Vitamin D status in renal transplant recipients.

Vitamin D plays an important role in calcium homeostasis. Renal transplant recipients may be more susceptible to reduced levels because of decreased sun exposure and steroid therapy. This study aimed to determine vitamin D status after renal transplantation and its effect on parathyroid hormone (PTH) and bone mineral density (BMD). We measured serum 25-hydroxyvitamin D levels (25-OHD) in 244 renal transplant recipients, divided into two groups, 104 recently transplanted (less than 1 year) and 140 long-term. Vitamin D status was defined according to NKF/KDOQI guidelines. Mean 25-OHD levels were 33 +/- 19 nmol/L and 42 +/- 20 nmol/L, respectively, for the recent and long-term transplant recipients. Vitamin D insufficiency was present in 29% and 43%, deficiency in 56% and 46% and severe deficiency in 12% and 5%, respectively. An inverse correlation was found between logPTH and 25-OHD (r=-0.2, p= 0.019) in long-term but not in recently transplanted patients. No correlation was found between 25-OHD levels and BMD. Hypercalcaemia was present in 40% of the recently transplanted recipients and 25% of the long-term. In conclusion 25-OHD was low in virtually all of our renal transplant recipients and may aggravate secondary hyperparathyroidism, but its correction may be difficult in patients with hypercalcaemia.

Increasing myocardial oxygen demand during prolonged halothane anesthesia in dogs.

The effect of prolonged halothane anesthesia on myocardial oxygen uptake and coronary blood flow is unknown. This 5.5-hr study was undertaken to determine whether myocardial changes occur in dogs during prolonged steady-state halothane anesthesia. Hourly data were collected beginning 1.5 hr after induction of steady-state anesthesia. When compared to values obtained at 1.5 hr of halothane anesthesia, no significant myocardial changes were observed during the initial 3.5 hr. However, after 4.5 hr, mean arterial blood pressure increased 14% (P less than 0.01), coronary sinus flow increased 22% (P less than 0.05), and myocardial oxygen uptake increased 19% (P less than 0.05). At 5.5 hr mean arterial pressure was 18% (P less than 0.01), coronary sinus flow 31% (P less than 0.01), and myocardial oxygen uptake 21% (P less than 0.05) above levels measured at 1.5 hr. At 5.5 hr whole body oxygen uptake was 6% (P less than 0.01) above the 1.5 hr value. Cardiac output, heart rate, and systemic and coronary vascular resistances did not change significantly. This study demonstrates that duration of anesthesia is an important factor in determining the metabolic oxygen requirements of the heart. During prolonged anesthesia, the increase in myocardial oxygen demands may have an unfavorable effect on the myocardial oxygen supply-demand relationship.

Safety of enflurane following administration of aminophylline in experimental animals.

The induction of halothane anesthesia following intravenous administration of aminophylline may cause ventricular arrhythmias. This study was designed to determine whether induction of enflurane anesthesia following intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with 2% enflurane in the absence of aminophylline. Three additional groups of six dogs were given intravenous aminophylline, 10, 25, or 50 mg/kg, respectively, followed 3 minutes later by 2% enflurane. No arrhythmias occurred at any time in any animal. In contrast to halothane induction of enflurane anesthesia following aminophylline appears to be safe and does not cause cardiac arrhythmias.

Halothane-induced cardiac arrhythmias following administration of aminophylline in experimental animals.

Cardiac arrhythmias often occur when patients receiving aminophylline are anesthetized with halothane. This animal study was designed to define what constitute arrhythmogenic doses of aminophylline when administered before halothane anesthesia. One group of six dogs was given aminophylline, 10 mg/kg IV, followed in 3 minutes by inhalation of 1% halothane. In two additional groups of dogs the same experimental protocols were used except that aminophylline doses were 25 mg/kg and 50 mg/kg. In the first group, two of six dogs developed ventricular arrhythmias during induction of halothane anesthesia. One of six dogs given 25 mg/kg of aminophylline developed a ventricular arrhythmia. Three of six dogs given 50 mg/kg of aminophylline developed ventricular arrhythmias. Sustained ventricular arrhythmias occurred in 33% of the animals with "therapeutic" serum theophylline levels and in 33% of the animals with "toxic" levels. Induction of halothane anesthesia within 15 minutes of aminophylline administration may be dangerous and is likely to result in severe and persistent ventricular arrhythmias.

Cardiovascular effects of ketamine following administration of aminophylline in dogs.

The induction of halothane anesthesia following intravenous administration of aminophylline may cause ventricular arrhythmias. Ketamine has been recommended for anesthesia induction and maintenance in patients with asthma. This study was designed to determine whether induction and maintenance of ketamine anesthesia following intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with intravenous ketamine, 5 mg/kg, followed by infusion of 5 mg/kg/hr. Three additional groups of six dogs were given intravenous aminophylline, 10, 25, and 50 mg/kg, respectively, followed 3 minutes later by intravenous ketamine, 5 mg/kg, and a 5 mg/kg/hr ketamine infusion. No arrhythmias occurred at any time in any animal. Ketamine use following aminophylline would appear to lack arrhythmogenic potential and may be advantageous in the clinical setting.