Impacts of ambient temperature on the burden of bacillary dysentery in urban and rural Hefei, China.

Bacillary dysentery continues to be a major health issue in developing countries and ambient temperature is a possible environmental determinant. However, evidence about the risk of bacillary dysentery attributable to ambient temperature under climate change scenarios is scarce. We examined the attributable fraction (AF) of temperature-related bacillary dysentery in urban and rural Hefei, China during 2006-2012 and projected its shifting pattern under climate change scenarios using a distributed lag non-linear model. The risk of bacillary dysentery increased with the temperature rise above a threshold (18·4 °C), and the temperature effects appeared to be acute. The proportion of bacillary dysentery attributable to hot temperatures was 18·74% (95 empirical confidence interval (eCI): 8·36-27·44%). Apparent difference of AF was observed between urban and rural areas, with AF varying from 26·87% (95% eCI 16·21-36·68%) in urban area to -1·90% (95 eCI -25·03 to 16·05%) in rural area. Under the climate change scenarios alone (1-4 °C rise), the AF from extreme hot temperatures (>31·2 °C) would rise greatly accompanied by the relatively stable AF from moderate hot temperatures (18·4-31·2 °C). If climate change proceeds, urban area may be more likely to suffer from rapidly increasing burden of disease from extreme hot temperatures in the absence of effective mitigation and adaptation strategies.

Effect of diurnal temperature range on the outpatient visits for acute bronchitis in children: a time-series study in Hefei, China.

OBJECTIVES: To determine the relationship between diurnal temperature range (DTR) and outpatient visits for childhood acute bronchitis (AB) in Hefei, China, to analyze whether DTR effect was delayed, and to explore the susceptible populations. STUDY DESIGN: An ecological study. METHODS: A Poisson generalized linear regression model combined with a distributed lag non-linear model was used to analyze the relationship between DTR and childhood AB from Hefei, China during 2010-2013, after adjusting for long-term trend and seasonality, mean temperature and relative humidity. RESULTS: An adverse effect of DTR on childhood AB was observed, and the impact of DTR was greatest at three days lag, with a 1.0% (95% confidence interval = 0.5-1.6%) increase of AB cases per 1 °C increment of DTR. Female children and children aged 0-4 years appeared to be more vulnerable to DTR effect than other children. CONCLUSIONS: Our study suggests that large DTR may increase the incidence of childhood AB in Hefei, particularly for those who are female and young. Caregivers and health practitioners should be made aware of the potential threat posed by large DTR.

The TNFAIP3 polymorphism rs610604 both associates with the risk of psoriasis vulgaris and affects the clinical severity.

BACKGROUND: Genome-wide association studies in white and Chinese Han populations have found that the single-nucleotide polymorphism (SNP) rs610604, at the tumour necrosis factor (TNF)-α-induced protein 3 (TNFAIP3) locus, is associated with psoriasis, and is also associated with response to TNF blockade in psoriasis. AIM: To examine whether this SNP is also associated with the clinical traits of psoriasis vulgaris (PV). METHODS: A hospital-based case-control study was performed, which involved 647 subjects [351 patients with PV and 296 healthy controls (HC)]. The rs610604 variants were typed using a SNaPshot assay. RESULTS: Both the G allele and the dominant model genotype (GG + GT) of rs610604 were associated with risk of PV (OR = 1.53; P = 0.01 and OR = 1.68, P < 0.01, respectively). In genotype-phenotype analysis, both the G allele and the GG + GT genotype were also associated with the clinical severity of PV. Severe cases [Psoriasis Area and Severity Index (PASI) > 6] had a higher frequency of the G allele and the GG + GT genotype compared with mild cases (PASI ≤ 6) (OR = 2.03, P = 0.001 and OR = 2.46, P < 0.001, respectively). In addition, rs610604 was significantly associated with almost all of the phenotypes in subphenotype-control analyses. CONCLUSIONS: SNP rs610604 in the TNFAIP3 locus is associated with the clinical severity of PV in a Chinese Han population.

Potential relationship between the canonical Wnt signalling pathway and expression of the vitamin D receptor in alopecia.

BACKGROUND: Vitamin D receptor (VDR) is expressed in dermal papilla cells and in the epidermis of the hair follicle. Patients with alopecia areata (AA) and alopecia universalis (AU) have VDR mutations. AIMS: We investigated expression of VDR in isolated hair follicles and epidermal keratinocytes from patients with AA or AU, and assessed changes in the expression of Wnt signalling regulation factors to determine the relationship between the occurrence of AA or AU and decreased expression of VDR. METHODS: Immunohistochemistry was performed for canonical Wnt signalling molecules, VDR, and proliferation and differentiation markers in the skin tissue of patients with AA or AU. After VDR small interfering RNA or Dickkopf-1 (DKK1) treatment of follicle dermal papilla (DP) cells, expression of VDR and Wnt signalling molecules was determined. DKK1 was used to treated keratinocytes and DP cells in a transwell coculture system. Western blotting analysis was performed to assay for VDR and ß-catenin. RESULTS: Expression of Wnt/ß-catenin signals and VDR was decreased in AA or AU lesions compared with nonlesional skin. Inhibition of Wnt/ß-catenin signals and VDR influenced differentiation and proliferation of epidermis and hair follicles. In the transwell coculture system, DKK1 reduced the expression of VDR and ß-catenin in cells in a dose-dependent manner. CONCLUSIONS: This study demonstrates that the decreased expression of VDR in AA and AU lesions is related to decreased expression of Wnt/ß-catenin signals, which inhibits proliferation and differentiation of hair follicles and epidermal cells.

Crystal structure of a three-tetrad, parallel, K+-stabilized human telomeric G-quadruplex at 1.35†Šresolution.

The crystal structure of the G-rich human telomeric DNA Tel22 has been determined at 1.35 Šresolution in space group P6. Tel22 forms a non-canonical DNA structure called the G-quadruplex. The space group and unit-cell parameters are comparable to those in the crystal structures with PDB codes 6ip3 (1.40 Šresolution) and 1kf1 (2.15 Šresolution). The G-quadruplexes are highly similar in all of the structures. However, this structure of Tel22 displays clear density for polyethylene glycol and two potassium ions, which are located outside the ion channel in the G-quadruplex and play an important role in stabilizing the crystal contacts. In addition, 111 water molecules were identified (compared with 79 and 68 in PDB entries 6ip3 and 1kf1, respectively) that participate in intricate and extensive networks providing high stability to the G-quadruplex.

Clinical characteristics and risk of melanoma development from giant congenital melanocytic naevi in Korea: a nationwide retrospective study.

BACKGROUND: Giant congenital melanocytic naevi (GCMN) are known risk factors for the development of melanoma. However, melanoma risk among Asians is rarely evaluated. OBJECTIVES: To evaluate the clinical characteristics and risk of melanoma development from GCMN in Koreans, we performed a nationwide retrospective cohort study in Korea. GCMN were defined as those comprising ≥5% body surface area in children or measuring ≥20cm in adults. METHODS: In total, 131 patients with GCMN were enrolled, with a mean age of 10·3years (range: birth-70years). RESULTS: The posterior trunk was the most common site (67, 51·1%), followed by lateral trunk, anterior trunk, legs, both anterior and posterior trunk, buttocks, and arms. Satellite naevi were present in 69 cases (52·7%), and axial areas were more commonly involved in patients with satellite naevi than in those without satellite lesions. Atypical features such as rete ridge elongation and bridges were seen, and, among these, pagetoid spread and ballooning cell changes were more common in patients <4years old. Proliferative nodules were found in three cases. Melanomas had developed in three of 131 patients (2·3%; a 6-year-old girl, a 14-year-old girl and a 70-year-old man), and the incidence rate was 990 per 100000 person-years. Melanomas in these three patients consisted of two cutaneous melanomas and one extracutaneous meningeal melanoma. CONCLUSIONS: We should be aware of melanoma development from GCMN, and lifelong follow-up is required due to the risk of melanoma arising in GCMN.

Genesis of a highly pathogenic and potentially pandemic H5N1 influenza virus in eastern Asia.

A highly pathogenic avian influenza virus, H5N1, caused disease outbreaks in poultry in China and seven other east Asian countries between late 2003 and early 2004; the same virus was fatal to humans in Thailand and Vietnam. Here we demonstrate a series of genetic reassortment events traceable to the precursor of the H5N1 viruses that caused the initial human outbreak in Hong Kong in 1997 (refs 2-4) and subsequent avian outbreaks in 2001 and 2002 (refs 5, 6). These events gave rise to a dominant H5N1 genotype (Z) in chickens and ducks that was responsible for the regional outbreak in 2003-04. Our findings indicate that domestic ducks in southern China had a central role in the generation and maintenance of this virus, and that wild birds may have contributed to the increasingly wide spread of the virus in Asia. Our results suggest that H5N1 viruses with pandemic potential have become endemic in the region and are not easily eradicable. These developments pose a threat to public and veterinary health in the region and potentially the world, and suggest that long-term control measures are required.

The combination of polymorphisms within MCP-1 and IL-1beta associated with ulcerative colitis.

Monocyte chemoattractant protein-1 (MCP-1) is a chemokine involved in monocyte recruitment to sites of inflammation. Raised level of MCP-1 has been widely demonstrated in the intestinal mucosa of patients with ulcerative colitis (UC), suggesting an important role of MCP-1 in the pathogenesis of UC. The -2518A/G polymorphism in the promoter region of MCP-1 gene affecting its transcriptional activation has been reported recently. In order to assess the potential role of this polymorphism in UC, we examined its distribution in 162 unrelated UC patients and 203 healthy controls. In addition, considering the gene regulatory association between interleukin-1beta (IL-1beta) and MCP-1, we further examined whether the gene polymorphisms between MCP-1 and IL-1beta exert synergetic effects on risk of UC. Our results show that the distribution of MCP-1 genotype or allele frequencies between UC patients and controls was not significantly different; however, the association between the polymorphism of MCP-1 -2518 GG and the polymorphism of IL-1beta-511 T in UC patients is significant (OR 2.062, 95% CI 1.034-4.113, P = 0.038). This is the first report describing the association between MCP-1 polymorphism and UC, and our data suggest that the MCP-1 -2518 polymorphism itself does not represent an independent genetic risk factor for UC. In contrast, the combination polymorphisms between MCP-1 and IL-1beta can increase UC risk significantly, which might help us understand the molecular mechanism underlying the development of UC.

Changes in lymphocyte subsets in the peripheral blood of patients with active pulmonary tuberculosis.

The aim of this study was to determine the percentage of lymphocyte subsets in peripheral blood in patients with active tuberculosis. A total of 21 patients with active tuberculosis and 15 healthy volunteers were included in the study. T-lymphocyte subsets, B-lymphocytes (CD19(+) cells), natural killer (NK) cells and cells positive for costimulatory molecules CD28 and CD152 were evaluated using flow cytometry. Patients with tuberculosis had a significantly decreased percentage of CD3(+) and CD3(+)CD4(+) cells, and a significantly decreased ratio of CD3(+)CD4(+) to CD3(+)CD8(+) cells compared with healthy controls. In contrast, the percentage of B-cells (CD19(+) cells), CD3(+)CD8(+) cells, CD28(+) cells, CD152(+) cells, and subpopulations of CD4(+)CD152(+), CD8(+)CD152(+) and CD8(+)CD28(+) T-cells were all significantly increased compared with healthy controls. There were no statistically significant differences in the percentages of NK cells or CD4(+)CD28(+) cells between patients and controls. These results indicate that patients with active tuberculosis have altered lymphocyte homeostasis.

Outbreak of human metapneumovirus infection in psychiatric inpatients: implications for directly observed use of alcohol hand rub in prevention of nosocomial outbreaks.

Nosocomial outbreaks of infectious diseases in psychiatric facilities are not uncommon but the implementation of infection control measures is often difficult. Here, we report an outbreak of an acute respiratory illness in a psychiatric ward between 29 July and 20 August 2005 involving 31 patients. Human metapneumovirus was detected in seven (23%) patients by reverse transcription-polymerase chain reaction and nucleotide sequencing. A review of outbreak surveillance records showed that six nosocomial outbreaks occurred in the year 2005, of which four (67%) were confirmed or presumably related to a respiratory viral infection. Directly observed deliveries of alcohol hand rub 4-hourly during daytime to all psychiatric patients was instituted in December 2005. Only one nosocomial respiratory viral outbreak occurred in the following year. The total number of patients and staff involved in nosocomial outbreaks due to presumed or proven respiratory virus infections decreased significantly from 60 to six (P<0.001), whereas those due to all types of nosocomial outbreaks also decreased from 70 to 24 (P=0.004). Alcohol hand rub has been shown to have potent bactericidal and virucidal activity against a wide range of nosocomial pathogens. Regular use of directly observed alcohol hand rub may decrease the incidence and scale of nosocomial outbreaks due to enveloped respiratory viruses especially in mentally incapacitated patients.

Expression and clinical significance of aquaporin-1 and ET-1 in urine of children with congenital hydronephrosis.

OBJECTIVE: Congenital hydronephrosis is induced by congenital obstruction of uretero pelvic junction, bladder vesicoureteral reflux, posterior urethral valve, stricture of ureter end and ureterocyst, which is extremely apt to cause end-stage renal failure in children. It becomes significant to explore the expression profile and clinical significance of aquaporin-1 (AQP-1) and ET-1 (endothelin-1) in the urine of children with congenital hydronephrosis. PATIENTS AND METHODS: 80 cases of children with congenital hydronephrosis were selected to be the observation group and another 40 cases of children with other diseases were served as control group. Pre-operative morning urine, intra-operative renal pelvis urine and morning urine at the 7th day after the operation of all the children were collected for the detection of the level of ET-1, Cr level and AQP1 in the urine. Urine various indexes of different diseases stages in children of both groups were compared. RESULTS: There was no significant difference between children with mild and children in control group (p > 0.05). In the observation group, the AQP-1 level during the operation was significantly lower than that before operation, but it was significantly higher in post-operation than that during the operation, which was still lower than that in control group (p < 0.05). Urine ET-1 level in observation group and its positive rate were significantly higher than that in control group (p < 0.05). Serum stress indexes in each stage of the observation group were significantly higher than that in control group (p < 0.05). CONCLUSIONS: The expression levels of urine AQP-1 and ET-1 of children with congenital hydronephrosis were obviously increased. The AQP-1 level during the operation was lower than that before operation. This post-operation level was significantly higher than before the operation. The expression of AQP-1 and ET-1 could be used as important indexes for clinical diagnosis.

Galectin-1 induces hepatocellular carcinoma EMT and sorafenib resistance by activating FAK/PI3K/AKT signaling.

Galectin-1 (Gal-1) is involved in several pathological activities associated with tumor progression and chemoresistance, however, the role and molecular mechanism of Gal-1 activity in hepatocellular carcinoma (HCC) epithelial-mesenchymal transition (EMT) and sorafenib resistance remain enigmatic. In the present study, forced Gal-1 expression promoted HCC progression and sorafenib resistance. Gal-1 elevated αvß3-integrin expression, leading to AKT activation. Moreover, Gal-1 overexpression induced HCC cell EMT via PI3K/AKT cascade activation. Clinically, our data revealed that Gal-1 overexpression is correlated with poor HCC survival outcomes and sorafenib response. These data suggest that Gal-1 may be a potential therapeutic target for HCC and a biomarker for predicting response to sorafenib treatment.

A novel locus for autosomal dominant non-syndromic deafness (DFNA41) maps to chromosome 12q24-qter.

We have studied 36 subjects in a large multigenerational Chinese family that is segregating for an autosomal dominant adult onset form of progressive non-syndromic hearing loss. All affected subjects had bilateral sensorineural hearing loss involving all frequencies with some significant gender differences in initial presentation. After excluding linkage to known loci for non-syndromic deafness, we used the Center for Inherited Disease Research (CIDR) to test for 351 polymorphic markers distributed at approximately 10 cM intervals throughout the genome. Analysis of the resulting data provided evidence that the locus designated DFNA41 maps to a 15 cM region on chromosome 12q24.32-qter, proximal to the marker D12S1609. A maximum two point lod score of 6.56 at theta=0.0 was obtained for D12S343. This gene is distal to DFNA25, a previously identified locus for dominant adult onset hearing loss that maps to 12q21-24. Positional/functional candidate genes in this region include frizzled 10, epimorphin, RAN, and ZFOC1.

Disassociation of intrinsic and haemodynamic responses in stenotic arteries.

OBJECTIVE: In stenotic arteries, constriction can decrease intraluminal pressure, which in turn can further decrease vessel size. Because of these pressure changes, the hypothesis that haemodynamic responses may be significantly different from intrinsic smooth muscle responses in stenotic arteries was tested. METHODS: In rabbits (n = 16), one iliac artery was denuded (stenotic), and the other iliac artery was untouched (hypercholesterolaemic). The rabbits were placed on a 2% cholesterol diet for three weeks. Iliac arteries from these and normal (n = 8) rabbits were removed and studied as rings or perfused segments. RESULTS: In arterial rings, maximal isometric tension in response to noradrenaline was significantly (p < 0.05) greater in hypercholesterolaemic [0.59(SEM 0.03) x 10(6) dynes.cm-2] and normal arteries 0.63(0.04) compared with stenotic arteries [0.28(0.04)]. Normal [EC50 = 6.99(0.07), -log(M)] and hypercholesterolaemic [EC50 = 7.00(0.12)] rings were more sensitive (p < 0.05) to noradrenaline than stenotic rings [EC50 = 6.49(0.24)]. All arterial rings vasodilated in response to glyceryl trinitrate, and changes in isometric tension occurred over a 1000-fold change in noradrenaline or glyceryl trinitrate concentration. In normal and hypercholesterolaemic arteries, flow was unaltered even at the highest noradrenaline concentration. In stenotic arteries, noradrenaline decreased distal pressure from 76.9(5.4) to 24.3(7.3) mm Hg (p < 0.05) and flow from 17.9(1.6) to 6.4(1.8) ml.min-1 (p < 0.05). After noradrenaline decreased flow, glyceryl trinitrate did not always successfully vasodilate the stenotic arteries and thereby re-establish flow. Lastly, in stenotic arteries, most of the haemodynamic response occurred at one incremental dose of noradrenaline or glyceryl trinitrate. CONCLUSION: Fundamentally different haemodynamic responses occur in stenotic v normal and hypercholesterolaemic arteries. As the intrinsic smooth muscle responses (from the stenotic rings) are weaker, the augmented responses in whole stenotic segments are probably related to the intraluminal pressure changes.

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.

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.

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.

The left ventricle affects the duration of right ventricular ejection.

OBJECTIVE: The aim was to determine if rapid changes in left ventricular pressure can acutely alter right ventricular systolic pressure and thus influence the length of right ventricular ejection. METHODS: The experiments were performed in six open chest anaesthetised dogs, weight 18-25.5 kg. Left and right ventricular pressures and pulmonary blood flow were recorded continuously as left ventricular pressure was abruptly decreased by opening a shunt in systole. From these data, the pressure and flow changes and the duration of right ventricular ejection were determined. RESULTS: Opening the left ventricular shunt caused left ventricular pressure to fall from 94.1(SD 10.5) to 62.6(11.3) mm Hg (p < 0.01), right ventricular pressure to fall from 30.3(4.6) to 27.0(3.6) mm Hg (p < 0.01), and pulmonary flow to fall from 69.5(14.2) to 57.5(13.9) ml.s-1. The duration of right ventricular ejection, determined from pulmonary flow, also decreased from 192.7(22.7) to 157.2(18.7) ms (p < 0.05) and was significantly related to the length of left ventricular systole. Time between end diastole and peak negative dP/dt decreased for both left and right ventricle. Left and right ventricular time intervals were related before (r = 0.99) and after (r = 0.75) opening the shunt. CONCLUSIONS: The duration of right ventricular ejection was decreased by a sudden decrease in left ventricular afterload and was significantly related to the length of left ventricular systole. The duration of right ventricular ejection may be coupled with left ventricular contraction through ventricular interdependence.

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.