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K S Li

Publications and source records attributed to K S Li.

30 records · Page 2Linked to original sources
PubMed1993

Contribution of each wall to biventricular function.

OBJECTIVE: Common muscle fibres encircle both ventricles and the ventricles share a common septal wall. This close anatomical association suggests that regional ischaemia and structural integrity may alter systolic function in both the right and the left ventricle. To examine this possibility, we investigated the contribution of each wall to biventricular function. METHODS: Isolated hearts, obtained from anaesthetised rabbits, were perfused with physiological salt solution under constant pressure. Balloons were placed in the right and left ventricles to measure isovolumetric pressure, and pressure-volume curves were obtained. In separate sets of experiments, the left ventricular free wall, right ventricular free wall, or septum was made ischaemic, incised, or injected with glutaraldehyde, respectively. Pressure-volume curves were obtained again. RESULTS: After left ventricular free wall ischaemia (n = 11), right ventricular developed pressure decreased significantly from 27.9(SD 8.9) to 14.1(6.6) mm Hg (p < 0.05), and remained depressed when the left ventricular free wall was further damaged by glutaraldehyde. Cutting the left ventricular free wall (n = 6) decreased right ventricular developed pressure from 28.9(8.6) to 17.8(4.8) mm Hg (p < 0.05), while reapproximating the left ventricular free wall by suturing re-established right ventricular developed pressure. After right ventricular free wall ischaemia (n = 7), right ventricular developed pressure decreased from 26.8(6.6) to 24.1(5.7) mm Hg (NS) and left ventricular developed pressure was unaltered. Cutting the right ventricular free wall (n = 7) had no effect on left ventricular developed pressure. Cutting the septum (n = 7) had no obvious influence on right ventricular developed pressure, but dramatically decreased left ventricular developed pressure from 79.2(55.2) to 43.7(32.2) mm Hg (p < 0.05). Injecting glutaraldehyde into the septum (n = 7) decreased both right and left ventricular developed pressures from 22.1(8.5) to 14.0(8.8) and from 78.2(50.5) to 47.9(37.9), respectively. CONCLUSIONS: The results show that the heart should be viewed as a mechanical syncytium. The left ventricular free wall plays a critical role in right ventricular systolic function and may help to explain the right ventricular response to left ventricular ischaemia. On the other hand, in the isolated heart preparation, right ventricular free wall ischaemia has only a minimal effect on left ventricular systolic developed pressure. Altering ventricular septal function affects both right and left ventricular systolic function.

Animals↗
PubMed1993

Ventricular coupling via the pericardium: normal versus tamponade.

OBJECTIVE: The aim was to examine how regional variations in pericardial pressure affect the mechanical coupling between the ventricles. METHODS: Canine hearts from 14 dogs (14.5-18 kg) were removed and placed in cold cardioplegia solution. Balloons were inserted into the left and right ventricles and the atria. Pericardial pressure over the left ventricle (Pclv) and the right ventricle (Pcrv) was measured with thin balloon catheters. Ventricular and pericardial pressures were measured, and ventricular and pericardial coupling was calculated, under control conditions and with increases in pericardial tension and fluid. RESULTS: At baseline, regional differences in pericardial pressure occurred [Pclv > Pcrv, 4.0(SD 0.9) v 2.9(0.6) mm Hg, p < 0.05]. Ventricular coupling via the pericardium was defined as delta Pclv/delta Pcrv for right ventricular volume increases and delta Pcrv/delta Pclv for left ventricular volume increases. This ratio increased more after increasing right ventricular volume than after increasing left ventricular volume [delta Pclv/delta Pcrv > delta Pcrv/delta Pclv, 1.14(0.33) v 0.51(0.15), p < 0.05]. Increasing the pericardial tension by clamping the pericardium increased pericardial pressures, yet did not alter the regional variations in pressure [Pclv > Pcrv, 8.4(2.2) v 6.4(2.5) mm Hg, p < 0.05] or pericardial coupling [delta Pclv/delta Pcrv > delta Pclv/delta Pcrv, 1.18(0.46) v 0.54(0.16), p < 0.05]. In contrast, creating a mild tamponade increased pericardial pressures, eliminated regional differences in pressure, and altered the coupling between ventricles [delta Pclv/delta Pcrv approximately delta Pclv/delta Pcrv, 0.95(0.11) v 1.05(0.08), p = NS]. These regional differences in pericardial pressure might have a geometrical basis. In four in vivo canine experiments using cine magnetic resonance, the short axis radius of curvature for the right ventricle was greater than for the left ventricle [38.3(4.4) mm v 29.2(3.8) mm, p < 0.05]. CONCLUSIONS: The pericardium partially protects right ventricular filling: regional differences in pericardial pressure normally occurred with lower pericardial pressure over the right ventricle, and left to right ventricular coupling was less. This protection of right ventricular filling was lost with even a small pericardial effusion.

Animals↗
PubMed1993

The order of dilator-constrictor administration affects stenotic hemodynamic responses.

This study tested the hypothesis that, due to intraluminal pressure changes, the order of constrictor-dilator administration alters stenotic hemodynamic responses. Canine carotid arteries were perfused with a physiologic salt solution under constant pressure (100 mm Hg). An intraluminal stenosis partially obstructed the arteries. Pressures proximal and distal to the artery and the flow were continually recorded as norepinephrine (10(-9)-10(-6) M) was added to the perfusate. Adding diltiazem (10(-7) M) before norepinephrine shifted the effective half maximum dose (ED50) of the norepinephrine flow curve from 7.35 +/- 0.66 X 10(-8) M to 6.39 +/- 0.72 X 10(-7) M (p < 0.05). More important, adding 10(-7) M diltiazem after norepinephrine-induced constriction did not reestablish stenotic pressure or flow: A 30-fold increase in diltiazem concentration (3.16 X 10(-6)M) was required to reestablish stenotic pressure (62.6 +/- 4.4 mm Hg) and flow (25.4 +/- 3.2 ml/min). Similarly, adding nitroglycerin (10(-7) M) before norepinephrine shifted the ED50 from 7.21 +/- 0.58 X 10(-8) to 5.94 +/- 0.78 X 10(-6) (p < 0.05). Adding 10(-7) M nitroglycerin after norepinephrine did not reestablish stenotic pressure or flow: 3.16 X 10(-6) M nitroglycerin was required to reestablish stenotic pressure (59.2 +/- 4.8 mm Hg) and flow (23.2 +/- 2.7 mL/min). This constrictor-dilation history did not occur in isolated arterial rings (norepinephrine + nitroglycerin = 38.1 +/- 13.9 g/cm2; nitroglycerin + norepinephrine = 42.2 +/- 9.4 g/cm2; p = not significant [NS]) or in normal arteries (norepinephrine + nitroglycerin = 4.89 +/- 0.14 mm [external diameter]; nitroglycerin + norepinephrine = 4.92 +/- 0.23 mm; p = NS). In stenotic arteries, intraluminal pressure influenced the order of constrictor-dilator administration on hemodynamic response, which was not observed in isolated arterial rings or in normal arteries. This pressure-dependent sensitivity affects vasomotor tone and may be important in the pathophysiology of ischemia.

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PubMed1992

Differential effects of positive end expiratory pressure and cardiac tamponade on left-right ventricular mechanical function in the dog.

OBJECTIVE: The aim was to examine the hypothesis that an increased coupling occurs between the ventricles during tamponade via a ventricular-pericardial-ventricular interaction, but that ventricular coupling would be unaltered or reduced with positive end expiratory pressure (PEEP). METHODS: An in situ arrested, canine heart preparation was used. Changes in left and right ventricular pressure (dPl, dPr) and volume (dVl, dVr) caused by increasing the volume of the other ventricle were measured at normal and at matched levels of raised pericardial pressures (Pp) caused by 20 cm H2O PEEP and by tamponade. RESULTS: With PEEP, the coupling between the ventricles was unaltered when compared to control. With tamponade, dPl/dPr, dVl/dPr, dPr/dPl, and dVr/dPl increased significantly (p less than 0.05) by 0.21 (SEM 0.03, unitless), 0.45(0.04) ml.mm Hg-1, 0.18(0.03), and 0.28(0.04) ml.mm Hg-1 respectively. CONCLUSIONS: Augmented ventricular interdependence occurs during tamponade but not with PEEP, which may help to explain the different haemodynamic patterns observed under these conditions.

Animals↗
PubMed1992

Platelet amplification of vasospasm.

Platelets may accentuate vasoconstriction in stenotic arteries capable of vasomotion. We examined the interaction of platelets, stenosis, and arterial vasoconstriction in normal and stenotic arteries with intact endothelium. Beagle carotid arteries (n = 38) were isolated, removed, and placed in an in vitro perfusion system. Platelet-rich plasma (PRP) or platelet-poor plasma (PPP) were perfused through the arteries under constant pressure (100 mmHg) and a fixed distal resistance. In intact arteries without a stenosis, angiotensin II (ANG II) decreased luminal diameter without altering flow during PRP perfusion. After creating an intraluminal stenosis, vasoconstriction produced by ANG II resulted in near total cessation of flow. During PRP perfusion, this effect was amplified, demonstrating suppression of flow at significantly (P less than 0.05) lower concentrations of ANG II (PRP, ED50 = 0.03 +/- 0.01 x 10(-8) M) compared with arteries perfused with PPP (PPP, ED50 = 2.7 +/- 0.8 x 10(-8) M). This accentuated vasoconstrictor response in the presence of platelets was not blocked by SKF 96148 (a thromboxane A2 antagonist) but was abolished by ketanserin (a 5-HT2-serotonergic blocker). This increased sensitivity to vasoconstriction was not due to significant platelet plugging inasmuch as no cyclic flow reductions were observed, aspirin (acetylsalicylic acid) did not prevent this accentuated vasoconstrictor response, and adventitial administration of nitroglycerin restored flow to baseline levels. These studies illustrate that 1) platelets amplify the effect of vasoconstrictors in stenotic arteries, 2) this amplification of vasoconstriction is primarily due to platelet release of serotonin, and 3) the amplification occurs in the absence of significant platelet plugging and endothelial damage.

Animals↗
PubMed1991

Comparative significance in systolic ventricular interaction.

STUDY OBJECTIVE: The aim was to measure the systolic coupling between the ventricles and to determine the relative importance of ventricular interaction in the pressure development of each ventricle. DESIGN: Acute studies were done in dogs to measure the changes in right and left ventricular pressures (dPr, dPl) caused by sudden changes in left ventricular pressure (dPl') with release of an aortic constriction, and sudden changes in right ventricular pressure (dPr') with release of a pulmonary artery constriction, respectively. The instantaneous cross talk gain [dPr/dPl' (Klr) or dPl/dPr' (Krl)] was calculated during the ejection phase. The potential systolic pressure generated by the contralateral ventricle was evaluated as the cross talk gain multiplied by the contralateral systolic developed pressure. EXPERIMENTAL MATERIAL: Studies were done in eight random source dogs (12-18 kg), anaesthetised with sodium pentobarbitone. MEASUREMENTS AND MAIN RESULTS: The maximal Klr was lower than the maximal Krl, at 0.09 (SD 0.05) v 0.25 (0.06), and the mean Klr also was lower than the mean Krl, at 0.04 (0.02) v 0.10 (0.03), p less than 0.05. The potential right ventricular pressures developed by the left ventricle [maximum 10.3(5.6), mean 4.8(2.7) mm Hg] were not significantly different from the potential left ventricular pressures developed by the right ventricle [maximum 8.8(2.7), mean 3.4(0.7) mm Hg]. However, the ratio between the potential transmitted pressure and the measured developed pressure was greater in the right ventricle [maximum 39.0(21.1), mean 17.8(8.9)%] than in the left ventricle [maximum 11.1(7.1)%, p less than 0.05; mean 3.9(1.5)%, p less than 0.01]. This suggests that about 20-40% of the right ventricular systolic pressure may result from the left ventricle and about 4-10% of the left ventricular systolic pressure may result from right ventricle. CONCLUSIONS: Although the pressure coupling was greater in right to left ventricular interaction, right ventricular pressure generation may be more dependent on the left ventricle. Systolic ventricular interaction may be more important for right ventricular systolic function. Further, the parameters of right ventricular systolic function currently used may be considerably affected by the left ventricle.

Animals↗
PubMed1990

Effects of increased pericardial pressure on the coupling between the ventricles.

STUDY OBJECTIVE: The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered. DESIGN: Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured. EXPERIMENTAL MATERIALS: Hearts from 10 random source dogs, weight 12.5-18 kg, were used. MEASUREMENT AND MAIN RESULTS: At control pericardial pressure levels, the magnitude of the pericardial-ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18 (0.03), p less than 0.01, and dV1/dPp was significantly greater than dV1/dPr, at -0.83 (0.09) v -0.24 (0.06), p less than 0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dP1/dPr approximately, dV1/dPr approximately, dPr/dP1 approximately, and dVr/dP1 approximately increased significantly (p less than 0.05) by 0.48 (0.03), 0.67 (0.13), 0.38 (0.05), and 0.61 (0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dP1/dPr increased, from 0.51 (0.03) to 0.79 (0.01), p less than 0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42 (0.03) v 0.44 (0.04), p greater than 0.5. CONCLUSIONS: Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade.

Animals↗
PubMed1989

[Urinary tract involvement from pancreas carcinoma].

Pancreas carcinoma is sometimes notoriously difficult to diagnosis. It is well known that pancreas carcinoma can invade contiguous organs, but no attention for urinary tract involvement is paid. Urinary tract is involved at a late stage but may represent the first symptomatic evidence of disease. In such case, pancreas carcinoma can be presented initially as urologic disease and patients' symptom may not be differentiated from urinary tract disease. Computed tomographic (CT) images and medical records of 50 patients with histologically proved pancreas carcinoma were reviewed. There were 10 cases with urinary tract involvement. Those of 8 were male and 2 were female. There was a high incidence of left urinary tract involvement (left:right:bilateral = 7:2:1). Although 9 cases were pancreas body and tail carcinoma, 1 case was pancreas head carcinoma. And those stages were all in IV. All cases have confirmed evidence of urinary tract involvement at autopsy within 4 months following CT studies. IVP study was performed in 8 of these cases. We compared those IVP, CT images and findings of autopsy. In those patients, 4 cases showed direct invasion of the kidney, 5 cases showed ureteral involvement and 1 case showed metastasis to the urinary bladder and ureters. IVP showed inferior displacement of the kidney and/or ureteral displacement on the affected side. And also, collecting system distortion was demonstrated, including hydronephrosis secondary to ureteral compression. CT scan showed abnormal mass which is contiguous to the pancreas, showing compression the kidney and/or retroperitoneal extension with ureteral involvement. Metastasis to the urinary bladder is also identified. The findings of autopsy were almost the same of the CT findings. Pancreas carcinoma characteristically remains silent until little chance for cure. Although urinary tract involvement is rare, it can mimic renal and ureteral pathology. In differential diagnosis of urinary tract lesion, the disease process originated from pancreas should be included as well as from contiguous structures.

Aged↗
PubMedDate not supplied

Acute alterations in systolic ventricular interdependence-mechanical dependence of right ventricle on left ventricle following acute alteration of right ventricular free wall.

The purpose of the study was to examine whether systolic ventricular interdependence can be acutely altered by changes in the mechanical properties of the ventricular wall. In eight acute canine studies, we released an aortic constriction during diastole. We measured right ventricular (RV) pressure changes (dPr) caused by sudden changes in left ventricular (LV) pressure (dPl). Measurements were obtained during control, 10 min after right coronary artery occlusion, and then 15 min after injecting glutaraldehyde into the RV free wall. By superimposing the pressure tracings of the beats immediately before and after the aortic release, the instantaneous pressure difference ratio (dPr/dPl) was calculated during systole. Maximal value of the pressure difference ratio decreased from control 0.11 +/- 0.04 to ischemia 0.08 +/- 0.03; (p < 0.05) and increased with glutaraldehyde 0.15 +/- 0.06; (p < 0.05). Thus, acute ischemia in RV free wall decreased the magnitude of systolic ventricular interdependence from LV to RV, while glutaraldehyde, which stiffens the RV free wall, increased the magnitude.

Animals↗
PubMedDate not supplied

No change in plasma corticosterone and splenic norepinephrine during humoral and cellular immune responses to sheep erythrocytes in C3H mice.

Host responses to immune stimulation, including antigenic stimulation and inflammation, have been described to involve the central neurotransmission, the hypothalamic-pituitary adrenal (HPA) axis, and the immune system. After antigenic stimulation, it has been hypothesized that the HPA axis is involved in a feedback mechanism which limits lymphocyte expansion linked to the immune response. However, such a stimulation of the HPA axis after immunization is not consistently reported in the literature. In the present experiments, we looked for a possible activation of the HPA axis, as well as for the involvement of the sympathetic nervous system during primary and secondary antibody synthesis and cellular immunity. C3H female mice were immunized with low or high doses of sheep red blood cells which induced delayed-type hypersensitivity (DTH) or antibody synthesis, respectively. Plasma corticosterone levels remained in normal ranges whether the animals developed primary or secondary humoral response or DTH. Splenic norepinephrine (NE) levels were unchanged during cellular immunity. During primary and secondary antibody responses splenic NE levels decreased, but no difference appeared between immunized animals and controls when the splenic NE content was expressed in milligrams per spleen because of a spleen enlargement in immunized animals. From these results, it can be concluded that immune responses, antibody synthesis and cellular immunity, in opposition to inflammation, may be induced without any detectable stimulation of the HPA axis or modification of the NE input in the spleen.(ABSTRACT TRUNCATED AT 250 WORDS)

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