Biomedical subjects

C X Jia

Publications and source records attributed to C X Jia.

At least 19 recordsLinked to original sources

PubMed2005

New genotype of avian influenza H5N1 viruses isolated from tree sparrows in China.

The 2004 outbreaks of highly pathogenic avian influenza H5N1 disease in China led to a great poultry loss and society attention. A survey of avian influenza viruses was conducted on tree sparrows (Passer montanus) collected in China in 2004. Four viruses were isolated from free-living tree sparrows. The results of the whole-genome analysis indicated that an H5N1 virus with a new genotype is circulating among tree sparrows. The hemagglutinin and neuraminidase genes of the new genotype were derived from Gs/Gd/96-like viruses and the nuclear protein gene descended from the 2001 genotype A H5N1 viruses, while the other inner genes originated from an unknown influenza virus. In experimental infection, all four viruses were highly pathogenic to chickens but not pathogenic to ducks or mice. The four tree sparrow viruses were different from the 2003 tree sparrow strain (genotype Z) in Hong Kong. The results suggested that H5N1 viruses might be distributed widely in tree sparrows.

Animals↗

PubMed2000

Improvement of rejection-induced diastolic abnormalities in rat cardiac allografts with inducible nitric oxide synthase inhibition.

OBJECTIVE: Inhibition of inducible nitric oxide synthase (nitric oxide II) activity has been proposed as a method to attenuate capillary leak and edema during rejection of heterotopically transplanted rat hearts. Myocardial edema has previously been implicated in diastolic dysfunction during allograft rejection. Accordingly, we tested the hypothesis that inducible nitric oxide synthase inhibition with aminoguanidine would alleviate left ventricular stiffening and myocardial edema formation in 4-day heterotopic rat heart allografts. METHODS: Passive left ventricular filling was studied in American Cancer Institute Lewis rats receiving heterotopic heart transplants receiving either aminoguanidine, a selective nitric oxide synthase inhibitor (n = 6); dexamethasone (1 mg. kg(-1). d(-1) administered subcutaneously) for 4 days after transplantation (n = 6); or intravenous saline solution (n = 6). American Cancer Institute-to-American Cancer Institute isografts (n = 6) were used as controls. RESULTS: Serum nitrite/nitrate levels in the aminoguanidine group (18 +/- 3 mmol/L) and dexamethasone group (22 +/- 4 mmol/L) were reduced versus the intravenous saline group (144 +/- 36 mmol/L [SEM]) to levels seen in controls (25 +/- 9 mmol/L). Left ventricular volume at 15 mm Hg for the aminoguanidine group was increased versus that for the intravenous saline solution group, similar to that for controls, and reduced versus dexamethasone-treated animals. Myocardial water content for the aminoguanidine-treated animals (78.3% +/- 0.4%) was similar to those of intravenous saline-treated animals (78.0% +/- 0. 3%) but greater than those of controls (77.1% +/- 0.2%) and dexamethasone-treated animals (76.7% +/- 0.3%). CONCLUSIONS: Nitric oxide II inhibition with aminoguanidine minimizes the reduction in left ventricular filling that is seen with allograft rejection through a mechanism that is not associated with attenuation of myocardial edema.

Animals↗

PubMed1999

Pressure volume curves in arrested heterotopic rat heart isografts: role of improved myocardial protection.

BACKGROUND: To minimize decreases in left ventricular (LV) compliance immediately after rat heart transplantation, we tested several different methods of myocardial protection. MATERIALS AND METHODS: Five groups of ACI rat hearts (n = 6 each) were arrested by coronary perfusion with 5 ml of UW (University of Wisconsin), UW-BDM (UW with 2,3-butanedione monoxime), CU (Columbia University), or CU-BDM solution or by LV injection of potassium chloride and Ringer's lactate immersion (KCl/RL). After abdominal isografting and blood reperfusion for 15 min, transplanted hearts (TxH) were arrested and excised. Diastolic LV pressure-volume curves (LVPVCs) were correlated with myocardial water content (MWC). Native hearts (NH) were arrested identically to TxH and maintained at 4 degrees C by immersion. LVPVCs were measured at 15-min intervals for 90 min. RESULTS: In three of four pressure intervals at Time 0, normalized LV volume (LVV) was smaller (P < 0.05, ANOVA) in KCl/RL native hearts than in the four perfusion groups. LVV decreased significantly in NH after 45-75 min; LVV decreased similarly with time in all groups. In TxH, postarrest LVVs were higher with UW-BDM, CU-BDM, and CU than with UW or KCl/RL (P < 0.05, ANOVA). Expressing LVV of TxH as a percentage of NH, UW-BDM, CU, and CU-BDM provided qualitatively better diastolic properties than KCl/RL and UW. CONCLUSIONS: Thus rat LVPVCs can be improved after heart transplantation with alternative strategies of myocardial protection. KCl arrest decreases LV filling volume in this model and should be avoided.

Abdomen↗

PubMed1999

Coronary perfusate composition influences diastolic properties, myocardial water content, and histologic characteristics of the rat left ventricle.

BACKGROUND: Recent studies found that edema, histology, and left ventricular diastolic compliance exhibit quantitative relationships in rats. Edema due to low osmolarity coronary perfusates increases myocardial water content and histologic edema score and decreases left ventricular filling. The present study examined effects of perfusate osmolarity and chemical composition on rat hearts. METHODS: Arrested American Cancer Institute (ACI) rat hearts (4 degrees C) were perfused with different cardioplegia solutions, including Plegisol (289 mOsm/L), dilute Plegisol (172 mOsm/L), Stanford solution (409 mOsm/L), and University of Wisconsin solution (315 mOsm/L). Controls had blood perfusion (310 mOsm/L). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. After glutaraldehyde or formalin fixation, dehydration, and paraffin embedding, edema was graded subjectively. RESULTS: Myocardial water content reflected perfusate osmolarity, being lowest in Stanford and University of Wisconsin solutions (p<0.05 versus other groups) and highest in dilute Plegisol (p<0.05). Left ventricular filling volumes were smallest in dilute Plegisol and Plegisol (p<0.05). Osmolarity was not a major determinant of myocardial edema grade, which was highest with University of Wisconsin solution and dilute Plegisol (p<0.05 versus other groups). CONCLUSIONS: Perfusate osmolarity determined myocardial water content and left ventricular filling volume. However, perfusate chemical composition influenced the histologic appearance of edema. Pathologic grading of edema can be influenced by factors other than osmolarity alone.

Adenosine↗

PubMed1999

Attenuation of reperfusion injury with probucol in the heterotopic rat cardiac isograft.

BACKGROUND: We tested the hypothesis that pretreatment with the antioxidant probucol attenuates reperfusion-induced diastolic abnormalities in the heterotopic rat cardiac isograft. METHODS: American Cancer Institute rats (n = 48) were divided into 6 groups. Hearts were arrested by coronary perfusion with 3 ml 4 degrees C University of Wisconsin solution at 60 mmHg. Eighteen donor hearts were divided into 3 groups of 6 and arrested either 1 hour after intraperitoneal injection of 3 ml oil with (Prob Tx) or without (Oil Tx) probucol (300 mg/kg) or without injection (Ctrl Tx). After a 90 minute storage period, abdominal isografting was performed with a total ischemic time of 2 hours. Following 15 minutes of blood reperfusion, donor hearts were rearrested and excised. Recipients' native hearts (NH, n = 18) were also arrested. Two additional groups with (Prob NR, n = 6) and without (Ctrl NR, n = 6) probucol pretreatment were arrested and subjected to 2 hours of ischemia without reperfusion. Postmortem LV pressure-volume curves and myocardial water content (MWC) were measured. RESULTS: At each pressure interval normalized LV volume (LVV) was significantly greater for Prob Tx than Oil Tx or Ctrl Tx. All isograft groups had significantly lower LVV at all pressure intervals and higher MWC than non-transplanted hearts. CONCLUSIONS: Pretreatment with probucol attenuates reperfusion-induced decreases in LVV in the heterotopic rat heart isograft model. Probucol, which is orally active in humans, merits further study for its potential to improve myocardial protection during cardiac surgery.

Abdomen↗

PubMed1998

A novel arresting solution for study of postmortem pressure--volume curves of the rat left ventricle.

OBJECTIVE: We have found diastolic properties of the rat heart extremely sensitive to the method used to induce arrest. Accordingly, we sought to develop a reliable solution for measuring the LV pressure-volume relationship (LVPVR) in the rat. MATERIALS AND METHODS: The study had five phases: (i) K120Na100, consisting of KCl (120 mEq/L) in NaCl (100 mEq/L) diluted with distilled water was developed in preliminary experiments. (ii) ACI rats were arrested with 3 cc of 4 degreesC KCl (n = 6) or K120Na100 (n = 6) infused into the aortic root. The LVPVR was expressed as normalized volume (Vn) at standardized pressures. Myocardial water content (%MWC) was determined. (iii) Six hearts were arrested with K120Na100 and LVPVRs observed over 1 h. (iv) Four hearts were instrumented with sonomicrometry crystals to compare in vivo and postmortem pressure diameter data. (v) The relation between body weight and dry heart weight was determined in 48 animals. RESULTS: In hearts arrested with KCl, mean Vn at pressures of 10, 15, and 20 mmHg (206 +/- 26, 306 +/- 21, and 336 +/- 25 microl, respectively) was significantly reduced vs K120Na100 hearts (345 +/- 11, 407 +/- 12, and 472 +/- 18 microl) (P < 0.05). Mean %MWC changed insignificantly. Vn at 20 mm Hg became significantly smaller vs initial data 60 min after arrest with K120Na100 (P < 0.05, ANOVA). No differences between in vivo and postmortem mean normalized diameter were observed. The correlation coefficient for the relation between body weight and dry heart weight was 0.80. Conclusions. K120Na100 at 4 degreesC reliably preserves LV diastolic properties in the rat heart for 30 min. Normalization of LV volume to body weight is justified.

Animals↗

PubMed1998

Retrograde coronary perfusion: effects on iatrogenic edema and diastolic properties.

BACKGROUND: The relative merits of antegrade infusion and retrograde infusion of cardioplegic solution in terms of heart weight, myocardial water content, and ventricular diastolic properties are undefined. Accordingly, we compared antegrade and retrograde flow of hemodiluted blood in isolated, hypothermic porcine hearts. METHODS: After cardiectomy, 1 L of cold heparinized blood diluted with lactated Ringer's solution to concentrations ranging from 100% lactated Ringer's to 50% lactated Ringer's and 50% blood was perfused in an antegrade (n = 6) or retrograde (n = 6) fashion at mean pressures of 62 +/- 2 mm Hg (+/- standard error of the mean) and 49 +/- 2 mm Hg, respectively. Heart weight, myocardial water content, and left ventricular pressure-volume relationships were obtained before and after perfusion. RESULTS: In the comparison of measurements before and after perfusion, changes in heart weight (36 +/- 4 g versus 5 +/- 2 g; p < 0.05), myocardial water content (6.9% +/- 1.0% versus 2.5% +/- 0.4%; p < 0.01), and ventricular filling measured by normalized left ventricular volume at 10, 15, and 20 mm Hg were greater in the antegrade group. CONCLUSIONS: In the isolated porcine heart, retrograde flow is distinguished from antegrade flow by less change in heart weight and myocardial water content and no diastolic dysfunction.

Animals↗

PubMed1998

Reversal of iatrogenic myocardial edema and related abnormalities of diastolic properties in the pig left ventricle.

OBJECTIVE: This study examines the resolution of iatrogenic edema and related changes in systolic and diastolic properties in the intact pig left ventricle. METHODS: The coronary arteries were perfused for 50 to 60 seconds with diluted blood (hematocrit value 10% +/- 1%, edema group, n = 5) or whole blood (hematocrit value 28% +/- 1%, control group, n = 6) infused into the aortic root during aortic crossclamping in conditioned, anesthetized pigs. After whole blood reperfusion, preload reduction by vena caval occlusion was used to define systolic and diastolic properties at 15-minute intervals. Left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography were recorded. RESULTS: Left ventricular mass (wall volume) in the edema group increased significantly compared with that in control pigs after crossclamp removal. Mass returned to preperfusion levels after 45 minutes. The ventricular stiffness constant (beta) increased significantly in the edema group versus the control group, returning to baseline by 30 minutes. The diastolic relaxation constant (tau) and base constant (alpha) did not differ between groups. There was no significant change in contractility. CONCLUSION: Increases in left ventricular mass and diastolic stiffness induced by coronary perfusion with hemodiluted blood resolve after 45 minutes of whole blood perfusion in pigs. This study defines physiologic effects of edema in the normal heart while eliminating most common confounding experimental errors.

Animals↗

PubMed1998

A method for detecting changes in left ventricular mass during variations in filling volume.

Two-dimensional echocardiography has been useful for measuring changes in left ventricular mass (LVM) at constant left ventricular end-diastolic volume (LVEDV). Two-dimensional echocardiographic measurement of LVM changes during variations in LVEDV requires definition of the LVM/LVEDV relation because two-dimensional echocardiographic measurements could be affected by asymmetrical redistribution of LVM. Echocardiography data were recorded during caval occlusions in pigs (n = 6). Results confirm that A(M) (left ventricular [LV] short-axis cross-sectional [SACS] wall thickness area), was inversely related to AL (LV SACS lumen area), the average relation being A(M) = -0.33 AL + 20 (r = 0.82 +/- 0.05 [SE]). In addition, we developed a model that computes normal relation between LV SACS wall thickness area (AMc) and LV SACS lumen area (ALc) over a physiologic range of LVEDVs based on a single end-diastolic two-dimensional echocardiographic SACS image. Each computed relation corresponds uniquely to an LVM (LVMc). Theoretically, a difference between AMc/ALc relation before an intervention and the computed relation after the intervention would indicate a change in LVM. To test the utility of this model, edema was induced in a second group of pigs (n = 6) by coronary hemodilution. Two conditions were tested: pre-edema and edema. Serial AMc/ALc and LVMc were computed. Pre-edema and edema AMc were compared at matched LV SACS end-diastolic areas (ALc = 15 cm2). Results showed a significant increase in LVMc (two-tailed p value < 0.05), as observed by two-dimensional echocardiography. We conclude that the A(M) and AL are inversely related. This relation is useful for detecting alterations in LVM during variations in LVEDV.

Animals↗

PubMed1998

Diastolic properties, myocardial water content, and histologic condition of the rat left ventricle: effect of varied osmolarity of a coronary perfusate.

BACKGROUND: Although myocardial edema is known to impair diastolic filling of the left ventricle, the interrelation of edema, histologic condition, and function has not been quantitated sufficiently for extrapolation to studies of multifactorial influences on diastolic properties. METHODS: Accordingly, ACI rat hearts arrested at 4 degrees C underwent coronary artery perfusion with a cardioplegia solution that was either unaltered (288 mOsm/L, P288 group, n = 6), diluted (144 mOsm/L, P144 group, n = 6), or concentrated (380 mOsm/L, P380 group, n = 6). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. Myocardial samples were fixed in varying dilutions of glutaraldehyde. After dehydration and paraffin embedding, edema was graded subjectively (0 to 5), and myocardial interstitial spaces were determined by use of a semiquantitative method. RESULTS: Mean normalized left ventricular filling volume at 20 mm Hg filling pressure in the P144 group, 189 +/- 16 microliters (SEM), was reduced versus both the P288 (278 +/- 26 microliters) and the P380 (332 +/- 18 microliters) groups (p < 0.05, ANOVA). Mean myocardial water content in the P144 group, 80.7% +/- 1%, was increased versus the P380 (76.7% +/- 0.4%, p < 0.05) but not versus the P288 group (78.4% +/- 0.8%). In hearts preserved with 2.5% glutaraldehyde, mean edema grade and interstitial space in the P144 group (4.0 +/- 0.3) were increased versus the P380 (1.8 +/- 0.3, p < 0.05) but not the P288 group (2.7 +/- 0.5). Derived linear regressions relate water content to filling volume and histologic condition. CONCLUSIONS: Coronary perfusate osmolarity is thus associated with predictable changes in myocardial water content, left ventricular filling volume, and edema. These correlations allow definition of new hypotheses for the study of cardiac allograft rejection in patients and experimental animals.

Animals↗

PubMed1998

Effect of improved myocardial protection on edema and diastolic properties of the rat left ventricle during acute allograft rejection.

BACKGROUND: Studies of myocardial edema and diastolic dysfunction in rat heart transplantation have been flawed by ischemic injury. This study uses improved methods to prevent ischemic contracture. METHODS: Hearts of 30 ACI rats were transplanted into the abdomen of Lewis rats by use of cold University of Wisconsin solution for improved preservation. Left ventricular diastolic properties were expressed as volume at standardized pressure intervals. RESULTS: On posttransplantation day 3, mean left ventricular volume at 15 mm Hg in allografts (290 +/- 9 microl, SEM) was not significantly different vs isografts (299 +/- 32 microl), allografts on day 0 (337 +/- 28 ml) or day 1 (324 +/- 20 microl), or native hearts (334 +/- 19 microl). However, volume was reduced to 173 +/- 17 microl on day 4 and to 70 +/- 23 microl on day 5 (p < 0.05). Similar findings were obtained for volume at 5 and 10 mm Hg. Allograft myocardial water content on day 3, 76.3% +/- 5%, similar to allografts on day 0 and 1 and to isografts on day 3, increased to 77.6% +/- 8% on day 4 (NS) and 79.4% +/- 6% on day 5 (p < 0.05 vs day 0). Histologically, rejection in allografts was mild on day 3, moderate on day 4, and severe on day 5. CONCLUSIONS: Reduced left ventricular filling volume during rejection is only partially explained by edema. Abnormalities of diastolic properties previously attributed to the unloaded state of nonworking heart models may actually reflect inadequate peritransplantation myocardial protection.

Adenosine↗

PubMed1997

Myocardial edema: comparison of effects on filling volume and stiffness of the left ventricle in rats and pigs.

BACKGROUND: This study compared the adverse effects of crystalloid-induced myocardial edema on left ventricular (LV) compliance in small and large hearts. METHODS: Plegisol (289 mOsm/L) was perfused into the coronary arteries of pigs (n = 8) and 1:1 dilute Plegisol (145 mOsm/L) into the coronary arteries of rats (n = 6). Pressure-volume relations, heart weight, and water content were then determined. The pressure-volume relations were compared using an LV volume at a pressure of 10 mm Hg. RESULTS: Edema in rats was associated with significant (p < 0.05) increases in heart weight (1.1 +/- 0.0 g versus 1.4 +/- 0.1 g [average +/- standard error of the mean]) and water content (76.8% +/- 0.4% versus 81.3% +/- 0.8%), but an increase in LV stiffness (7.91 +/- 0.52 versus 9.27 +/- 1.42) and a decrease in the LV volume at 10 mm Hg (0.25 +/- 0.02 mL versus 0.14 +/- 0.05 mL) were not statistically significant. Edema in pigs was associated with statistically significant (p < 0.05) increases in LV stiffness beta (0.050 +/- 0.004 versus 0.072 +/- 0.008), heart weight (207 +/- 8 g versus 274 +/- 9 g), and water content (79.8% +/- 0.6% versus 85.3% +/- 0.6%) and a significant decrease in the LV volume at 10 mm Hg (88.4 +/- 5.8 mL versus 60.4 +/- 6.8 mL). CONCLUSIONS: Myocardial edema is associated with an increase in water content and LV stiffness and a decrease in the LV volume at 10 mm Hg in both species. In rats, however, the water content is smaller in the control state and a more hypotonic perfusate is needed to induce a given degree of edema.

Animals↗

PubMed1996

Validation of right and left ventricular conductance and echocardiography for cardiac function studies.

BACKGROUND: Continuous estimation of left ventricular volume from instantaneous conductance has compared favorably with "gold standards," is less labor intensive, and provides real-time data. Little information exists, however, correlating right ventricular conductance with such gold standards or examining the effects of an electrical field generated in the opposite ventricle. METHODS: In open-chested sheep, right and left ventricular conductance, two-dimensional echocardiography, and thermodilution cardiac outputs were measured at steady-state conditions. After these measurements, postmortem pressure-volume relations, ventricular mass, and ventricular casting were performed. RESULTS: The corrected end-diastolic volume measured by conductance correlated well with volumes measured by echocardiography (r = 0.89), postmortem pressure-volume relations (r = 0.84), and casts (r = 0.85). Left ventricular end-diastolic volume measured by conductance did not differ significantly from other standards by analysis of variance. The presence of an electrical field in the opposite ventricle did not affect measured conductance in the studied ventricle. CONCLUSIONS: Conductance is useful for the measurement of right and left ventricular end-diastolic volumes in the beating heart and is not affected by the presence of an electrical field in the opposite ventricle. Hence, conductance is a useful tool in studies involving interventricular dependence and function.

Animals↗

PubMed1996

Iatrogenic myocardial edema: increased diastolic compliance and time course of resolution in vivo.

BACKGROUND: Perfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals. METHODS: Edema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion. RESULTS: In the edema group, average left ventricular mass (132 +/- 7 [standard error of the mean] versus 106 +/- 4 g) and ventricular stiffness constant (0.15 +/- 0.02 versus 0.05 +/- 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 +/- 6 versus 116 +/- 4 g) and ventricular stiffness (0.06 +/- 0.01 versus 0.05 +/- 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups. CONCLUSIONS: Crystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction.

Animals↗

PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation in pigs.

Ventricular fibrillation (VF) is induced during implantable cardioverter defibrillator insertion and can result in cardiovascular collapse. The relation between repeated VF trials of varying duration and systolic blood pressure (SBP) recovery rate was studied in 6 pigs. Two implantable cardioverter defibrillator patches were placed on the heart, and VF was varied in a cyclic pattern until cardiovascular collapse occurred. A negative logarithmic relation between SBP recovery rate and duration of VF was found in 4 of the pigs with correlation coefficients of 0.62 to 0.97 (p < 0.05). The overall correlation coefficient was 0.51 for all 116 data points (p < 0.001). Although there was a significant (p < 0.05) decrease in average (+/- standard error of the mean) baseline SBP in the second half of each experiment (83 +/- 5 mm Hg versus 77 +/- 6 mm Hg), no significant difference in SBP was observed during VF (17 +/- 1 mm Hg versus 16 +/- 1 mm Hg) or after 15 seconds of SBP recovery (51 +/- 4 mm Hg versus 46 +/- 3 mm Hg) between the two halves of the experiments. Cardiovascular collapse occurred without warning; epinephrine was effective in reversing it. In conclusion, SBP recovery rate and duration of VF have a negative logarithmic relation consistent with a negative effect on left ventricular contractility with prolongation of VF. The onset of cardiovascular collapse during implantable cardioverter defibrillator testing cannot be predicted on the basis of monitored blood pressure alone.

Animals↗

PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation/flutter in humans.

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 +/- 2, and the mean drop in systolic pressure was 84 +/- 16 mmHg. The mean recovery time for systolic pressure was 10 +/- 6 seconds, the average systolic pressure recovery rate was 13 +/- 14 mmHg/sec, and the mean percent systolic pressure recovery was 94% +/- 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.

Adult↗

PubMed1994

Extrinsic factors influencing left ventricular conductance in situ.

BACKGROUND: The accuracy of conductance measurement of left ventricular (LV) volume is affected by parallel conductance (Vp) from right ventricular (RV) volume as well as surroundings of the heart. No studies have quantified the extrinsic influences on Vp. METHODS AND RESULTS: In six anesthetized pigs, using a median sternotomy and pericardial well, implantable cardioverter defibrillator patches, normal saline, or echocardiography gel were introduced and removed. LV end-diastolic pressure (LVEDP) did not change significantly with these interventions. Raw LV conductance was used to estimate end-diastolic volume (LVEDV), end-systolic volume (LVESV), and stroke volume (SV). Saline significantly increased mean +/- SEM calculated LVEDV from 106 +/- 8 to 131 +/- 6 mL and calculated LVESV from 81 +/- 7 to 110 +/- 5 mL; calculated SV decreased from 25 +/- 3 to 21 +/- 2 mL (P < .05, paired t test). Implantable cardioverter defibrillator patches and gel did not significantly change calculated LV volumes. LV conductance was also measured in arrested hearts during LV filling (5 to 60 mL) at four levels of RV volume (RVV). Using a fixed value for Vp, calculated mean LV volume was 30 +/- 3 mL at RVV = 0, 32 +/- 3 mL at RVV = 20, 33 +/- 3 mL at RVV = 40, and 36 +/- 3 mL at RVV = 60 (P < .01, repeated-measures ANOVA). CONCLUSIONS: While implantable cardioverter defibrillator patches and gel have no statistically significant effect, saline and RVV affect LV volume calculations by conductance, requiring special techniques during cardiopulmonary bypass or caval occlusion.

Animals↗

PubMed1994

Diastolic function in the heterotopic rat heart transplant model. Effects of edema, ischemia, and rejection.

Decreased systolic ventricular function and compliance and increased left ventricular edema and mass have been demonstrated in cardiac allograft rejection. Whether decreased left ventricular compliance in rejection is caused by myocardial edema has not been examined, and compliance in the Ono-Lindsey model has not been reported. Heterotopic rat abdominal cardiac transplantation was performed in ACI isografts (n = 24) and in ACI to Lewis allografts (n = 24). Subgroups were studied on posttransplantation days 0, 1, 3, and 5 (each n = 6). Both transplanted hearts and native hearts were arrested with potassium for the assessment of myocardial water content, heart weight, and the left ventricular pressure-volume relation. In transplanted hearts, myocardial water content did not change in isografts but increased on posttransplantation day 5 in allografts (81.1% on posttransplantation day 5 versus 76.1% on day 0, 77.2% on day 1, and 77.5% on day 3, p < 0.05). Wet and dry heart weight also increased on posttransplantation day 5 in allografts (p < 0.05). The left ventricular pressure-volume relation in transplanted hearts shifted to the left when compared with that in native hearts in all subgroups; these volume differences were statistically significant (p < 0.01) for all pressures above 7.5 mm Hg. This pattern was similar in isografts and allografts on posttransplantation days 0, 1, and 3, and no significant differences between isografts and allografts were demonstrated. On posttransplantation day 5, however, the pressure after a 0.05 ml injection in allografts was greater in transplanted hearts than in native hearts (24 +/- 3 versus 3 +/- 1 mm Hg, p < 0.01). The pressure difference between transplanted and native hearts was also significantly greater in allografts than in isografts (22 +/- 2 versus 6 +/- 1 mm Hg, p < 0.01), indicating an increase in stiffness of allografts. Thus edema and impaired diastolic properties occur concurrently with allograft rejection. Left ventricular volume is abnormal from posttransplantation days 0 to 5 in transplanted hearts but not native hearts in the Ono-Lindsey model with current methods, apparently because of ischemic injury during transplantation.

Animals↗