during a 15 minute left circumflex (LCX) coronary artery occlusion (CAO) and at 10 minutes, 4 and 8 hours reperfusion. Heart rate, left ventricular pressure, and Vsys, Viso, Vfill, and Pejt of the anterior myocardium remained unchanged throughout the experiments. During CAO, systolic wall-thickening of the posterior wall was reversed to systolic wall-thinning. Upon reperfusion, Vsys started to recover (2.5 +/- 3.2 mm/s at 10 minutes) and gradually improved over 8 hours of reperfusion (4.6 +/- 3.2 mm/s at 4 hours, 6.4 +/- 1.5 mm/s at 8 hours). Viso became positive during CAO (9.4 +/- 7.1 mm/s vs. -5.6 +/- 3.9 mm/s under control conditions) and was unchanged at 10 minutes reperfusion (7.9 +/- 5.2 mm/s). After 4 hours and 8 hours of reperfusion, Viso recovered to 1.2 +/- 9.2 mm/s and -0.3 +/- 10.7 mm/s, respectively. Vfill also became positive during CAO (1.5 +/- 6.2 mm/s vs. -18 +/- 8.7 mm/s under control conditions). There was a quick recovery of Vfill (-9.4 +/- 7.5 mm/s) with the onset of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effect of a bradycardic agent on the isolated blood-perfused canine heart.

Bradycardic agents could limit the consequences of myocardial ischemia via two mechanisms: by decreasing myocardial oxygen demand (MVO2) and by increasing diastolic coronary blood flow (CBF). We investigated whether the benzazepinone UL-FS 49 affects only sinus node cells or also smooth muscle and/or myocardial cells. To avoid confounding interactions with the periphery, we performed experiments on 11 isolated, blood-perfused canine hearts. Injection of UL-FS 49 (1 mg/kg i.c.) significantly reduced heart rate (HR) from 104 +/- 7 to 93 +/- 7 min-1 (mean +/- SEM) and increased stroke volume (n = 6: 9.8 +/- 1.1 vs. 13.2 +/- 1.6 ml), so that cardiac output remained unchanged (n = 6: 1.1 +/- 0.1 vs. 1.2 +/- 0.1 l/min). The contractile state, assessed by isovolumic peak systolic pressure, was unaltered by UL-FS 49 (n = 5: 72 +/- 6 vs. 72 +/- 6 mmHg). At a constant coronary arterial pressure (CAP) of 80 mmHg, mean CBF was slightly decreased (102 +/- 11 vs. 97 +/- 10 ml/[min.100 g]) by UL-FS 49, such that mean coronary resistance remained unchanged (0.9 +/- 0.1 vs 1.0 +/- 0.1 mmHg.min.100 g/ml). The slight decreases in arteriovenous oxygen content difference (n = 6: 6.6 +/- 0.7 vs. 6.5 +/- 0.7 ml/100 ml) and in CBF lead to a calculated, significant decrease in MVO2 (n = 6: 6.9 +/- 0.5 vs. 6.0 +/- 0.4 ml.100 g/min). In conclusion, UL-FS 49 at the dose used decreases MVO2 by reducing HR in isolated canine hearts. In the absence of negative inotropic and vasodilating effects, cardiac output is maintained via increased stroke volume, and CAP will likely be preserved in situ. Thus, this specific bradycardic agent could be useful in treating ischemic myocardial disease.

Animals↗

PubMed1991

[Down-regulation and hibernating myocardium].

Some homeothermic animals can survive adverse conditions by hibernation, i.e., by reducing their body temperature in accordance with ambient temperature, thus reducing metabolism and vital functions. Six years ago, the term hibernation was introduced to describe a particular state of the myocardium. Although the meaning is different from that used in zoology and, thus, is misleading, it is used increasingly to describe a condition induced by moderate reduction in coronary flow. Some evidence in the literature suggests that the myocardium can actively reduce its mechanical function as a consequence of reduced coronary flow in order to prevent ischemia-induced injury. It is conceivable that the hibernating myocardium is the result of such a down-regulation of function. The hibernating myocardium can be characterized by decreased function in the hypoperfused area, which still exhibits active metabolism and remains viable. This is in contrast to "stunned" myocardium, which represents dysfunction during postischemic reperfusion, i.e., with coronary blood flow being close to normal. In analogy to hibernation in its original meaning, down-regulation and hibernating myocardium are considered to represent a protective mechanism, because such myocardium can quickly regain its initial function after restoration of physiologic blood flow. Because hibernating myocardium is salvageable, it has to be distinguished from other dysfunctional tissue that has lost its function due to ischemic damage, so that appropriate clinical interventions can succeed in restoring normal coronary blood flow.

Adaptation, Physiological↗