Biomedical subjects

B B Chiang

Publications and source records attributed to B B Chiang.

4 recordsLinked to original sources

PubMed2000

Chemoreflexes: an experimental study.

HYPOTHESIS: Transmyocardial laser revascularization (TMLR) will not denervate the heart, because it does not destroy all of the afferents. This study was designed to determine if stimulation of cardiac sympathetic and vagal afferents from an area of the left ventricle treated with TMLR could evoke reflex effects, and thus whether TMLR would denervate the heart. METHODS: The effect of TMLR on reflexes evoked by chemically stimulating cardiac afferents was examined in 9 dogs. Bradykinin and capsaicin were applied topically or injected into the left anterior descending coronary artery before and after TMLR and after bilateral vagotomy and sympathectomy. Aortic (AoP) and left ventricular pressures (LVP) and electrocardiography were monitored. The first derivatives of LVP (dP/dt) were calculated. RESULTS: Topical bradykinin elicited variable hemodynamic responses. Topical capsaicin evoked pressor responses, increasing mean (+/- SEM) AoP (105+/-9 to 115+/-9 mm Hg; P<.001) and positive dP/dt (+dP/dt) (1032+/-81 to 1159+/-10 mm Hg/s; P<.01) before TMLR. Intracoronary capsaicin evoked a depressor response before TMLR. Pressor responses remained intact after TMLR with increases in mean AoP and +dP/dt (115+/-6 to 128+/-5 mm Hg and 1039+/-98 to 1136+/-100 mm Hg/s, respectively; P<.01). Depressor responses also remained intact after TMLR (91+/-10 vs 101+/-11 mm Hg [P<.02], and 865+/-104 vs 931+/-104 mm Hg/s [P<.05], respectively). Hemodynamic responses were diminished after bilateral vagotomy and abolished after bilateral sympathectomy. CONCLUSION: Since activation of cardiac afferent nerves and reflex responses remained intact after TMLR, but changed after vagotomy or sympathectomy, TMLR does not denervate the heart sufficiently to be the cause of improved angina after TMLR.

Afferent Pathways↗

PubMed1997

Variable effects of cardiomyoplasty on left ventricular function.

Cardiomyoplasty (CMP) has been considered as a possible treatment for patients with heart failure. Symptomatic improvements occur almost uniformly among survivors with CMP, but changes in left peak ventricular systolic pressure (PVSP) and stroke volume vary in patients. This study examined whether there is variability present shortly after cardiomyoplasty surgery. Cardiomyoplasty was performed in 11 mongrel dogs with normal ventricular function. Nine to twelve days after CMP, left ventricular (LV) function was evaluated by simultaneously measuring LV volume (conductance catheter) and pressure (Millar catheter). The latissimus dorsi muscle (LDM) was stimulated synchronously with ventricular systole in a ratio of 1:4 to 1:7 to avoid muscle fatigue. Data were analyzed on a beat by beat basis. The PVSP, and maximum dP/dt (+dP/dt) increased, but the absolute value of minimum dP/dt (-dP/dt) decreased in stimulated beats in 7 dogs while 4 dogs did not respond. The net changes in stimulated beats versus nonstimulated beats of PVSP were 6.1 +/- 1.8 mm Hg (4.3%), of stroke work was 4.5 +/- 1.9 gm x m (29.5%), of +dP/dt was 185 +/- 47 mm Hg/s (8%), and of -dP/dt was 168 +/- 43 mm Hg/s (7.8%) (p < 0.05) for all these net changes in the responding group while these variations were not significant in the nonresponding group. From the results of our study, active LDM assist improves left ventricular systolic function, occurring in only 7 of 11 experiments. This improvement is inconsistent and varied individually. The integrity of the LDM, tightness of wrapping, and adhesions might contribute to the variability which is present early after surgery and before the LDM is converted into a fatigue resistance muscle.

Animals↗

PubMedDate not supplied

Two step cardiomyoplasty with vascular delay: effect of stimulation of latissimus dorsi muscle on diastolic function.

A common concern in cardiomyoplasty is whether latissimus dorsi muscle (LDM) stimulation impairs diastolic function. This study determined the time course of left ventricular (LV) contraction and relaxation and their relationship to the diastolic function. Ten mongrel dogs underwent vascular delay of the left latissimus dorsi muscle 2 weeks before cardiomyoplasty. Fourteen to 18 days later, the effects of LDM stimulation were evaluated. Our study demonstrated that LDM stimulation significantly increased peak LV systolic pressure (131.3 +/- 7.5 to 152.0 +/- 7.5* mm Hg), +dP/dt (1585 +/- 151 to 2088 +/- 176 x mm Hg/s), stroke volume (10.8 +/- 1.5 to 13.8 +/- 1.9* ml), stroke work (17.2 +/- 2.7 to 25.6 +/- 3.8* gm x m), and peak aortic flow (4751 +/- 698 to 6712 +/- 926* ml/min), and significantly decreased the pre-ejection time (113.9 +/- 12.6 to 92.3 +/- 7.8* ms) and total systolic time (366.0 +/- 26.9 to 333.6 +/- 21.3* ms) (*p < 0.05). As for diastolic function, LDM stimulation decreased -dP/dt (-1462 +/- 116 to -1781 +/-116* mm Hg/s) and tau (64.0 +/- 6.1 to 52.1 +/- 2.9* ms). The diastolic filling time (Tdf) was significantly longer (177.9 +/- 17.6 to 213.7 +/- 18.7* ms) during the beat immediately after LDM stimulation. These changes reflected an overall stronger contraction and faster relaxation. Our results imply that with vascular delay, stimulation of LDM not only assists systolic function but also improves diastolic function in cardiomyoplasty.

Animals↗

PubMedDate not supplied

Cardiomyoplasty: hemodynamic benefit to normal and depressed canine left ventricular function.

This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To improve viability of the latissimus dorsi muscle (LDM), vascular delay was performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two weeks after cardiomyoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimulated at a ratio of 1:4-1:7 synchronously with ventricular systole. Microspheres (90 mu) were sequentially injected into the left coronary artery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 +/- 2 to 161 +/- 2* mmHg, the peak rate of change of LV pressure (+dP/dt) from 1888 +/- 46 to 2584 +/- 43* mmHg/sec, aortic systolic pressure (AoSP) from 140 +/- 2 to 159 +/- 2* mmHg, stroke volume (SV) from 11.2 +/- 0.3 to 13.3 +/- 0.3* ml, stroke work (SW) from 19 +/- 1 to 26 +/- 1* gm.m, peak aortic flow (P Qa) from 5542 +/- 142 to 7190 +/- 161* ml/min, and decreased -dP/dt from -1683 +/- 31 to -1689 +/- 49* mmHg/sec (* = p < 0.05). Microsphere injections depressed LV function, but did not affect the magnitude of the net changes between stimulated and nonstimulated beats. However, the percent changes significantly increased. Preconditioning of LDM with vascular delay augments cardiac function in LDM assisted beats. This improved performance was present in both normal as well as depressed LV function groups. Thus, investigations of cardiomyoplasty may not necessarily require a model of severe myocardial dysfunction. Vascular delay offers an important preconditioning method of LDM to augment cardiac function in cardiomyoplasty.

Animals↗