Isoflurane-enhanced Recovery of Canine Stunned Myocardium: Role for Protein Kinase C?

Background: Isoflurane enhances the functional recovery of postischemic, reperfused myocardium by activating adenosine A1 receptors and adenosine triphosphate-regulated potassium channels. Whether protein kinase C is involved in this process is unknown. The authors tested the hypothesis that inhibition of protein kinase C, using the selective antagonist bisindolylmaleimide, attenuates isoflurane-enhanced recovery of stunned myocardium in dogs.

Methods: Fifty dogs were randomly assigned to receive intracoronary vehicle or bisindolylmaleimide (2 or 8 [mu]g/min) in the presence or absence of isoflurane (1 minimum alveolar concentration). Five brief (5 min) coronary artery occlusions interspersed with 5-min reperfusion periods followed by 180 min of final reperfusion were used to produce myocardial stunning. Hemodynamics, regional segment shortening, and myocardial blood flow (radioactive microspheres) were measured at selected intervals.

Results: There were no differences in baseline hemodynamics, segment shortening, or coronary collateral blood flow between groups. Isoflurane significantly (P < 0.05) decreased heart rate, mean arterial pressure, rate pressure product, and the maximum rate of increase of left ventricular pressure (+dP/dtmax) in the presence or absence of bisindolylmaleimide. Sustained contractile dysfunction was observed in dogs that received vehicle (recovery of segment shortening to 12 +/- 8% of baseline), in contrast to those that received isoflurane (75 +/- 7% recovery). Bisindolylmaleimide at a dose of 2 [mu]g/min alone enhanced recovery of segment shortening (50 +/- 7% of baseline) compared with vehicle-pretreated dogs, and isoflurane in the presence of 2 [mu]g/min bisindolylmaleimide further enhanced recovery of contractile function (79 +/- 8% of baseline). In contrast, 8 [mu]g/min bisindolylmaleimide alone (32 +/- 12%) or combined with isoflurane (37 +/- 17%) did not enhance recovery of segment shortening compared with vehicle-pretreated dogs.     

Bridge to recovery for postcardiotomy failure: is there still a role for centrifugal pumps?

BACKGROUND: Early implantation of centrifugal devices in patients with postcardiotomy cardiogenic shock may provide a bridge to recovery and allow subsequent long-term survival. METHODS: Since January 1989, 62 patients were supported with centrifugal pumps because of failure to wean from cardiopulmonary bypass. Indications were postcardiotomy cardiogenic shock (PCCS) (n = 60), bridge to cardiac retransplantation (n = 1), and right ventricular failure (n = 1). Patients' ages ranged from 23 to 78 years; 40 were men (65%), and 22 were women (35%). Twenty-two patients (35%) had a left ventricular assist device; 9 patients (15%) had a right ventricular assist device; and 31 patients (50%) had a biventricular assist device. Length of support ranged from 1 day to 19 days. RESULTS: Forty-two patients (68%) were weaned successfully; 27 patients survived to discharge (44%). Complications included bleeding (n = 41, 66%), renal failure (n = 28, 45%), and respiratory failure (n = 26, 42%). Currently, 23 patients survived 10 or more years (n = 1), 6 to 10 years (n = 7), 1 to 5 years (n = 10), and less than 1 year (n = 5). CONCLUSIONS: Centrifugal pumps are available, easy to use, and relatively inexpensive. Our experience justifies their continued use as a bridge to recovery for patients with postcardiotomy cardiogenic shock, despite the availability and increasing use of more expensive devices.     

Head injury outcome prediction: a role for protein S-100B?

INTRODUCTION: Prediction of the likely outcome of head injury from the outset would allow early rehabilitation to be targeted at those with most to gain. Clinical evaluation of a head injured patient may be confounded by intoxicants such as alcohol. Imaging modalities are insensitive (CT) or impractical (MR) for screening populations of such patients. A peripheral marker that reflected the extent of brain injury might offer an objective indication of likely adverse sequelae. This review evaluates the evidence for Protein S-100B as such a marker. METHODS: A search of published literature revealed 18 studies designed to evaluate the relation between serum S-100B and measures of outcome after head injury. RESULTS: A cut-off point of 2.5microg/L is related to dependent disability in those presenting with low conscious level, and may be a specific test for this. There appears to be a relation between initial serum S-100B concentration and measures of disability as well as post-concussion symptoms for those with seemingly mild injuries. There does not appear to be a relation between S-100B and measures of neuropsychological performance. CONCLUSION: Patients with high levels of S-100B at initial assessment (>2.5microg/L) may represent a high risk group for disability after head trauma.     

Management of glenohumeral arthritis: a role for arthroscopy?

When nonoperative measures fail in the treatment of glenohumeral arthritis, arthroscopy has emerged as a viable therapeutic option. It is valuable as a diagnostic and therapeutic intervention and has a low morbidity and low complication rate. Arthroscopic techniques can be performed in the younger patient or athlete wishing to delay arthroplasty or in the elderly patient with associated comorbidities wishing to avoid a larger operation. In those with inflammatory arthropathies, arthroscopy with associated debridement and synovectomy can relieve pain, improve function, and delay progression of the disease. In the athlete and young patient with osteoarthritis, arthroscopy allows recognition and treatment of coexisting pathologies in which procedures such as subacromial decompression and capsular release have proven to be of benefit. Arthroscopic debridement, abrasion arthroplasty, and microfracture techniques seem to be of some benefit; however, it remains unclear who the ideal candidate is. Overall it is generally viewed that patients improve and benefit most when intervention is early in the course of the disease. Although the role of arthroscopy in the treatment of glenohumeral arthritis is evolving, in certain situations and patients it is thus a viable option and another tool in the armamentarium of the orthopedic surgeon.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

Depression: a role for neurosurgery?

After providing an overview of depression this article briefly reviews the development of psychosurgery and outlines the current procedures in use world wide. Stereotactic subcaudate tractotomy (SST) is described in particular detail, and the rationale for its use in the treatment of resistant depression is then discussed by considering the findings of neuropsychological, neurophysiological and neuroimaging studies. The emerging evidence suggests that the prefrontal cortex subserves an essential function in emotion and that disruption of its connections modifies mood.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.     

The role of CPI-17 in vascular calcium sensitivity regulated by protein kinase Cα and Cε in rats with hemorrhagic shock

Objective To observe the role of PKC-potentiated inhibitory protein for protein phos-phatase 1 of 17×103(CPI-17) in vascular calcium sensitivity regulatedy by protein kinase Cα (PKCα) and Cε (PKCε) in rats with hemorrhagic shock (HS). Methods Eight Wistar rats were used to reproduce 2 h HS model. Superior mesenteric artery (SMA) rings from HS rats were randomly divided into 2 h shock group( without treatment), PKCα agonist group (with addition of thymelea toxin into the nutrient solution), CPI-17 antibody + PKCα agonist group [ incubation with thymelea toxin and CPI-17 antibody (1: 800)], PKCε agonist group ( with addition of carbachol into the nutrient solution), and CPI-17 antibody + PKCe ag-onist group [ incubation with carbachol and CPI-17 antibody (1:800)]. SMA rings from another eight nor-mal rats were used as normal control group. Calcium sensitivity indices (Emax, pD2) of SMA rings were measured by isolated organ perfusion system. Hypoxic VSMCs in primary culture were randomly divided into 2 h hypoxia group, PKCct agonist group ( with above-mentioned treatment), PKCε agonist group ( with a-bove-mentioned treatment), normal VSMCs were used as normal control group. Protein expression and phos-phorylation of CPI-17 were measured via Western blot. Results Emax and pD2 in all the experimental groups were lower than those in normal control group (P<0.01). Emax in PKCα agonist group and PKCε agonist group was increased (5.8±0.8, 5.8±0.9 mN, respectively) as compared with that of 2 h shock group (4.1±0.6 mN, P <0.01 ). Protein expression and phosphorylation of CPI-17 in VSMC were signifi-cantly decreased in 2 h hypoxia group, compared with those in normal control group (P<0.05 ), and those in PKCα agonist and PKC agonist groups (P<0.05 or P<0.01 ). Conclusions PKCα and PKCε may regulate vascular calcium sensitivity through change in protein expression and activity of CPI-17 in HS rats.